I don’t often provide a lot of background into HIV science or HIV denial, instead referencing previous posts I’ve made or websites such as AIDStruth.org or the NIAID fact sheet. For those of you who may be looking for more background in a nice, concise format, HealthDot has a 20-minute interview with John Moore and Jeanne Bergman (both who help run AIDStruth.org) regarding the issues of HIV science and HIV denial–including a few minutes on what journalists can do.

Comments

  1. #1 Joe
    June 29, 2007

    Tara, Thanks for all this. I expect you will be inundated by more denialists. Fifteen years ago I was pretty well informed on the subject because I was designing and synthesizing protease inhibitors. The question I have for all the denialists is: what qualifies you to come to your conclusions?

    This is not a social issue that is decided by persuasion; this is a technical issue that is decided on the data, by people qualified to understand the data.

    There is an article (warning- PDF) that I find useful, it is about how people who know the least about a subject have the strongest opinions http://www.apa.org/journals/features/psp7761121.pdf .

    Before denialists play the Duesberg card- I have read his early arguments, while doing so I thought “there must be a psychiatric diagnosis for his condition.” Sure, he is an authority on retroviruses; but, on HIV-AIDS he is irrational.

  2. #2 apy
    June 29, 2007

    If I remember correctly, some people such as Lynn Margulis appear to not be convinced HIV causes AIDS. Do their ideas have any ground to them? Someone like Dr Margulis have a fairly strong scientific background and don’t appear to just be some crackpot.

  3. #3 Richard Jefferys
    June 29, 2007

    Lynn Margulis got her views from Peter Duesberg & Harvey Bialy and particularly from Harvey Bialy’s biography of Duesberg. The fact that Margulis recently parroted those views in a blog posting (including canards like all pregnant women testing positive) suggests that whatever her scientific background, it has not served her well on this topic. I do not know enough about her to know if she’s a crackpot, but the people she’s getting her information from certainly are, e.g. here is Harvey Bialy attempting to “debate” Nick Bennett:

    http://deanesmay.com/posts/1105628771.shtml

    Bialy subsequently admitted that “Eccles the Idiot” was also him.

  4. #4 Adele
    June 29, 2007

    Thanks for linking that interview Tara. I’m so jealous of how Jeanne Bergman and John Moore communicate! The analogies were just great.

  5. #5 apy
    June 29, 2007

    I suppose we can’t be masters of all knowledge. Has she submitted any sort of withdrawal if her statements?

  6. #6 cooler
    June 29, 2007

    I thought the denialists were nuts until i saw the video Hiv Fact or fraud last summer. Its pretty rude that many reputable scientists have questioned the hiv hypothesis, and have been insulted by many. Here is the video I saw last Year.

    http://video.google.com/videoplay?docid=5064591712431946916

    Keep in mind that most scientists who question hiv have no conflicts of interest, unlike John Moore.

    People question HIV because there is no reliable animal model (virtually every animal injected does not die of aids) and there is not much virus present, (its only in a small fraction of T cells) Like 1 in a hundred or so.

    Many take the middle road, Like Luc montagnier the discoverer of HIV, Who in his book “virus” in 2000 still stresses the need for co factors, specifically shyh ching Lo’s mycoplasma penetrans. This microbe causes disease and death in every animal injected as lo showed. DR. Nicolson has found this microbe via pcr in CFS, ALS, GWI and you can see his research here.

    http://www.aegis.com/pubs/atn/1990/ATN09501.html

    Garth Nicolsons new book must be read about mycoplasma and Gulf war Syndrome.

    http://www.projectdaylily.com

    Im not saying that HIV does or Does not cause AIDS but there needs to be more study, and scientists who questioned should be debated publicly, not insulted personally.

  7. #7 Dan
    June 29, 2007

    Oh dear,

    Tara’s doing some “damage control”.

    Another study comes out (see sidebar) that should get any thinking person to question which way is “up” in “AIDS research”.

    I like the way Jeffreys basically states the Lynn Margulis can’t think for herself. Obviously, Duesberg needs to hold her hand, otherwise she wouldn’t question the HIV=AIDS hypothesis. Lame

    Anyhoo,
    in response to “Joe”, who’s aware that this really isn’t a scientific issue, but a sociolgical one (but states the opposite)…as soon as you science folks lose the gays on this one, it’s a done deal. San Diego’s Gay Lesbian Times recently published an article that gave the dissidents a fair shake. The editor goes on to say that the GLT will continue to keep the debate open. Oh, dear…

  8. #8 Adele
    June 29, 2007

    I don’t think Dr. Margulis retracted. I don’t know her but from what she says I think she has a very regimented anti establishment world view. Not a surprise I guess since she got alot of flak for her own contirbutions to symbiosis theory back then. Also the main denialists are good friends with Margulis. And she at least when she made those statements had only read denialists not the published science.

    The problem is, the establishment isn’t always wrong or always completely wrong or always made up only of capitalist pigs.

  9. #9 Richard Jefferys
    June 29, 2007

    Well, if saying “you’re all nuts” is offering to keep the debate open. It could have positive effects though, maybe they can get more of them to renounce their past homophobic comments. Do you see Margulis’s statement that all pregnant women test HIV positive as a triumph of independent thinking?

  10. #10 Dan
    June 29, 2007

    Richard,

    go back and read the whole statement by the editor.

    I’m sure he’s quite well aware of the bold step his paper has taken, so, unfortunately, he’s got to do some token dissident-bashing. He does go on to say that the debate should be kept open…which is a terribly inconvenient thing for those who promote the AIDS paradigm. They don’t want debate. Debate=bad!

    If you stood on such firm ground, you would enter debate with open arms and minds. And! If you were the scientists you romanticize yourselves to be, you’d understand that any question or challenge can be revisited, including a complete revision of a paradigm:)

  11. #11 Nullifidian
    June 29, 2007

    Keep in mind that most scientists who question hiv have no conflicts of interest, unlike John Moore.

    Don’t they?

    Take Harvey Bialy for an example. He might not have any perceived financial conflicts of interest, but those aren’t the only conflicts of interest worth considering. In fact, a more salient conflict of interest worth considering is Harvey Bialy’s raging and mentally unbalanced hate of homosexuals. In his case, AIDS denialism is either a way of attempting to convince HIV-positive homosexuals the treatment that they need and so contributing to their deaths, or a way of shifting the blame for the disease from an ethically neutral virus to a “lifestyle disease” for which he can blame homosexuals. Perhaps it’s a bit of both. In either case, dispassionate evaluation is not common to HIV-denialists.

  12. #12 apy
    June 29, 2007

    The claim that debate=bad for those that “promote the AIDS paradigm” is a bit off point isn’t it? I am not a doctor nor do I have any experience in AIDS research, but from what I’ve been reading neither do the denialists. Debate is certainly useful when the two parties of relatively equal understanding of the concepts. It seems like those who “promote the AIDS paradigm” have been hearing the same arguments over and over and have promptly shown that the research disagrees. At this point, what use is debate?

    I apologize if what I have said is off base, I have just been reading up on the AIDSTruth website, so perhaps my understanding of the current situation is poor.

  13. #13 Dan
    June 29, 2007

    Apy,

    do you watch “The Simpsons”?

    You sound like Ralph Wiggum.

    Lisa’s 2nd grade class had just gotten finished watching a film about the evils of vegetarianism where vegetarians were described as “grade A morons”. The children, young and easily susceptible to propagandam, started calling Lisa (a vegetarian) a “grade A moron” for not eating the tripe presented to them.

    The fact that you call people “denialists”, shows that you’ve just watched the film (AIDStruth).

  14. #14 Adele
    June 29, 2007

    Insults based on “The Simpsons”? Really dan. That’s almost as good as cooler/911Truther BillyBipBip’s comment consisting almost completely of the word “woo” and variations on it.

  15. #15 apy
    June 29, 2007

    I preceded and ended my comment with the fact that I am rather new to this entire discussion. I am certainly willing to educate myself more if you would provide information rather than insults.

  16. #16 cooler
    June 29, 2007

    I was mocking you, you’re the one that said woo first. I propose a new law that anyone over 80 years old can not say “woo” LOL

  17. #17 Dan
    June 29, 2007

    Apy,

    For a site that isn’t high in the google ratings, and presumably gets only 150 hits a day, you seemed to find AIDStruth without a problem.

    You’re willing to educate yourself. Are you eager to educate yourself?

    If you’re eager, you’ll go out and read everything you can and discern for yourself what’s going on. Or you can just rely on AIDStruth. Your choice.

  18. #18 Adele
    June 29, 2007

    apy,

    If you want to look at “alternative” sources of information, here are some ideas.

    Barnesworld dot blogs dot com This was set up by Harvey Bialy who’s views on homosexuality were mentioned up there and a right-wing lawyer whose employers were even embarased by this. Some of the articles on the site talk about HIV and AIDS. Bialy also photoshops alot of monkeyheads onto photos of John Moore and he had one of Barack Obama as Osama bin Laden. Definitely one of your more intellectual denialist pages.

    newaidsreiview dot org This one is from a long time denialist “journalist” named Liversedge. There isn’t much science on it but you can see more photos of monkeys and John Moore and read amusing arguments between people like “Forty” and “Pope” a guy named Claus Jensen about if John Moore is a closet denialist.

    rethinkingaids dot com Has alot of links to other HIV denialist sites and it doesn’t have such a distracting thing with ridiculing John Moore. The president is Etienne Deharven who is a emeritus scientist. They have a list of people who supposedly think HIV doesn’t cause AIDS. The problem with it, alot of people on there never signed it or they’re dead, of AIDS. Also denialists like to say everyone who’se on the list is a scientist but they’re not.

    duesberg dot com From the head honcho of bad science himself. Has all his like three thousand bad reviews linked legally or illegally I don’t know. It all makes sense when you read it until you start looking at the references he uses and there are alot of them, he’s lying about it all or using bad logic. All the time.

    alive and well dot org. This one wants HIV positive mothers breastfeed their kids even though breastfeeding is a transmission risk. People on their board are people who make money “treating” these patients with “alternative” medicine. Cooler would call it woo. I call it cynicism and conflict of interest too.

    There are more but they’re all linked together. Read them but be critical. I’ve read most of em and I could lose one hand and still have enough fingers to count the facts I saw.

  19. #19 Evion
    June 29, 2007

    Not all of us are microbiologists or virologists, yet we have an important obligaton to question academic HIV research, and demand an accounting, especially when HIV research is suspected to be tainted by academic misconduct, unethical or immoral conduct, or influenced by drug company money sponsorship. The danger of leaving oversight to academics in the ivory tower is the same as placing the fox to guard the chicken house.

    A favorite false argument by the AIDS apologists is the one you raised, which is, don’t raise any questions because only the highly trained HIV virologists and HIV immunologists in their ivory towers can actually know anything about HIV, and the rest of us poor souls should thank them while we submit to HIV testing, and deadly anti HIV drugs like nevirapine which had once been banned by the CDC ( January 2001).

    When science enters our living room, then that gives us the right and obligation to question mandatory HIV testing with false positives that can send life into upheaval, or even trigger the administration of toxic deadly drugs, or removal of a child by social agencies. This has become an even more serious issue in the past 30 years with a long list of bad drugs approved by the FDA and later withdrawn, and other serious problems with the health care system which have come to light as mentioned in books by Abramson and Angell. It is also imperative for the taxpayer to demand an accounting of all the billions of taxpayer public dollars spent on HIV research with no vaccine, no animal model and no mechanism of disease.

    The basic questions that need to be answered are:

    1) has medical science proven the hypothesis that HIV causes AIDS? If so, where are the medical references? So far, none of the drug company reps or paid political activists has posted these in spite of repeated requests. They have given us a few links from the AIDS truth web site, such as this Gallo NEJM article

    Who among you here accepts this article as the one that proves HIV causes AIDS?

    2) Where are the placebo controlled studies showing safety and efficacy of nevirapine and the other HIV drugs? There aren’t any. This is a disgrace.

    3) Where is the animal model for HIV causing AIDS. There isn’t any. This is a disgrace.

    4) Where are the hundreds of healthcare workers who contracted AIDS from occupational exposure to AIDS patients needle sticks? There is a governement CDC report of occupationally acquired AIDS which are problematic, there are no other peer reviewed medical literature reports of interns, residents, surgeons, and nurses catching AIDS from needle sticks from AIDs patients. This experiment injecting human “primates” (ie health care workers) with HIV laden needle sticks has been a colossal failure, same as the colossal failure to cause AIDS in chimps by injecting them with HIV. Chimps don’t get AIDS.

    It is a disgrace that deadly toxic drugs are being administered to mothers and babies without scientific proof of the causation between HIV and Aids, and without a placebo controlled drug study showing safety and efficacy of the toxic drugs.

    For more info see; reviewingaids DOT com

  20. #20 Dan
    June 29, 2007

    Adele,

    oh my. What a difference it would have made had you simply listed the sites without commentary.

    It would have given you some credibility, and in doing so, shown the supposed strength of your position.

    I hope Apy’s interest is real, and will embark on a journey of discovery.

  21. #21 apy
    June 29, 2007

    “For a site that isn’t high in the google ratings, and presumably gets only 150 hits a day, you seemed to find AIDStruth without a problem.”

    It’s linked to twice in the post you are commenting on.

    “You’re willing to educate yourself. Are you eager to educate yourself?”

    I don’t know what this means. This isn’t some world changing event where I decide to take the blue pill. I’m just reading some websites.

    “If you’re eager, you’ll go out and read everything you can and discern for yourself what’s going on. Or you can just rely on AIDStruth. Your choice.”

    You seem fairly willing and eager to criticize rather than suggest some reading sources.

    Adele,
    Thanks for the site listing, I’ll look it over when I can.

    “oh my. What a difference it would have made had you simply listed the sites without commentary.”

    You are willing to speak fairly negatively about the aidstruth website but criticize someone which speaks negatively about the ‘other side’? Perhaps arguing against specific points might help?

  22. #22 apy
    June 29, 2007

    Evion,
    Certainly you raise some useful points. The most important being “who to trust”. For many issues, one can look at the arguments themselves and determine which one is more likely to be valid, for instance the sun travels around us or we around the sun. However, something like AIDS has been studied for years upon years by very intelligent people with obviously controversial results, perhaps it will take a bit more than just reading a few webpages to come to a conclusion that one can consider their own. After reading a few web pages I cannot say that I understand the fine details any more than before, I can only regurgitate what various people have stated and present their arguments, none of which are the result of any research I have on the subject.

    More importantly, you point out that nobody has given any solid proof that HIV leads to AIDs. From what I have found on the AIDSTruth.org website seems to suggest this is very well known and presents a few links to documents.

    The AVERT web site (http://www.avert.org/evidence.htm) states:
    The alternative definition of AIDS requires a CD4+ cell count consistently below 200 cells per cubic millimetre of blood, which cannot be explained by any factor other than HIV (such as cancer, malnutrition, radiation or chemotherapy). No HIV test is required.

    It turns out that the vast majority of people diagnosed with AIDS fit these criteria. They form a population that barely existed before 1980, but which now numbers hundreds of thousands in the USA and Europe alone. People with such severe immune deficiency are at very high risk of developing serious illnesses and usually die within months (unless they take antiretroviral drugs).10, 11, 12 We can use this simple, unambiguous definition to test the association between HIV and AIDS.

    I am not going to say if this is valid or not, I simply don’t know. But given that some people are arguing that HIV does not lead to AIDS, do they have any evidence of an alternative? Do they have an animal model? Certainly lacking these does not mean dissidents are wrong, since the pro HIV to AIDS community does not either, but if both choices are on equally poor footing, what tips the balance in the way of the non-HIV theory? Is there any research which shows an overpowering existence of a counterexample to HIV causing AIDS? This would most definitely sway a number of people wouldn’t it?

    Finally, if the statement is HIV does not cause AIDS, and from what I understand even some of the most outspoken dissidents agree that HIV does exist, certainly if they all inject themselves with HIV and don’t get AIDS that would be a pretty strong counter example. It looks win-win for both sides too.

  23. #23 Adele
    June 29, 2007

    Dan,

    Is there anything untrue about my “commentary”? Did Harvey Bialy put monkey heads on John Moore or not? Did all the people on deharven’s “list” actually sign it or not? Are there people on there who died of AIDS or not? Does the Alive and Well board include alot of people who make money from giving patients “alternative” treatments or not?

    The disgrace here “Evion” is people who can’t come up with one original objection to solid HIV science in the last twenty years. Like asking for the “one” paper that proves this or that. Or insisting that “hundreds” or thousands or whatever of healthcare workers should have got AIDS when the reasons why it’s lower were given again and again and then just this afternoon by people like DT on the other thread. Or saying yet again there aren’t any placebo controlled studies when they know there are or they’re just repeating what some other denialist said.

    Every denialist argument is like this at least the ones I’ve seen. They’re old. They were mostly crap even when they first came out with a few exceptions that were answered since then. They require you to ignore the evidence or else lie about it like we’ve seen Andrew Maniotis do here and like Duesberg has done since the eighties.

  24. #24 Pope
    June 29, 2007

    Perhaps arguing against specific points might help?

    Is that so Apy? Why don’t you mention some specific points you’d like to discuss then?

    Following Adele, do you want to discuss homophobia, right wing lawyers, composite pictures, the definition of ‘long time denialist “journalist”‘, “a lot of people whose problem is they didn’t sign or they’re dead of AIDS”, whtehre Duesberg the “head honcho of bad science” links legally or illegally, or wheteher the above are all – gasp – linked together?

    Come on take your pick, show your genuine interest in the science. You look pretty well informed after all

    Perhaps your specific points are “what an animal model shows HIV doesn’t cause AIDS” Well tell us what such a model looks like, apart from no animals get AIDS from HIV and we’ll try to accomodate you

    Don’t be shy now, you’re among powerful friends, so please go ahead and tell us what the “overpowering existence of a counter example to HIV causes AIDS” would be. We’ll try to find one that satisfies you.

  25. #25 apy
    June 29, 2007

    I don’t know, but the specific post you are referencing I made was referring to some sort of model for what dissidents do think causes AIDS. I’m asking for an experiment that can be preformed that is reproducible that causes AIDS. Sorry for the confusion.

  26. #26 Pope
    June 29, 2007

    I’m asking for an experiment that can be preformed that is reproducible that causes AIDS.

    Apy, I’m sure you know that such an experiment would take a long time and cost a lot of money. Do you know somebody who’d like to finance and publish it?

  27. #27 apy
    June 29, 2007

    Mr Bialy claims to be very rich. Rich people often know rich people, perhaps he could work something out?

  28. #28 Adele
    June 29, 2007

    apy,

    HIV research has SIV models of AIDS. HIV was a zoonosis it came from SIV in primates that infected an injured hunter or someone preparing the meat. So the ideal model of AIDS would be using the same virus or a similar virus in a host that hadn’t seen that virus before. If you infect a primate with a SIV from another species it gets symptoms of AIDS. T-cells go down, it gets OIs actually most of the AIDS symptoms have been seen at one time or another. So there is a model. It’s not perfect but what animal model of disease is? There are alot of questions left but we’re working on them.

    On the other side, most denialists have a drug or stress theory of HIV causing AIDS. There’s a large block of research on drugs of abuse and other drugs and animals. The only drugs that cause anything like AIDS are immunosuppressives. Drugs don’t cause AIDS. Stress doesn’t cause AIDS. There’s nothing out there you can link from an animal model to everyone who has AIDS. Except for a lentivirus you can find in every AIDS patient.

  29. #29 Pope
    June 29, 2007

    Ah, Adele, you never answered my question, have chimps always been such an imperfect animal model as in the case of HIV/AIDS?

    The only drugs that cause anything like AIDS are immunosuppressives. Drugs don’t cause AIDS

    Thank you for that. I’m confident Apy can draw his own conclusions from that piece of logic without comment – if he wants to…

  30. #30 Adele
    June 29, 2007

    Duesberg knows rich people too. His lab got funded by rich ultraconservatives. Duesberg’s had twenty years to make a contribution to AIDS research. What has he done? Published a bunch of repeated reviews that are an embarassment to the journals who published them. Lies, distortions, childish logic. Why didn’t he do some of these drug studies to prove he was right? He’s supposed to be the modern Galileo, what gives?

  31. #31 apy
    June 29, 2007

    “The only drugs that cause anything like AIDS are immunosuppressives. Drugs don’t cause AIDS

    Thank you for that. I’m confident Apy can draw his own conclusions from that piece of logic without comment – if he wants to… ”

    I can’t draw a conclusion yet, I need another piece of data. It sounds like you are implying AIDS is caused by drugs. So, have a statistically relevant portion of AIDS patients been proven to have taken a drug that is shown to have immunosupressive effects?

  32. #32 Adele
    June 29, 2007

    When I wrote immunosuppressive I meant drugs used to prevent organ transplant rejection. Some steroid use can do the same thing.

    Illegal drugs? Take heroin. There’s been alot of interest in heroin and HIV since alot of people get HIV by injecting drugs together with someone who already has it. So there’s been alot of research on this. The people in these studies with HIV have about half the CD4 T-cells that drug users without HIV have. Jon Cohen did a article about drug use and Duesberg in Science over ten years ago.
    http://www.sciencemag.org/feature/data/cohen/266-5191-1648a.pdf

    Different drugs do different things to the immune system. These all get outweighed by what HIV does. HIV infection ends up depleting a specific population of cells and that leaves you helpless to the fungi and bacteria you normally fight off every day.

  33. #33 Evion
    June 29, 2007

    Adele said

    The disgrace here “Evion” is people who can’t come up with one original objection to solid HIV science in the last twenty years. Like asking for the “one” paper that proves this or that. Or insisting that “hundreds” or thousands or whatever of healthcare workers should have got AIDS when the reasons why it’s lower were given again and again and then just this afternoon by people like DT on the other thread. Or saying yet again there aren’t any placebo controlled studies when they know there are or they’re just repeating what some other denialist said. Every denialist argument is like this at least the ones I’ve seen. They’re old. They were mostly crap even when they first came out with a few exceptions that were answered since then. They require you to ignore the evidence or else lie about it like we’ve seen Andrew Maniotis do here and like Duesberg has done since the eighties.

    1) Adele, you seem to be in agreement that there is not one paper that proves HIV causes AIDS? Right? And at the same time, you seem to feel that there is no problem with the fact that there is not one paper that proves HIV causes AIDS. We dont need any papers that prove HIV causes AIDS. Do you agree with this Adele? How about two, three four or five papers? How many papers does it take to prove HIV causes AIDS? 100 papers, a thousand, the entire medical literature? Is this what you think Adele, that a collection of thousands of papers collectively prove HIV causes AIDS, but they cannot be listed individually? Correct? Which is it Adele? Will you be evasive and/or lie about this or give it straight this time?

    2) Adele, you seem to agree that there are enough occupationally acquired AIDS reported in the medical literature to preserve the hypothesis that HIV acquired by health care workers causes AIDS? What about Brazil?

    “Brazil ranks among the countries with the highest numbers of AIDS case reports in the world. By the end of the year 2000, 203,353 cases and 100,494 deaths due to AIDS had been reported by the National System. Although there are 99 documented or possible cases of occupational exposure to HIV in the world literature, no cases had been reported in Brazil up to the present date.”

    The first case of AIDS due to occupational exposure in Brazil

    Brazilian Journal of Infectious Diseases vol.6 no.3 Salvador June 2002, , Naila Janilde Seabra Santos et al.

    This is the number 200,000 AIDS cases by end of year 2000, and ZERO reported occupationally acquired AIDS, until this ONE case of AIDS? One is a very lonely number. Sorry, Adele, although I would like to be a believer, you are not very convincing. Remember the numbers, 200,000 AIDS cases and ONE nurse gets AIDS from a patient, thats ALL. Something smells fishy in Denmark.

    3) Adele, this is what your DT colleague says is a placebo for the placebo controlled nevirapine trial. The drug group received nevirapine and 2 more toxic HIV drugs, the placebo group received a placebo (instead of nevirapine) and two more toxic HIV drugs. Adele, so you really believe that this charade is a placebo controlled trial? The “placebo” is in actuality 2 toxic drugs. What ever happened to the old way, one group receiving the drug and the other group receiving a placebo? (not a placebo and two toxic drugs?) This is very sick twisted logic which is a disgrace to humanity and medical science. Do you agree with this Adele, that 2 toxic drugs can be called a “placebo”? You want to talk about crap? This is crap.

  34. #34 Adele
    June 29, 2007

    Where’s the one paper that proves evolution? Honestly. You have access to the medical literature so look it up. Although you’re probably a creo.

    I’m satisfied with Bob Gallo’s first group of papers plus Jay Levy’s independent isolation. But none of that would’ve worked without the four years of publications by doctors and other people describing AIDS and what it was and how its infectious. If you want those papers and there are hundreds, go get them. They’re not a secret. After 1984 there were still issues to solve. A lot of them were , some not. That’s why we still work on it. But the causation is proven as much as you can prove something.

    If you’re interested in stick-infection, go read DT on the other thread.

    Your placebo is really pissing me off. When you know a drug can save someone’s life you don’t give them a salt pill. So if you come up with a maybe better drug, you compare the first drug to the second one. It’s called ethics. But there’s not a single paper proving ethics, is there, I admit it.

  35. #35 noreen Martin
    June 29, 2007

    If you want to compare drugs, why not compare those on any antiretrovirals to a group of patients only on LDN. Let’s see which group fares the best and who lives the longest. It would not be unethical to do this because those of us on LDN are on it by choice and it is being prescribed legally. Maybe some are afraid of the results that would be found.

  36. #36 Pope
    June 29, 2007

    Different drugs do different things to the immune system. These all get outweighed by what HIV does.

    Makes you wonder what exactly the HIV test measures doesn’t it?

    Apy, You seem to have lost interest in animal models almost as quickly as Adele and have instead started speculating in how rich people are tied together:

    Mr (sic) Bialy claims to be very rich. Rich people often know rich people, perhaps he could work something out

    Are you suggesting philantropist millionaires should fund alternative medical research with no view to profit? But that would subvert the pharmaceuticals, perhaps our whole enlightened capitalist democracy wouldn’t it?

    You’re not a commie are you Apy, or perhaps an islamist?

  37. #37 Kevin
    June 29, 2007

    If you were the scientists you romanticize yourselves to be, you’d understand that any question or challenge can be revisited, including a complete revision of a paradigm:)

    Well said, Dan! Exactly the point that I have been making in another thread while addressing the anti-scientific stance of Dr. Aust.

    Since Tara added this “damage control” post right after my last post in the other thread, I’m reposting part of my “two questions” post, here. Posters like “Joe” seem to believe that ordinary people have no business assessing the successes and failures of HIV science, even though the failures can easily be identified as outnumbering the successes by a wide margin. He obviously doesn’t realize how dangerous his obsequious attitude is–particularly given the high-levels of corruption in modern medicine. It isn’t Duesberg stance that is irrational, but rather, it is “Joe” and his eagerness to legitmize the “secret” language of HIV that is irrational.

    _____________________

    Because people fool themselves without knowing they are doing it. — Dr. Aust

    Your most recent testimonial proves that you understand a thing or two about fooling yourself. I’ve got two very basic questions for you, Doctor…two questions questions that you do not seem to want to honestly answer, yet they are the best place to begin our evaluation.

    Are people still dying from HIV/AIDS?
    and
    How are they dying?

    Before we answer these questions, let’s look at why HIV apologists, such as yourself, try to invalidate my right, and more importantly, the rights of fellow scientists to ask these two very basic questions. This implicit censorship, among professionals, is very telling. After all, the evidence exposing HIV/AIDS as a mistaken explanation is quite apparent; twenty years of shoddy science is not easily defended. I find one example particularly telling; the ridiculous back-peddling often employed by those who “study” HIV is unmistakable, and their scripted recantations are downright Orwellian–such an unbecoming environment for producing good science–yet, Dr. Aust, and others on this blog, prefer to remain oblivious.

    Science is not alone in the loss of self-correcting mechanisms. The hollow testimonies of the numerous shills in our society are unavoidable, and they would be almost entertaining, that is, if they weren’t so goddamn disconcerting. Whether its housing, education, or health care, those in control of the funding have proved to be more interested in using that money to increase personal wealth, to obscene levels, in spite of obvious detriments to the integrity of the social institutions they purport to serve. The economy (housing bubble), civic responsibility (cynical citizens who don’t vote) and personal health (profiteering trumps care concerns) are all riddled with damning examples of frequent and blatant abuses of public trust by those in control. Consequently, a culture of accepted corruption–across institutions–has become normalized while legitimate endeavors and concerns suffer from neglect. Such massive corruption has eroded the self-correcting mechanisms that previously assured the integrity of these institutions, and those responsible for the decline should be held accountable. In fact, many of those who now hold professional status should lose it.

    Where HIV/AIDS is concerned, a system of rituals and a “secret” language disguised as specialized science has replaced the system that has worked for so long–a system based primarily on independent inquiry, real Science! Scientists and doctors, alike, are complicit in allowing this to happen. The abandonment of “do no harm” is an important component to understanding how this could happen to such a damaging degree. Once again, professional complicity was absolutely required before such specious science could ever become normalized. Don’t you agree, Dr. Aust? Regardless, accountability will be necessary before change can occur.

    __________________________

    The negative results of endemic corruption are obvious throughout our society, and the pathetic and impotent claims produced by HIV science provide some of the most absurd examples:

    “HIV is very enigmatic but always fatal…well, at some point in the future it’s fatal…we just can’t tell you the when or the how, unless you take these pills 12 times a day; then, we can tell you…because we can monitor your “markers” for HIV, as you get sicker from the drugs. Also, we’ll continue to ignore these debilitating and deadly side effects, while also refusing to recognize the irrelevance of HIV markers, in spite of research suggesting otherwise. We also ignore the obvious changes in cause of death and the disparities in disease presentation in different parts of the world. Remember, it’s a very enigmatic virus…just take your pills and the side effects, take those too…they’re part of the deal. You’ll die if you don’t. Did I mention that? We haven’t even gotten to the conflicting mutation theories but boy do they mutate…”

    Dr. Aust, you and your colleagues, have had twenty years to come up with an answer, and this is the best that you can do. HIV/AIDS is a money tree for Big Pharma, and it’s inability to explain the realities of this disease condition are becoming ever more apparent. Your posturing has grown tiresome, and it is a danger to public health.
    ____________________
    Finally, let’s answer those two basic questions, shall we?

    Are people still dying from HIV/AIDS?

    Yes…the number that are dying from “AIDS” is virtually unchanged. While the ranks of healthy HIV positives has grown due to scaremongering and increased testing, the connection between the two appears to be quite dubious. Thus, HIV positivity is a red herring, unless of course you continue to shoot Meth and/or begin a regimen of life-ending retrovirals.

    How are they dying?

    This is where things get even more interesting…whether apologists will admit it or not, many more “AIDS” patients are dying from the medications. Organ failure, including liver and heart, along with physical deformities have become normalized and synonymous with HIV/AIDS, which is in stark contrast to the defining ailments that characterized the condition early on. Of course, the apologists refuse to acknowledge the significance of this fact and continue to argue that the alternatives are worse, but as Noreen and myself understand, the “real” alternatives can mean the difference between living and dying. This is a human tragedy, and the killing by prescription has to stop.

    As for HIV, the only thing that mutates faster than the virus are the laughable theories used to explain-away its numerous explanatory deficiencies.

    Kevin

  38. #38 Evion
    June 29, 2007

    Dear Adele,

    OK I understand you feel that HIV causes AIDs has been proven, and this proof is recorded openly somewhere in the medical literature. Fine. If this is so, then why no occupationally acquired AIDS cases in Brazil after 200,000 AIDS patients were treated in Brazilian hospitals upto the year 2000, at which time a single AIDS case was reportedly acquired from an AIDS patient? Doesn’t this strike you as rather odd, and inconsistent with the “proven” hypothesis that HIV causes AIDS? Only one case?

  39. #39 apy
    June 29, 2007

    “You seem to have lost interest in animal models”
    What do you mean? I asked if there was an animal model for what dissidents think causes AIDS. Do I have to mention it in every post from then on?

    noreen Martin,
    What is LDN?

    “Are you suggesting philantropist millionaires should fund alternative medical research with no view to profit? ”
    I’m just suggesting a possibility to acquire funds to research it. Someone expressed an issue with testing dissident theories due to lack of funds, but if many of the head dissidents are very wealthy perhaps they could fund their own research. If it pays off they could possibly pull a profit out of it, depending on what they find. I’m not sure why you feel the need to accuse me of being a commie or an islamist, I don’t see what that has to do with funding research.

  40. #40 noreen Martin
    June 29, 2007

    LDN or low dose naltrexone is a wonderful drug that is helping many with immune deficiency diseses from cancers to autimsm, MS, AIDS and a lot more in between. It works by a differnt concept, meaning that it does not directly kill anything. Instead, it works by boosting the body’s own endrophin levels in the brain so that the body can ward off diseases. It is taken late at night and not in a time-release form so that all through the next day the body’s levels are normal. It has been found that many people with immune diseases have low levels of endrophins and this helps to correct this problem.

    This drug is not new and Dr. Bihari used it in the early 80′s for his AIDS patients. It has done great things for M.S. and some studies have been done on it. As stated earlier, it is cheap, non-addictive, no side effects and it works. I swear by this drug and you can take from that what you may. Having had AIDS and many of the AIDS-defining diseases, this drug has helped to keep me healthy. Since being on it, I haven’t even had the common cold.

  41. #41 Pope
    June 29, 2007

    So what’s the balance on Harvey Bialy’s bank account, and who else is rich, Ape? How much does it cost to keep theAIDS Inc. research machine running for a year? I’ll give you a clue, it ain’t millions.

  42. #42 Kevin
    June 29, 2007

    I don’t know, but the specific post you are referencing I made was referring to some sort of model for what dissidents do think causes AIDS. — apy

    I realize that I am only one example,but I suffered severe immune dysfunction, in the form of AIDS-defining ailments, while consistently testing HIV-negative. I’ve only recovered by my health after existing conventional care and by finding an MD who practiced holistic treatment for immune failure. He also realized that my health was being severely compromised by opportunistic fungal infections, which is also found in virtually all HIV-positive AIDS cases. For example, PCP and candida are both common AIDS-related fungal infections. Regardless, my health has drastically improved over the past two years, using primarily alternative treatments.

    I have posted about my experiences numerous times on this blog. If you are truly interested in learning about an alternative interpretation of “AIDS”, you can review my previous posts on the subject:

    Here and Here

    In trying to find answers, I’ve found others, both test-positive and test-negative who have similar histories. The positive ones were usually placed on ARVs, which seems to help for a short period, but the negative patients, like me were left with few answers, unless we found them on our own, which I did! As long as conventional medicine prefers to remain in the dark about the realities of this condition, effective treatments for all “AIDS” cases will be a long-time coming, and perhaps, that’s exactly what Big Pharma and modern medicine want…it certainly assures big profits and job security.

    In my opinion, there will never be an easy, all-encompassing answer for AIDS, for it obviously has multiple causes. Unfortunately, or perhaps fortunately, HIV doesn’t appear to be one of them. What I do know is that the most effective treatments for restoring immune health will require a holistic understanding by both patient and doctor, and pharmaceuticals will definitely play a smaller role if the goal is long-term immune reconstitution. That’s a fact.

    Kevin

  43. #43 Kevin
    June 29, 2007

    Having had AIDS and many of the AIDS-defining diseases, this drug has helped to keep me healthy. Since being on it, I haven’t even had the common cold.

    Noreen, I’ve been trying to get my HMO-doctor to prescribe LDN for me, so that I can add it to my regimen. It’s a new HMO-doctor, so he’s only known me since I’ve recovered my health, though he has access to my entire health history since I had my files sent to him. Even so, he refuses to prescribe it for me. I’m looking for a new doctor but, of course, my experience is that they are all mostly the same. I guess I could drive 400 miles to see the holistic doctor who helped me get well. Perhaps, I’ll just call him, but I was hoping my insurance will cover it.

    Is the $22/month, pre or post insurance, Noreen?

    Kevin

    It so hard to get good care in the country. I highly recommend Sicko to all the blog readers here. It opens nationwide tonight, I believe.

  44. #44 JD
    June 29, 2007

    Jeane Bergman is awesome and speaks like a true concerned human being scientist:

    The HIV denialists say that the young children at ICC could not refuse the drugs or fight off the “researchers” who gave them their medications. Should children of two or even 12 years get to decide if they will or will not take their medicine? Of course not, particularly when irregular dosing may result in drug-resistant HIV.”

    Because kids don’t know that not taking drugs will make their viruses be drug resistant – so you’ve got to make them understand by force. I get that fine, my father used to hit us with his belt buckle when we didn’t understand that he was thirsty for his brown water. But we learned, and so should everyone.

    But, please, one thing I’m still trying to figure out, what’s the standard, for testing I mean, because no one will tell me, except by not answering. And I have a clinic to run, in Australianus, where my Aboriginees are depending on me to figure out who gets to die first on the lifesaving drugs.

    Please help! What is the purified, particulate standard for hiv tests, that shows you that the 12-year old in Jeane Bergmans’ article can’t make a decision for himself?

    I just keep coming up with no answer, on every test they always say that the other test is the standard, and then that there is no standard, adn I know what this means, because I took an HIV educators seminar, where they said that tests test for a particle that causes BIIIG problems in homosexuals and black peoples, but we had to ask everybody to get tested anyway, but relaly, just the blacks and gays were important. And I said, why? and they said, because they have the particle, and you know that from the tests. And I said – OOOOHHHH – I get it, they have the particle, and you know that beause you hvae it in the Smithsonian.

    And they said, well, I guess they didn’t say anything. So, I’m stuck, with all these bad batched old tests adn all these Aboriginees in Australianus, so please, someone tell me, what is the standard? You know, the single, purified, particulate, magic bean that is the reference point on the map for my old tests?

    Because I paid a lot of money to set up this clinic, because I knew I could get the welfare checks out of their big, brown hands, if I tried hard enough – so please, don’t let me down!!!

    What’s teh standard? What’s the purified particulate standard?

    Pleaase!! Tell me!

  45. #45 noreen Martin
    June 29, 2007

    Kevin,
    The cost is before insurance, plus shipping because the drug has to be filled by a compounding pharmacy. Some of these are listed on the lowdosenaltrexone.org site. I hope that you can find a holistic, environmental or other open-minded doctor who will fill the prescription. I wouldn’t try AIDS or infectious disease doctors because most will not go there, which is a shame because this drug is usefull and helping so many. What section of the country do you live in?

  46. #46 JD
    June 29, 2007

    SPeaking of standards, I found this on the internet (which I know is mostly horsepoop), so is this true, or am I really out of luck with my testing clinic?

    “Along the same lines, no one is HIV viral load negative. All samples of human blood, tested by PCR Viral Load, always demonstrate the presence of copies of “HIV RNA.” The standard protocol for HIV Viral Load declares a blood sample negative if less than 400 copies of HIV RNA are found.”

    Is that true? Why isn’t anyone negative on the hiv pcr tests?

    Similarly, the ultrasensitive protocol for HIV viral load declares a blood sample negative if less than 50 copies of HIV RNA are found (Roche 2003). No single human being is, therefore, entirely free of copies of “HIV RNA” in his/her blood. We all are “HIV Viral Load” positive to some degree. Whether this is due to minimal expression of endogenous retroviruses or to universal exposures to stressor agents remains to be analyzed.

    Man, this sucks. I don’t know what to do anymore. Or who to believe! Won’t somebody help? WHy isn’t anyone negative? Are we all going to die????

    Oh NO! I just ordered a Wii. Now I’ll never get to use it.

  47. #47 Alan Kellogg
    June 30, 2007

    His name was Ryan Boelle. Everybody knew him as Angels Boi because he had a huge crush on the actor who played the part. Ryan was a small person, had a weak immune system, and was a homosexual. Ryan had a fight with his lover, they split, and during the split Ryan went to a sex party. There he was among a number of people who fellated an HIV positive man. Ryan had a tooth abcess.

    Ryan quickly developed a high virus count, concurrently his T-cell count crashed. He had trouble with the initial cocktail. He had trouble with getting on Medicaid because state bureaucrats had to have everything done right. Because of this is was off his medication for some time.

    Finally things got straightened out, he started his drug regime again, and he got better. But damage had already been done. Ryan would spend the last two years of his life swinging between full-blown AIDS and having the virus under control. Each time the virus held sway more damage was done.

    He lost energy. He healed more and more slowly. It took more and more medication to suppress the virus. Until, finally, there was nothing that could be done. About three years ago his family had him taken off life-support. He died an hour later.

    Ryan was a friend of mine. Never met him in person, only over the Internet, but he was a friend. He was bright, lively, inquisitive, and enthusiastic. He loved life, he loved people, he loved Dungeons & Dragons. He was a constant source of ideas and advice regarding the game. It hurt him when he had to quit the boards where he discussed his hobby. It hurt even more when his health became so bad he could no longer play. Yet through all his troubles he reached out to people to help, to advise, to communicate. For all throughout his ordeal he loved people.

    Ryan did abuse drugs when he was younger. He did have some at the party, for the first time in years. His T-cells crashed at the same time as his viral count exploded. With his weak immune system you’d think his previous drug history would’ve led to drug triggered AIDS back when he was a teen. If drug abuse does cause AIDS then why did he get better whenever his viral count went down? If the drugs do nothing, then why did viral count drop when he was on medication, and rise when he wasn’t? Why is this true for people besides Ryan Boelle?

    The HIV-AIDS connection has been tested by people who know the scientific method. Nobody has yet shown a more accurate explanation. I don’t think they’re even trying, despite decades of opportunity. HIV denial has become a matter of faith, and that is poisonous to critical thought.

  48. #48 noreen Martin
    June 30, 2007

    “HIV has become a matter of faith” where is the evidence that HIV causes AIDS? We are suppose to take this on faith. And I suppose that AZT never hurt anyone too. If must be great not to pursue other avenues or theories because then the mainstream can never be wrong. Hell, they won’t even debate the issue. So I ask you why should we take all of this on blind faith? Why should we believe what Gallo has to say when he was convicted of scientific misconduct? At least the rethinkers consider both sides of the issue because most started out with the mainstream’s point of view.

    If one looks at the 30 AIDS, defining diseases, they are not new and each are treatable. When one hasn’t any symptoms then one is not sick. It’s as simple as that. Not to be cruel but with many diseases, one will get better or not. There is no mystery to this. AIDS, a new classification, was the perfect storm. Events fell into place and many took advantage of this for the almighty dollar.

    Mow, much to many’s dismay, many of us have tossed the meds and are healthy. This brings up serious doubts about the situation. We cannot be explained away or sweep under the carpet. We are real and not theories to tear apart. I will leave you’ll on that one and let you argue your “theories” back and forth. Several months from now I will check back in with you and let you know how things are going.

  49. #49 Kevin
    June 30, 2007

    HIV denial has become a matter of faith, and that is poisonous to critical thought. — Alan Kellogg

    Bullshit.
    Your telling of Ryan’s story is a blatant propaganda piece, and it is AIDS propaganda that is poisonous to critical thought. For another example of the AIDS propaganda machine, one only has to review the literature and choose from the myriad of insanities contained therein. A particular favorite of mine is Immune Reconstitution Syndrome

    Rather, than admit that long-term immune reconstitution is impossible for those on HAART, the AIDS propaganda machine has created an entirely new syndrome to absolve the drugs from their obvious responsibility for further compromising the immune systems of patiets. Unbelievable! One might be led to believe by such antics, that long-term immune reconstitution is not the goal of current HIV treatment, and that’s a crime against all of us. A favorite quote from the link:

    “After a couple weeks on his HIV regimen, he developed a fever, blurred vision, and swelling around his eye. The odd thing was that his CD4 count had gone up dramatically since starting HIV medications. So what was going on? His immune system was better (oh, really?), yet his eye looked horrible. LZ was seen by his doctor and was diagnosed with immune reconstitution syndrome.”

    Brilliant. It’s the drugs, Stupid. As Noreen can affirm, a patient’s well-being is a far better indicator of immune health and a far better template by which to base future care decisions than surrogate markers. For example, if someone has low CD4′s but is not ill, don’t make them ill just so your “surrogate marker theory” looks good. If Ryan would have had doctors who actually cared about his well-being, perhaps, they would not have been so quick to poison him to death, Alan.

    ______________________

    Thank you for the LDN info, Noreen. I’ll try to find a physician who’ll prescribe it. My insurance won’t cover it unless my HMO-doctor prescribes it. I used to have separated drug coverage which allowed me to choose any doctor, but that changed this year, as my HMO tauted a “new and improved” coverage plan. Yeah, right….

    22 bucks isn’t so bad but it’s the principle, and it’s further prove of just how rotten health care in this country actually is. Ignorant posters like “Raven” may be satisfied with our 37th ranking, right behind Costa Rica, but I think we can do better.

    _______

    That’s for funny stuff, JD. You aim is right on target. Injecting a little humor into this mess is always welcome, if done with tact. Thanks.

    Kevin

  50. #50 cooler
    June 30, 2007

    I thought the denialists were nuts until i saw the video Hiv Fact or fraud last summer. Its pretty rude that many reputable scientists have questioned the hiv hypothesis, and have been insulted by many. Here is the video I saw last Year.

    http://video.google.com/videoplay?docid=5064591712431946916

    Keep in mind that most scientists who question hiv have no conflicts of interest, unlike John Moore.

    People question HIV because there is no reliable animal model (virtually every animal injected does not die of aids) and there is not much virus present, (its only in a small fraction of T cells) Like 1 in a hundred or so.

    Many take the middle road, Like Luc montagnier the discoverer of HIV, Who in his book “virus” in 2000 still stresses the need for co factors, specifically shyh ching Lo’s mycoplasma penetrans. This microbe causes disease and death in every animal injected as lo showed. DR. Nicolson has found this microbe via pcr in CFS, ALS, GWI and you can see his research here.

    http://www.aegis.com/pubs/atn/1990/ATN09501.html

    Garth Nicolsons new book must be read about mycoplasma and Gulf war Syndrome.

    http://www.projectdaylily.com

    Im not saying that HIV does or Does not cause AIDS but there needs to be more study, and scientists who questioned should be debated publicly, not insulted personally.

  51. #51 Tara C. Smith
    June 30, 2007

    and scientists who questioned should be debated publicly,

    Just like evolution deniers? The debate has already taken place in the literature, and the deniers’ pet theories haven’t stood the test.

  52. #52 Pope
    June 30, 2007

    Just like evolution deniers? The debate has already taken place in the literature, and the deniers’ pet theories haven’t stood the test

    Yes just like evolution deniers. What’s wrong with debating evolution in public? Why is it that scientific debate must be hidden from the public’s eye in “the literature”

    But ok, maybe Tara could point us to the literature where the debate with Duesberg and others has taken place, and tell us which theories have been tested according to the suggestions made by Duesberg and others.
    One notable debate which didn’t take place in “the literature” is Robert Gallo’s promised rebuttal to Duesberg’s PNAS article Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome: Correlation But Not Causation http://duesberg.com/papers/ch3.html

  53. #53 cooler
    June 30, 2007

    I’m talking about a public jury of millions, not a group of scientists who have many conflicts of interest, and many others that are afraid to speak out. A public jury usually gets the verdict right in a criminal case, and experts because of conflicts of interest get it wrong in our judicial system.

    The real reason there is no public debate is because of fear, ie millions of people would start asking tough questions, so the hiv orthodoxy, much like a prosecutor with a bad case, does everything from letting the public hear another side of the argument. A good prosecutor would not care about the public hearing another side of an issue, thats why John Moore is spending so much time trying to prevent people from hearing an argument, he’s insecure.

    John Moore is like a corrupt prosecutor who tells a jury “you cant hear another side of an argument because you might beleive it” Any responsible juror would demand to hear both sides of an issue to get to the truth.

    If you have read Orwells’s 1984, bad science/ideas can advance in many countries that don’t allow the public to hear both sides of an issue. For example, in Mao’s China or Stalin’s Russia if you were an economist and you wanted to publish an academic paper saying their economic policies were fraudulent, would the academic establishment have ever allowed it?

    Of course not, because in many societies the academic establishment is heavily influenced by government/orthodox propaganda that exerts it’s influnece in several ways such as financial influence, and other more subtle ways, as Orwell spoke about via “Thought control”

    Again here is a list of many scientists that have questioned HIV at one time or another.

    Luc montagnier
    Shyh Ching Lo Cheif Of the infectious unit of the AFIP
    Walter Gilbert nobel prize winner
    Kary Mullis nobel prize winner
    Peter Duesberg Retroviral expert
    Richard strohman UCB

    Many more

    Millions of Americans have a right to hear the other arguments and make up our own mind.

  54. #54 Nullifidian
    June 30, 2007

    I’m talking about a public jury of millions, not a group of scientists who have many conflicts of interest, and many others that are afraid to speak out. A public jury usually gets the verdict right in a criminal case, and experts because of conflicts of interest get it wrong in our judicial system.

    This is too funny. There are articles upon articles in legal journals detailing precisely how prosecutors and defense attorneys routinely misuse statistics, withhold or massage vital data, and then put ignorant people in the jury box because they’re going to not be able to recognize the distortions being fed to them. It happened to me once. I was removed “for cause” in voir dire because I admitted to being a biologist.

    This is behind the denialists’ campaign for public debate, and the creationists’ campaign, the relativity-deniers’ campaign, etc. People without the technical background can be led by the nose in a way which is less likely when the data is laid out and the arguments circumscribed by the necessity to put forth one’s claims in a manner which evaluates it against the existing literature, rather than using mere rhetoric to wow the public.

    Your list of scientists is misplaced. Nobody cares. You’re just putting forth stupid rhetorical tricks again. I got my degree from a university (UCSD) with seven Nobel laureates in its biology department, the most for any university in the US. The second is the U of Chicago, and they have six laureats of only the fake Nobels in economics given out by the Bank of Sweden.

    And it may shock you to discover that nobody gave a damn that person X had won a Nobel prize. It is the quality of their research that matters, not the name, the degree, or anything else which people like you latch on to try to give a veneer of credibility to an argument that has no basis in reality.

  55. #55 William Miller
    June 30, 2007

    Tara,

    you write that the ‘evolution deniers’ debate has already taken place ‘in the literature’, but ‘hasn’t withstood the test.’

    I see a debate ongoing, spilling into the public sphere, gaining momentum and a great deal of ink spilled in the press. I am familiar with the historical debates, reaching back to Ernst Mayr, I know of no serious scientist who would claim any debate to be over because of putsch-like arguments forwarded by a medical elite.

    I am not a Christian, by the way, and I am agnostic on most evolutionary claims, although I reject the neo-Darwinian simplification of descent as a means and natural selection – ie sexual congress – as the means for speciation.

    The symbiogenicists are much further along the right path, in my opinion.

    I think that is an expression you should learn, quickly: “In my opinion.”

    Science is always an opinion. The ancient greeks knew this well, and gave us the words:

    Doxa, opinion

    and

    Episteme, knowledge

    The reason for the disjunct was the unreliability of human senses to correctly interpret the world.

    You’re no doubt so clever a sophist, an Orthodoxist, that you will find a way to retort any criticism and claim it as a further victory for your cause.

    But some of your readers might appreciate knowing that you are arguing, as a constant theme, from rationalized authority, and almost never, that I have witnessed, from actual humbling critical thinking.

    Good luck to those who continue in this forum, it is an exercise in immoderate self-abuse for those bringing interesting ideas to challenge the entrenched, and bilious, new church.

  56. #56 William Miller
    June 30, 2007

    I’m sorry to add this before allowing a response, but I happened across it, and it gave me a reason to doubt your Wisdom, Tara, yet again:

    http://news.bbc.co.uk/2/hi/health/6230580.stm

    Lack of certainty

    Researcher Professor Jaroslav Stark, from Imperial College London, said: “Scientists have never had a full understanding of the processes by which T helper cells are depleted in HIV, and therefore they’ve been unable to fully explain why HIV destroys the body’s supply of these cells at such a slow rate.

    “Our new interdisciplinary research has thrown serious doubt on one popular theory of how HIV affects these cells, and means that further studies are required to understand the mechanism behind HIV’s distinctive slow process of cellular destruction.”

    The researchers think one possible explanation could be that the virus slowly adapts itself over the course of the infection.

    But they stress that further analysis is needed to verify this alternative theory.

    Ah-hah, we see the permissiveness of the Orthodoxy in allowing generous re-writing of The Theory, as long as, I suppose, it doesn’t abandon it altogether.

    Why wouldn’t the theories of the ‘denialists’ count for even more, as they predicted the absolute failure of the central dogma I think, at least a decade ago?

    I expect nothing but shrill argument in response, Tara, but I hope your readers will not be cowed, and will stand up for their rights to think.

    regards,

    Wm. Miller
    private citizen
    language teacher

  57. #57 Tara C. Smith
    June 30, 2007

    Yes just like evolution deniers. What’s wrong with debating evolution in public? Why is it that scientific debate must be hidden from the public’s eye in “the literature”

    Nothing is “hidden.” Rather, as is easily seen in the comments thread on here, it’s all too easy for deniers to misrepresent literature and outright lie–and it takes much more time to rebut them and set people straight than it does for them to just throw out their dishonest claims. Look up what a “Gish gallop” means to the evolution debate, and then look how Maniotis has done much the same thing in the other thread.

    Duesberg’s ideas have been falsified. If drug use causes AIDS, then why is only those HIV_ drug users who develop the syndrome? Why do HIV+ individuals who’ve never used drugs develop the syndrome? (Oh, right, according to Duesberg and others, they’re all lying about their past drug use, sorry.)

    William,

    I am familiar with the historical debates, reaching back to Ernst Mayr, I know of no serious scientist who would claim any debate to be over because of putsch-like arguments forwarded by a medical elite.

    I’m not claiming there are no controversies left wrt evolutionary biology. Certainly there are–including what the most important mechanisms of speciation are, for one. But the question “does evolution happen?” certainly is answered in the affirmative (even creationists accept “microevolution”, they just deny that it had anything to do with humans), the question “does RM + NS cause evolution” is answered in the affirmative (many, many experiments in bacteria), etc etc etc. Questions remain to be sure, but the debate that remains is much about the details, not about the big picture.

  58. #58 cooler
    June 30, 2007

    So according to you we should abolish the constitution and have experts to decide trials!
    Experts who if you watch Court TV say anything if the price is right. You’re a total moron.

    The HIV debate shouldnt be decided by frauds like Gallo who can tell the american people anything, make millions of his ridicolous hypothesis without hearing the many scientists that think he’s full of it.

    Its not rocket science, this is 8th grade stuff, Kochs postualtes. How do you prove a microbe causes disease in humans?

    Animal model………..oh jeez 99% of animals injected with hiv nothing happens!

    Have it be detectable in large amounts…………awwwwww, according to Gallo in his book Virus Hunting hiv is in only 1 of 10,000 t cells! I just talked to that fool JOel Gallant and he admitted HIV is now an autoimmune disease and theres not much direct cell killing because he admitted it doesnt infect enough cells! Great speculation to save the hypothesis!

    There should be some epidmiological sense, but according to the Army HIV is split evenly between the sexes, while AIDS is 90% male! This makes a lot of sense

    Why arent people informed that AZT is a Chemotherapy that kills cells, why are they told it’s an “antiretroviral” another lie.

    You are pretty unamerican to force this disinformation on the public. Its called informed consent, People have a right to hear another side of an argument, people are not stupid, if some group of scientists argued that eating 20 pizzas a day was good for you, nobody would believe it, unless you bar americans for learning about other sides of issues, than they would believe anything, as in the case with HIV!

  59. #59 cooler
    June 30, 2007

    the previous post is directed at nullifidian, for being a condescending worm.

  60. #60 apy
    June 30, 2007

    I did a quick google search for execptions to Koch’s postulates, I found:
    http://ic.ucsc.edu/~flegal/etox80e/SpecTopics/microbial.html
    As with almost every, if not all, postulates in science, there are limitations and exceptions to Koch’s postulates. For example, virulent strains of the bacteria that cause syphilis, Treponema pallidum, or leprosy, Mycobacterium leprae, have never been cultured in artificial media. Similarly, some infectious diseases, such as nephritis, may be caused by several different pathogens; and some pathogens can cause several different disease conditions, including Streptococcus pyogenes that can cause sore throat, scarlet fever, erysipelas (skin infections), puerperal fever, and osteomyleitis (bone inflammation).

    I don’t know how powerful any of this is to the argument, but the existence of some exceptions suggests the possibility that there might be more exceptions.

    “So according to you we should abolish the constitution and have experts to decide trials!
    Experts who if you watch Court TV say anything if the price is right. You’re a total moron.”

    cooler, I don’t believe anyone has said this. For starters, science is international, the constitution is not. Secondly, jury’s depend on the testimony of various experts to form their judgement. They are also wrong very often. Many guilty people have been found innocent and vice versa. Jury’s are also not free to take what an expert claims and then test it on the defendent to validate it.
    It would certainly be nice if a layman could spend 20 minutes listening to both sides adn be educated enough to make a decision about which side is correct but that is not the case. You are free to make your mind up either way but eventually you are relying on trusting what someone has said in order to form your opinion. I don’t see how a jury of millions of laypeople would change this at all. Let’s say the entire world decides to come to a majority rules verdict. In the end it comes down to how many people believed one side over the other and their verdict is not guranteed to be correct just because a majority agree to it.

  61. #61 cooler
    June 30, 2007

    AIDS does not inevitably lead to death, especially if you suppress the co-factors that support the disease. It is very important to tell this to people who are infected. I think we should put the same weight now on the co-factors as we have on HIV. Psychological factors are critical in supporting immune function. If you suppress this psychological support by telling someone he’s condemned to die, your words alone will have condemned him. ”

    - Luc Montagnier Virologist, Discoverer of HIV

  62. #62 Alan Kellogg
    June 30, 2007

    Cooler et al,

    You can’t handle the evidence. We place something before you and you turn your head. We use reason, and you use snark. We show you micrographs of AIDS viruses lysing a T-cell, and you see a man in an ape suit. You want things your way, and fuck the facts.

    You are a true believer, just like any other creationist and Holocaust denier. It contradicts your beliefs it has to be a lie, and is not to be countenanced in any manner. I have to ask, aren’t you getting tired of hauling those goal posts around?

    I know how science works, and I know how scientists work. Tain’t perfect, but at least scientists do make an honest effort to correct their errors when they are wrong.

    And BTW, go over to ENWorld and ask about Ryan “Angles Boi” Boelle. Or do a Gigablast on the name. You want to accuse somebody of lying, know what the fuck you’re talking about.

  63. #63 Alan Kellogg
    June 30, 2007

    BTW, here’s the result page for a search on “angelsboi”. I’m now waiting for your apology, and I’m ready to wait till Hell freezes over.

  64. #64 Chris Noble
    June 30, 2007

    AIDS does not inevitably lead to death, especially if you suppress the co-factors that support the disease. It is very important to tell this to people who are infected. I think we should put the same weight now on the co-factors as we have on HIV. Psychological factors are critical in supporting immune function. If you suppress this psychological support by telling someone he’s condemned to die, your words alone will have condemned him. “

    - Luc Montagnier Virologist, Discoverer of HIV

    You forgot to give a reference for this quote.
    It’s from an interview that appered in Omni magazine in December 1988 v11n3

    You also forgot to include the rest of the paragraph.

    “… have condemned him. It simply isn’t true that the virus is one hundred percent fatal. If you lead a normal life — sleep regularly at night, avoid alcohol, coffee, and tobacco — your immune system could perhaps resist the diseas for ten or fifteen years. By then we might have found an effective therapy”

    This hardly supports your claim that Montagnier is really a closet
    “rethinker”. Various co-factors almost certainly have a strong effect on the rate of progression. The single key factor is HIV.

  65. #65 cooler
    June 30, 2007

    He said in 1990 that hiv “might be benign” and in his book in 2000 “virus”, he stressed the need for cofactors.

    Anyways im sick of talking to you, youre like a robot, talking to you is not fun, go out and get some sun, son.

  66. #66 Chris Noble
    June 30, 2007

    Along the same lines, no one is HIV viral load negative. All samples of human blood, tested by PCR Viral Load, always demonstrate the presence of copies of “HIV RNA.” The standard protocol for HIV Viral Load declares a blood sample negative if less than 400 copies of HIV RNA are found. Similarly, the ultrasensitive protocol for HIV viral load declares a blood sample negative if less than 50 copies of HIV RNA are found (Roche 2003). No single human being is, therefore, entirely free of copies of “HIV RNA” in his/her blood. We all are “HIV Viral Load” positive to some degree. Whether this is due to minimal expression of endogenous retroviruses or to universal exposures to stressor agents remains to be analyzed.

    HIV TESTS CANNOT DIAGNOSE HIV INFECTION

    If your aim was to find a textbook example of the sort of illogical HIV Denialism that you can find on the internet then you have succeeded.

    Less than 50 includes 0. A viral load measurement of less than 50 copies/uL does not mean that there are some copies of HIV RNA present. It measn exactly what it says.

    It’s hard to come up with any response other than “Duhhhhh”;

  67. #67 Independence Day
    June 30, 2007

    As discussed above, the CDC report of 26 cases of occupationally acquired AIDs out of 24,000 AIDS cases in healthcare workers, 99.9% of which were not occupationally acquired is a problematic study for reasons which have been amply explained.

    The case of Brazil illustrates that Duesberg’s original 1987 statement, that AIDS is not contagious and not occupationally acquired by healthcare workers is correct. Yes, healthcare wotkers seroconvert. But they dont get AIDS.

    Brazil has 200,000 AIDS cases treated in Brazilian hospitals up to the year 2000 with not one single occupationally acquired AIDS case until one report was made of a nurses aide, that appears to be a text book case of AIDS. Problem is that there is only one single report when there should be hundreds. Is this one case prrof that Duesberg is wrong and proof that AIDs is occupationally acquired? I say no, because it is only one SINGLE case when hundreds are expected. This makes the actual report suspect.

    The First Case of AIDS in a Health Care Worker Occupationally Acquired in Brazil

    Even though health care workers seroconvert after the needle sticks, the few single or isolated reports of AIDS are not sufficient to convince a reasonable person that AIDS is an occupational hazard of taking care of AIDS patients in hospitals.

    The AIDS political activists and drug company reps can puff out and froth at the mouth, but the evidence in the medical literature is plain and clear, casting a serious doubt on the HIV causes AIDs hypothesis.

    Independence Day is approaching; this is a day to celebrate freedom from taxation without representation. Let us declare our freedom from taxation which pays for academic misconduct and fraud in AIDS research which soaks up our hard earned public dollars.

    Let us declare our freedom of speech in the media. Let us declare freedom from the brownshirted AIDS political activists, and drug company reps who use intimidation, lies, tricks and gimmicks to oppress honest scientists who stand up and speak the truth about the glaring falsehoods of HIV science. There is no animal model of HIV causing AIDS, no mechanism of disease, and no placebo controlled drug study showing efficacy of drug treatment. There is no gold standard for the HIV tests. This is a disgrace.

    Is there proof in the medical literature that HIV causes AIDS? No, this proof that HIV causes AIDS has not been presented here or anywhere else, in spite of ample opportunity. This is a disgrace.

  68. #68 Michael
    June 30, 2007

    Hello Alan.

    My name is Michael and I just read your comments up above about your friend and his illness and passing. If cooler does not apologise for his assumption that your friend was a real person or your story was made up, then I certainly do. My condolences for the loss of your friend. I too have lost many friends that at one time I too believed were due to HIV. My beliefs, however, have evolved since then.

    I do think that you are only giving us a very small and partial picture of the situation and factors involved with your friend, his illness, and his passing, and not a full enough picture of the situation to do anything with but jump to premature and unknowledgeable conclusions, although I am sure it is accurate as to the best of your knowledge and memory of 3 years ago. As you said, Ryan was an internet friend of yours, not an intimate friend that you personally spent one on one time with, so we readers are now getting the information 3rd hand.

    I would like to point out to you, Alan, some things you may not have considered, and one being that people do not die of AIDS. They die of something specific, and you did not share with us, what specifically, your friend died of nor any of what his specific symptoms were, nor what his treatments were, nor how his body reacted to the treatments. What was the cause of death? Was it hepatitis, TB, pneumonia, thrush, KS, PCP, or what? Or was it liver failure or kidney failure or heart failure? Was it something viral, bacterial, or was it related to his treatment. Please understand that without the full and complete picture, Alan, it is impossible for anyone to understand or do anything except jump to conclusions and assumptions of whether your friends death was HIV related or not. What were the other influencing factors if any? What was going on with him emotionally? What was going on in his relationship with his family? Did they accept him as a gay person, or did they reject him for this. Was he a person who expected to live, or did he have expectations of sickness or death? Did he even possibly have an inner death wish that he did not even share with you? You mentioned that he had formerly had drug problems, are you sure he resolved the drug addiction as well as the underlying emotional issues that drove his addiction? One can be sober and still suffer deeply from emotional stress that weakens ones immune system. Psychological factors can intensely affect one’s immune system.

    The reason I ask, is because I feel you are making assumptions that it is all about HIV, when his situation and exact illness was deeper than that even if it were partially true that HIV was a factor. Ignoring all of the other factors does not change them and make only HIV true. And the factors that could also have affected his situation are also much deeper than what little you have shared with us, and perhaps even deeper than the limited parts of his life that your friend had even shared with you over the internet.

    I would hope you will also come to understand, that even though you believe you “knew” your internet friend well, there is yet much more you do not know, from which position it is very easy for you to jump to conclusions based on very limited information.

    You wrote: “HIV denial has become a matter of faith, and that is poisonous to critical thought”.

    That statement is a double edged sword Alan, and one that can just as easily take a piece out of the opposite side of the issue.

    I would only hope you would keep a more open mind on this issue Alan, although it seems you are already married to only one side of the issue.

  69. #69 cooler
    June 30, 2007

    Dear corn flake, oh I’m sorry, Kellog,

    Scroll back i never mentioned anything about your friends passing liar, you are confusing me with someone else, ive never replied to any of your posts here in fact! Jesus, scroll back, why do you people lie with impunity?

  70. #70 Nullifidian
    June 30, 2007

    So according to you we should abolish the constitution and have experts to decide trials!
    Experts who if you watch Court TV say anything if the price is right. You’re a total moron.

    I’m a total moron because you’ve made up a wholly fictitious argument and attributed it to me? Well, doesn’t that just scream “intellectual honesty” of the kind that has given the AIDS denialist camp its numerous successes in the courtroom?

    If you want to know what my proposals for overhauling the currently established “expert testimony” is, just ask me. For one, I think that unannounced, blinded trials of forensic technicians should be done on at least a biannual basis, and that the results of these trials should form the basis for reporting any probabilities of a forensic “match”.

    I think that random samples should be elicited from populations by disinterested parties (i.e. not the police) in order to evaluate the degree of population substructuring in a given geographic area and that should be another basis for reporting any probabilities of a forensic DNA match.

    I think that the product rule should be banned entirely when reporting the likelihood of a forensic DNA match since it skates the line of perjury.

    And I think that the state should fund labs and forensic experts to replicate results, evaluate results, and testify on behalf of the defense, thus preventing situations where the defense doesn’t raise a challenge to forensic evidence despite previous challenges to its legitimacy and known errors and frauds.

    The HIV debate shouldnt be decided by frauds like Gallo who can tell the american people anything, make millions of his ridicolous hypothesis without hearing the many scientists that think he’s full of it.

    Virologists, epidemiologists, etc. have already heard the so-called ‘many’ scientists who are HIV denialists and they’re unconvinced.

    Its not rocket science, this is 8th grade stuff, Kochs postualtes. How do you prove a microbe causes disease in humans?

    You don’t. Next!

    At best you can just establish a reasonable degree of confidence based on the correlation of diseases to symptoms. There are many organisms for which one or more of Koch’s postulates do not obtain, so waving it about as if were the final answer to everything while not being equally skeptical about whether Mycobacterium leprae, for example, causes leprosy is fundamentally dishonest.

    Animal model………..oh jeez 99% of animals injected with hiv nothing happens!

    So Koch’s postulates include the assumption that every disease will be transmissible across every animal on the planet? Uh, no, I think you just made that up.

    Have it be detectable in large amounts…………awwwwww, according to Gallo in his book Virus Hunting hiv is in only 1 of 10,000 t cells!

    As has been explained to you repeatedly, CD4+ cells are t-cells, but not all t-cells are CD4+ cells. Anyone who cannot get this by now is either a moron, someone irreversably committed to the denialist position come what may, or both. Which are you?

    I just talked to that fool JOel Gallant and he admitted HIV is now an autoimmune disease and theres not much direct cell killing because he admitted it doesnt infect enough cells! Great speculation to save the hypothesis!

    You can’t tell the difference between an immunodeficiency disease and an autoimmune disease, and you’re staking the claim that it’s virologists, immunologists, and epidemiologists who have to satisfy you that HIV is the causative agent in a certain immunodeficiency disease?

    Way to support, by example, anything I could possibly say about the general public not being qualified to make a judgment on the matter.

    There should be some epidmiological sense, but according to the Army HIV is split evenly between the sexes, while AIDS is 90% male! This makes a lot of sense

    This is so incoherent that it’s difficult to parse, but I assume it’s about how the incidence of AIDS patients in “the Army” (I assume the U.S. one, since it seems to be certain Americans alone who think that nowhere else in the world exists) is skewed to men, while HIV-positive women equal the number of HIV positive men.

    If that’s so, it could be explained several ways, one of the easiest being that, since AIDS takes a long time to progress, it would be primarily seen in “lifers” who were HIV positive early in their career, and the demographics of lifetime military people in the Army skews to men, rather than women. Wow, something that’s consistent with what we know about the demographics of the army, plus what is known about the progression of the disease, predicts a skew between male and female AIDS patients in the Army. One could think that’s because the virologists, epidemiologists, etc. etc. are right!

    Why arent people informed that AZT is a Chemotherapy that kills cells,

    Because it doesn’t. It may damage mitochondria, and people are told about that. Mitochondria haven’t been independent cells for over two billion years.

    why are they told it’s an “antiretroviral” another lie.

    Because it is an antiretroviral.

    You are pretty unamerican to force this disinformation on the public.

    Oh boo hoo. I’ve got news for you: I’m “unamerican” in more ways than that. I’m an anarchist. As such, I fully support your right to, if you are HIV positive, not take antiretrovirals if you don’t want to. But you certainly had better disclose your status to any future sexual partners, so that they can make an autonomous decision of their own. However, I do not support misleading large swaths of people in ways which are likely to lead to thousands of preventable, or at least postponeable, deaths. In fact, I view it as genocide.

    Its called informed consent,

    The only consent that matters is the consent of the patient to take or not take the antiretrovirals, and I fully support the doctor giving the patient a full and frank explanation of all that is known about HIV. What the denialists claim is not known. In fact, it’s a collation of bullshit, stupid misunderstandings, and demagoguery.

    People have a right to hear another side of an argument,

    Yes, but the issue is not that you want them to hear it, but you want us all to be forced to believe it. We’ve all heard the arguments of the denialists and found them to be utter crap.

    What you hope to gain by doing public debates outside of the literature is to get public assent for your views even though you know they can’t hack it among a genuinely skeptical audience of scientists. Given the human consequences of proposing stuff that you know is false and has already been debunked in the area of virology, it amounts to nothing more nor less than a prescription for genocide.

    You disgust me.

  71. #71 Alan Kellogg
    June 30, 2007

    Cooler,

    You do know what “et al” means.

    Michael,

    You will find my reply on my site. For here I have a new phrase for you, “Contributory factor”. Learn it well, it can take you far.

  72. #72 JD
    June 30, 2007

    I keep seeing this word “hiv” coming up, and I still dont’ know what the pure particulate purified gold standard smithsonian museum reference for this particle is.

    no one will tell me. Spongy Noble believes in hiv like Peter Pan believes in fairies, and I know that Spongy must KNOW what the purified particulate molecule is that is also the where the buck stops here’ gold standard for all and each and every ‘hiv’ test.

    Spongy made a ‘duhhhh’ before, but I was wondering if it’s true that you can call someone pcr ‘negative’ if they’re, you know, below 400 whatever it is per cubic crapulmiter.

    Please, Will someone tell me what the pure particulate purified gold standard is? I’ve been asking for days and days, and everybody keeps using the word ‘hiv’, and I know that you’re not just making it up, you know, by believing in it – I know you have the purified gold standard reference particle for each and every test that corresponds with the tests so that all the true positives are positives and all the false positives are just misplace white people… anyway…

    Can you please just send it to me in Australianus? The gold standard, just in a shoe box or something. I need a standard, because we have white straight people where I live as well as the Aboriginees, so you know, I can use the high-risk strategy for the brown-skins, but what do I do for the nice white ladies (I try to sleep with them, but I’m a restless sleeper and kick a lot, and that bothers their husbands).

    Please, somebody, please, please, please,

    what is the singular one-of-a-kind always there purified particulate gold reference standard for hiv tests?

    What is it? Where is it? Why isn’t it here at this special place, with Spongy and the gang? Please help.

  73. #73 Why Not Selenium?
    July 1, 2007

    If HIV is NOT the cause of AIDs, then what is?

    There have been a number of requests for an alternative explanation. We are all familiar with the drug hypothesis by Professor Duesberg as one alternative explanation.

    Here is another.

    The role of micronutrients such as selenium has been largely ignored by the mainstream medical system. Recent studies have implicated selenium deficiency as a key to AIDS pathogenesis. It is well known that the HIV genome encodes for glutathione peroxidase which causes selenium depletion.(1) Selenium deficiency impaires the immune system.

    HIV positive patients who are supplemented with cheap inexpensive, nontoxic selenium tablets, have 30% less hopitalization (2)

    and show dramatic improvements in CD4 cell count and HIV reduction by PCR measurements. (3)

    This improvement in CD4 cell count and surrogate markers with selenium is much more impressive than any of the HAART drug cocktail studies, none of which are REALLY placebo-controlled.

    An excellent review article on all micronutrients and HIV can be found here. (4)

    For Noreen and Kevin, for a non-toxic cost effective approach, this makes sense. Diagnostic testing for selenium, B12, and other micronutrients is straight forward with blood testing with the large national labs like Quest and Labcorp.

    Organic Acid testing is available with US Biotek, Great Plains, Genova, Metametrix. Organic Acids are commonly used for diagnosis of nutritional deficiencies in autistic kids, and are quickly becoming the latest cutting edge method for evaluating nutritional deficiencies in adults and kids.

    Supplementation with selenium is a no-brainer. It is non-toxic and cheap. Other micronutrients such as B12, and vitamin C are mentioned in the review article.

    It is well known that malnutriton is a direct cause of immune-suppression, which in fact , is the definition of AIDS. Depletion of key nutrients like selenium could be a possible mechanism which could explain why HIV could produce a syndrome indistinguishale from starvation in Africans and North American drug abusers who are already suffering from malnutrition. It could also explain why well nourished non-drug users who are HIV positive become long term non-progressors. They are better nourished and better able to withstand micronutrient deficiencies.

    This information is available in the public domain and is not original by any means.

    (1) Biochemistry, Molecular modeling and in vitro activity of an HIV-1-encoded glutathione peroxidase Lijun Zhao et al. PNAS June 6, 2000 vol. 97 no. 12 6356-6361

    (2) HIV Clin Trials. 2002 Nov-Dec;3(6):483-91.Impact of a selenium chemoprevention clinical trial on hospital admissions of HIV-infected participants.

    (3) Suppression of Human Immunodeficiency Virus Type 1 Viral Load With Selenium Supplementation, A Randomized Controlled Trial, Barry E. Hurwitz, PhD Arch Intern Med. Jan 27, 2007;167:148-154.

    (4) American Journal of Clinical Nutrition, Vol. 85, No. 2, 333-345, February 2007 REVIEW ARTICLE

    Micronutrients in HIV-positive persons receiving highly active antiretroviral therapy.Paul K Drain, Roland Kupka, Ferdinand Mugusi and Wafaie W Fawzi

    Compared with HIV-negative person, HIV-infected persons have lower serum concentrations of several micronutrients and more commonly have micronutrient deficiencies (35-42). Among HIV-positive persons not receiving HAART, Observational studies have shown low or deficient serum concentrations of several micronutrients, including thiamine, selenium, zinc, and vitamins A, B-3, B-6, B-12, C, D, and E to be individually associated with either low CD4 cell counts, advanced HIV-related diseases, faster disease progression, or HIV-related mortality (43-57). In addition, micronutrient interventions have been shown to have cellular and clinical benefits in HIV-positive persons not receiving HAART. In randomized placebo-controlled trials, a daily supplement of vitamins C and E for 3 mo reduced oxidative stress (61), a daily multivitamin supplement for 48 wk reduced mortality in subjects with baseline CD4 counts <100 cells/µL (62), and a single large dose of vitamin A to neonates improved survival at 6 wk in those who were HIV-positive by polymerase chain reaction (63). In a randomized placebo-controlled trial in HIV-infected pregnant women, a daily multivitamin resulted in significant reductions in clinical HIV disease progression, improvements in CD4 and CD8 counts and HIV viral loads, and a reduction in HIV-related mortality (64, 65).

  74. #74 cooler
    July 1, 2007

    Step off, you disgust me.

    If we were in Stalins Russia, Mao’s China or Hitlers Germany a young Thomas Paine like myself would come up to a brainwashed loser like you and say, The policies of our leaders are crazy and are killing millions, you’re reply would be “all the experts agree with it so shutup”

    Experts are going to agree with the party line regardless of its merits most of the time, and only a brave few scientists will speak out. Why did experts in many historical instances supported corrupt policies as they did in Russia and Germany for example?

    There are several reasons, thought control, money, funding, fear of speaking out, and a establishment that prevented the public from hearing the other side of an argument. All these circumstances are present here in America today.

    An open public debate is the only way to get to the truth, and most Americans are unaware of the “denialists” arguments because of facsists like you, once they do, the gig is up. Im not saying hiv has nothing to do with AIDS, but I Agree with experts that are not bought and paid for that

    “AIDS is much more complicated than HIV”

    Shyh Ching Lo MD PHD
    Cheif of the infectious disease dept
    Armed Forces Institute of pathology

  75. #75 cooler
    July 1, 2007

    I suggest people read http://www.projectdaylily.com
    and you’ll find out a lot more about Lo and the mycoplasma/biowarfare program. Unlike hiv this microbe kills every animal thats injected with it and it is slowly spreading through the population causing a wide array of diseases like CFS etc.

  76. #76 Nullifidian
    July 1, 2007

    Step off, you disgust me.

    Nice to see you can only insincerely parrot me.

    If we were in Stalins Russia, Mao’s China or Hitlers Germany a young Thomas Paine

    You envision yourself as a latter-day Thomas Paine?! Bwahahahahahah!!

    like myself would come up to a brainwashed loser like you and say, The policies of our leaders are crazy and are killing millions, you’re reply would be “all the experts agree with it so shutup”

    Your is different than you’re. One is a possessive, the other is a contraction. Thomas Paine knew the difference.

    And if you want to go to historical analogies, Stalinist Russia provides us with an unqualified hack ruining Soviet biology by promoting a contrarian view (Lysenkoism) which was refuted by the experience and experiments of experts in the field.

    Given this, you look more like Lysenko than I do.

    Experts are going to agree with the party line regardless of its merits most of the time, and only a brave few scientists will speak out.

    Wrong. There is not a “party line” in science. There’s what works, and what doesn’t. In situations where the evidence is ambiguous, like whether things combusted due to “phlogiston” or oxygen in the 17th century, there is debate. Where things have proven their utility as a predictive and explanatory model like evolution or the transmissibility of HIV as a causative agent of AIDS, there is minimal to no scientific debate about these essentials, and attention turns to finding out more beyond the basics which have already been established.

    If one has evidence that the basics are fundamentally wrong, one can publish a refutation in the literature, where it will be evaluated. What you object to is that scientists aren’t pushovers for your stupid form of argumentation, so you want us to engage in a game of public debate which would lend your view unwarranted credibility and allow you to pull the cheap tricks you can’t get away with from scientists, because you know that your position cannot stand up to scrutiny in the full light of day. That is immoral.

    Why did experts in many historical instances supported corrupt policies as they did in Russia and Germany for example?

    Because everyone of them who didn’t were purged, kept their opinions to themselves, or fled the country. Duh.

    There are several reasons, thought control, money, funding, fear of speaking out, and a establishment that prevented the public from hearing the other side of an argument. All these circumstances are present here in America today.

    So you name “thought control” as the #1 reason that people don’t accept your shit for shinola? Wow. Got to dust off the tinfoil hats, those government mind control rays are way too strong for me!

    An open public debate is the only way to get to the truth,

    Wrong. Where was the “open public debate” and vote on the validity of the general theory of relativity? Inflationary theory? The atomic theory of matter? The chromosomal theory of heredity?

    One would have to be a moron to think that reality changes when you vote on it.

    and most Americans are unaware of the “denialists” arguments because of facsists like you,

    You misspelled “factists”.

    once they do, the gig is up.

    There is no “gig”. People who go into virology, epidemiology, etc. do not want it to be the case that there’s a virus out there which is currently uncurable, and for which there is no vaccine, and which cuts one’s life expectancy down by several decades. They would much rather that AIDS be due to “poppers”, drug use, etc. because those are relatively fixable, compared to a virus.

    Your conspiracy theories are infantile, moronic, unrealistic, and are currently leading people doen the road to death because this cavalcade of bigots and nuts that makes up the public ‘scientific’ face of HIV denialism has achieved some level of traction in countries like Gambia.

    Im not saying hiv has nothing to do with AIDS, but I Agree with experts that are not bought and paid for that

    “AIDS is much more complicated than HIV”

    Shyh Ching Lo MD PHD
    Cheif of the infectious disease dept
    Armed Forces Institute of pathology

    I see. So the taint of government support shows that people cannot possibly be trusted except when they say things that you can mangle until you like them. What sterling intellectual consistency you display.

  77. #77 Independence Day
    July 1, 2007

    I did watch the 20 minute video with Moore and Bergman, and noticed there are comments below the video. Here is one from Michael, and I must agree with Michael points, he is correct. The next comment there is about selenium supplementation, which has been reported in the medical liteature and referred to by the video as a “quack” remedy. A “quack” remedy is defined as anythng that costs a nickel and works better than the toxic drugs peddled by Big Pharma.

    Michael said;

    Dear readers, when someone such as the two fools interviewed in this video tell you there is only one side to an issue, namely their own, you better roll up your pants and put on your boots as quick as you can.

    To begin with, the host, John Mikytuck, introduces these two politicians as doctors: Dr. Moore and Dr. Bergman. But they ain’t medical doctors. These two have NEVER medically or even psychologically dealt with ill or healthy HIV patients. They simply have PHD’s and you don’t even know what their PHD was even in! “Doctor” Bergman is a lawyer, with a P”iled” H”igher & D”eeper” PHD in law at the New York HIV Law Center that relies on funding from pharma companies. Moore is the recipient of AIDS drug manufacturer Bristol-Myers Squibb’s $500,000 “Freedom To Discover” grant and the man HIV dissidents refer to as the most “unashamed” spokesperson for the AIDS establishment.

    Moore says their is no dispute that HIV causes AIDS “among the serious credible scientists”. What a joke. So if you happen to disagree with him, you simply are not serious or credible??? There are hundreds if not thousands of quite serious credible medical doctors and bio scientists that quite vehemently disagree with Moore’s well paid political stance that HIV is the cause of AIDS. Check the list for yourself at the “RethinkingAids.org” website. It includes more than 1000 medical doctors and bio researchers, including Nobel Laureates who disagree with “doctor” Moore.

    “doctor” Bergman, tries her best to paint the top dissidents as somehow rascist and homophobic. Nice try Bergie! But who are you kidding besides yourself? I am a gay man with a black lover who regularly enjoys the company and the friendship of some of the TOP DISSIDENTS who you call rascist and homophobic! I talk to Peter Duesberg and Harvey Bialy quite often, as well as David Rasnick and Charles Geshekter and Henry Bauer, and several of the other leading dissident scientists. They are more supportive of me and my black lover than anyone else I know including my own birth family! Does Bergman really think that Bialy and Duesberg and Black Historian and AIDS dissident Charles Geshekter and David Rasnick are rascist? What a load of crap! They are all willing and unpaid appointees of the South African Presidential AIDS Commission for chrissake! Rasnick and Geshekter and Bialy have DONATED (Hey Bergie, that means, unlike yourself and dr. Moore, unpaid for their services), many months of their lives in assisting health issues throughout Africa!

    Pharma funded doctor Moore tries to show some animations and pictures of who knows what from who knows where as some kind of proof of HIV. What a joke! How does he know what these are pictures of? The dissident scientists say HIV has NEVER even been isolated from a human host, let alone proven to be the cause of AIDS, and that these jokers don’t have a clue if their pictures are of HIV or syphillis or who knows what.

    At least Bergie admits that the “Hit Hard Hit Early” treatment of the late 90′s was a huge mistake, but she fails to mention the greatest mistake of all, which was the 10 years of High Dosage AZT monotherapy that was given to all HIV positives from 1987 to 1997. The average patient taking that poison lived 8 months to 1-1/2 years! Now there are 300,000 gay men that are dead from it including many of my friends! And by the way, 300,000 is FIVE TIMES the number who were killed in Vietnam. All I can say is Bergie should be voted among the top enemies of the gay and black communities! With drug pusher Doctor Moore right beside her!

    Moore warns us that the stuff found on the internet is disinformation, lies, and distortion. Does that include his AIDSTRUTH internet site? You betcha it does!

    Bergie says the black community has had a long tragic relationship to medicine and science, and is justifiably suspicious since the Tuskeegee experiments, but “this time is different”. Who is she kidding? This time it is even worse, because liver failure, directly related to who is taking the HAART drugs, is currently the leading cause of death among those told they are HIV positive.

    The host asked “doctor” Moore “Are there studies that show the difference between those treated with AIDS drugs and those who are untreated? Moore, carefully ignores this simple yes/no question (which by the way the true answer is NO there are no studies of untreated versus treated) and Moore goes back into drug pusher mode with his answer: “There are multiple studies that show the benefits of antiretroviral therapies”. Yeah, of course there are, and they are all done by the very drug companies that are pushing these poisons! There certainly ain’t no studies out there done by any independent non drug company paid groups!

    Bergie goes on to say that “the prime leaders of the denialist movement are overwhelmingly heterosexual, white males who are highly educated, very elite, and most are remarkably hostile to communities of color, african Americans, and gays and lesbians”. Well, just who the hell does she think is running the mainstream 10 billion dollar HIV research thing? Blacks and gays? No indeed, just the very same white/hetero/educated/elite such as Doctor Moore who is sitting right beside her! Not to mention Dr. Gallo of the NIH, Tony Fauci-the head of NIAIDS, and ALL of the US GOVERNMENT HIV researchers and big pharma HIV drug developers. They are all exactly what she says the dissidents are! This woman is seriously in denial!

    The host asks Moore and Bergie if their AIDSTRUTH site is funded by the drug companies. Of course they answer with a “No, it is not funded by drug company money”, but conveniently leave out the fact that both of their own day job paychecks DO COME FROM the drug companies. And Moores most recent check was a straight up cool half million dollars from AIDS drug manufacturer Smith Kline!

    But “doctor” Moore tops it all off when he says: “As a scientist, I find it hugely offensive that there is disinformation, distortion, and lies peddled by people with PHD’s and MD’s who are at least in theory scientists. I them in deep contempt for the perversion of the science that they try to pass to others. They are the people responsible for this death and destruction”.

    What a laugh. He must be talking about himself in this one, but obviously is to enthralled with his half million to listen to his own advice for even a moment. Just remember dr. Moore, when you point at others there are three of your own fingers pointing back at your own self!

  78. #78 cooler
    July 1, 2007

    You preach and whine, but you dont have much evidence to back your position. If you have a brain, you’ll realize there was never any debate on HIV after the Orwellian press conference in 1984. But you don’t have a brain, so please dont send me another sanctimonious tirade, I dont even read half of your idiotic posts.

    Can you give me a link of a scientific study/experiment that was designed to confirm/disprove Gallo’s hypothesis? Guess what, all the studies after Gallo’s claim in 1984 were designed with the premise that HIV already caused AIDS and were measuring something else entirely, had these studies been designed to test the hiv hypothesis they would have designed totally differently.

    So what’s an idiot like you left with? Gallo’s original papers that were published AFTER his government sponsored press conference. What did he have? A partial correlation with no animal model and a microbe that was present in 1 out 1000 t cells that was seemingly nuetralized by antibodies. If you think that alone is enough to prove causation you’re even dumber that I thought.

    Please dont tell me of the “20 years of confirmatory evidence since Gallo” NONE OF THOSE STUDIES/EXPERIMENTS WERE DESIGNED TO TEST THE HIV HYPOTHESIS, THEY ASSUMED IT TO BE TRUE AND WERE DESIGNED TOTALLY DIFFERENTLY BECAUSE OF THAT!

  79. #79 Chris Noble
    July 1, 2007

    Please, Will someone tell me what the pure particulate purified gold standard is? I’ve been asking for days and days, and everybody keeps using the word ‘hiv’, and I know that you’re not just making it up, you know, by believing in it – I know you have the purified gold standard reference particle for each and every test that corresponds with the tests so that all the true positives are positives and all the false positives are just misplace white people… anyway…

    Go here NIH AIDS Research and Reference Reagent Program for HIV viral isolates, purified, proteins, infectious molecular clones, viral load standards, PCR primers, monoclonal antibodies etc.

    Of course you can tell from your armchair that all this is just pixie dust and that thousands of scientists that both contribute to the reagent project and get reagents (for free) are all completely stupid.

  80. #80 Nullifidian
    July 1, 2007

    You preach and whine,

    Wrong again! I’ve neither preached nor whined. I’ve just refused to yield to a known liar.

    but you dont have much evidence to back your position.

    Wrong again!

    If you have a brain, you’ll realize there was never any debate on HIV after the Orwellian press conference in 1984.

    Also incorrect, but when you’re on a roll, why not go for the gusto?

    But you don’t have a brain, so please dont send me another sanctimonious tirade, I dont even read half of your idiotic posts.

    I see. I don’t have a brain because I accept that the widespread acceptance of HIV as the causative agent of AIDS is due to the weight of the evidence and not due to “thought control”.

    It would be funny if the human consequences were not so dire.

    Can you give me a link of a scientific study/experiment that was designed to confirm/disprove Gallo’s hypothesis? Guess what, all the studies after Gallo’s claim in 1984 were designed with the premise that HIV already caused AIDS and were measuring something else entirely, had these studies been designed to test the hiv hypothesis they would have designed totally differently.

    Okay, then wow us with your grasp of immunology and how to design a scientific experiment and tell us how these thousands of published studies and experiments should have looked, given your manifestly extensive expertise in the subject (which leads you to confuse immunodeficiency diseases for autoimmune diseases, for example).

    You’ve made enough unsourced claims. Now’s the time for the rubber to hit the road.

    So what’s an idiot like you left with? Gallo’s original papers that were published AFTER his government sponsored press conference.

    And nearly every other paper to do with HIV in the immunological literature since then.

    What did he have? A partial correlation with no animal model and a microbe that was present in 1 out 1000 t cells

    So is it 1 out of 1,000 or 1 out of 10,000? Or is it 1 out of pi? One out of e? One out of 58 x log 7?

    It has already been explained to you, by others previously and me most recently, that t-cells and CD4+ cells are not the same thing. CD4+ cells are t-cells, but not all t-cells are CD4+ cells. Since repeating arguments based on assumptions known to be false is to be a known liar, why should I give a damn about anything you have to say?

    Please dont tell me of the “20 years of confirmatory evidence since Gallo” NONE OF THOSE STUDIES/EXPERIMENTS WERE DESIGNED TO TEST THE HIV HYPOTHESIS, THEY ASSUMED IT TO BE TRUE AND WERE DESIGNED TOTALLY DIFFERENTLY BECAUSE OF THAT!

    Okay, so how would they be designed if they didn’t allegedly assume HIV-as-the-causative-agent-of-AIDS wasn’t true? I’m sick and tired of you making wild accusations you can’t support. If you can’t show any basis for your claims in fact, then you should admit that and retract that, or if you’re a more abashed soul just shut up and go away. Continuing to try to face those of us who know better out brazenly is a strategy which could only be convincing to a complete babe in the woods.

  81. #81 trrll
    July 1, 2007

    dele, this is what your DT colleague says is a placebo for the placebo controlled nevirapine trial. The drug group received nevirapine and 2 more toxic HIV drugs, the placebo group received a placebo (instead of nevirapine) and two more toxic HIV drugs.

    This is a remarkably deceptive argument. There is not a human subjects ethics committee in the country that would approve such a study, because a fundamental principle of medical ethics is that it is unethical to carry out a placebo controlled study of a life-threatening or painful disease when an effective treatment is available. Instead, studies are required to compare new drugs against the best current treatment. Placebo controlled studies were carried out with first generation drugs such as AZT, when it was unclear whether they would be beneficial or harmful to patients. The landmark AZT study was terminated early (again, as required by ethics rules) when the patients in one treatment group showed dramatically lower AIDS symptoms than the other. When the double-blind code was broken, the group showing reduced progression to AIDS turned out to be the AZT group. Since that time, it has been unethical to carry out placebo controlled studies on anti-HIV drugs. Rather, the drugs are compared against other drugs that have already been established to be effective. Originally, this was AZT. When newer drugs were shown to work better than AZT, these in turn became the standard for the control group.

  82. #82 Chris Noble
    July 1, 2007

    So what’s an idiot like you left with? Gallo’s original papers that were published AFTER his government sponsored press conference. What did he have? A partial correlation with no animal model and a microbe that was present in 1 out 1000 t cells that was seemingly nuetralized by antibodies. If you think that alone is enough to prove causation you’re even dumber that I thought.

    Gallo’s original paper had passed peer-review before the press conference.

    You are also displaying symptoms of DTWS (Denialist Time Warp Syndrome).

    Only a small percentage of lymphocytes are in peripheral blood. The majority of lymphocytes are in the gut.

    It is now recognised that a high proportion (~60%) of CD4+ cells in the gut are infected during acute infection and that the majority of CD4+ cell depletion occurs in the gut at this stage.

    HIV pathogenesis: the first cut is the deepest.

    The same pattern is seen in the SIV/macaque models of HIV infection.

  83. #83 Chris Noble
    July 1, 2007

    3) Adele, this is what your DT colleague says is a placebo for the placebo controlled nevirapine trial. The drug group received nevirapine and 2 more toxic HIV drugs, the placebo group received a placebo (instead of nevirapine) and two more toxic HIV drugs. Adele, so you really believe that this charade is a placebo controlled trial? The “placebo” is in actuality 2 toxic drugs. What ever happened to the old way, one group receiving the drug and the other group receiving a placebo? (not a placebo and two toxic drugs?) This is very sick twisted logic which is a disgrace to humanity and medical science. Do you agree with this Adele, that 2 toxic drugs can be called a “placebo”? You want to talk about crap? This is crap.

    You seem to be claiming that three different drugs, A, B and C are all highly toxic and provide no benefit.

    What does the “dissident” theory predict will happen to two groups that take
    a) Drugs A, B and a placebo C
    b) Drugs A, B and C

    ?

    If you look at any set of ethical guidelines for clinical experiments you will find that it is considered unethical to test a new drug against no treatment where there is an existing treatment.

    In fact pharmaceutical companies are often criticised for doing exactly this. When a pharmaceutical company develops a new me-too drug to compete on the market there is an obvious incentive to sponsor research that compares the new drug to placebo rather than the existing treatments. If they do an experiment comparing their new me-too drug with the best existing treatment and it performs worse then it doesn’t look good. If they do an experiment comparing the new me-too drug with a placebo and it is better than placebo then it looks good.

  84. #84 Independence Day
    July 1, 2007

    For the drug compnay reps and paid AIDS political activists, repeating again, a placebo controlled study is one in which the study group is divided into two arms. The placebo group gets the inert tablet with no pharmacologic activity, and the drug group gets the drug with the pharacologic activity.

    For HIV drugs, these rules have been thrown out the window, and it is common practice to do these unethical studies in Africa where the data cabinet sometimes is found missing and the data “recontructed”. Scientific misconduct and outright fraud has been publicly exposed in a number of these studies. These studies are paid by the drug maker, and if you believe these tainted studies, then I have a bridge to sell you.

    Again, the use of two toxic drugs for the placebo arm and three toxic drugs for the drug arm of a study is NOT a placebo controlled study. It is a charade and a disgrace to science and humanity. For a real placebo controlled study see reference number 3 below in which a simple nontoxic mineral that costs a nickel performed better than any HIV drug study.

    Repeating, NONE of the HIV drug studies were REALLY placebo controlled. AIDS political activists are paid to repeat their dogmas and actually believe in it. The rest of the free world is not required to.

    If HIV is NOT the cause of AIDs, then what is?

    There have been a number of requests for an alternative explanation. We are all familiar with the drug hypothesis by Professor Duesberg as one alternative explanation.

    Here is another.

    The role of micronutrients such as selenium has been largely ignored by the mainstream medical system. Recent studies have implicated selenium deficiency as a key to AIDS pathogenesis. It is well known that the HIV genome encodes for glutathione peroxidase which depletes serum selenium. (1)

    HIV positive patients who are supplemented with cheap inexpensive, nontoxic selenium tablets, have 30% less hospitalization. (2)

    and show dramatic improvements in CD4 cell count and HIV reduction by PCR measurements. (3)

    This improvement in CD4 cell count and surrogate markers with selenium is much more impressive than any of the HAART drug cocktail studies, none of which are REALLY placebo-controlled.

    An excellent review article on all micronutrients and HIV can be found here. (4)

    For Noreen and Kevin, for a non-toxic cost effective approach, this makes sense. Diagnostic testing for selenium, B12, and other micronutrients is straight forward with blood testing with the large national labs like Quest and Labcorp.

    Organic Acid testing is available with US Biotek, Great Plains, Genova, Metametrix. Organic Acids are commonly used for diagnosis of nutritional deficiencies in autistic kids, and are quickly becoming the latest cutting edge method for evaluating nutritional deficiencies in adults and kids.

    Supplementation with selenium is a no-brainer. It is non-toxic and cheap. Other micronutrients such as B12, and vitamin C are mentioned in the review article.

    It is well known that malnutriton is a direct cause of immune-suppression, which in fact , is the definition of AIDS. Depletion of key nutrients like selenium could be a possible mechanism which could explain why HIV could produce a syndrome indistinguishale from starvation in Africans and North American drug abusers who are already suffering from malnutrition. It could also explain why well nourished non-drug users who are HIV positive become long term non-progressors. They are better nourished and better able to withstand micronutrient deficiencies.

    This information is available in the public domain and is not original by any means.

    1) Biochemistry, Molecular modeling and in vitro activity of an HIV-1-encoded glutathione peroxidase Lijun Zhao et al. PNAS June 6, 2000 vol. 97 no. 12 6356-6361

    (2)HIV Clin Trials. 2002 Nov-Dec;3(6):483-91.Impact of a selenium chemoprevention clinical trial on hospital admissions of HIV-infected participants.

    (3) Suppression of Human Immunodeficiency Virus Type 1 Viral Load With Selenium Supplementation, A Randomized Controlled Trial, Barry E. Hurwitz, PhD Arch Intern Med. Jan 27, 2007;167:148-154.

    (4) American Journal of Clinical Nutrition, Vol. 85, No. 2, 333-345, February 2007 REVIEW ARTICLE
    Micronutrients in HIV-positive persons receiving highly active antiretroviral therapy. Paul K Drain, Roland Kupka, Ferdinand Mugusi and Wafaie W Fawzi

    Compared with HIV-negative person, HIV-infected persons have lower serum concentrations of several micronutrients and more commonly have micronutrient deficiencies (35-42). Among HIV-positive persons not receiving HAART, Observational studies have shown low or deficient serum concentrations of several micronutrients, including thiamine, selenium, zinc, and vitamins A, B-3, B-6, B-12, C, D, and E to be individually associated with either low CD4 cell counts, advanced HIV-related diseases, faster disease progression, or HIV-related mortality (43-57). In addition, micronutrient interventions have been shown to have cellular and clinical benefits in HIV-positive persons not receiving HAART. In randomized placebo-controlled trials, a daily supplement of vitamins C and E for 3 mo reduced oxidative stress (61), a daily multivitamin supplement for 48 wk reduced mortality in subjects with baseline CD4 counts <100 cells/µL (62), and a single large dose of vitamin A to neonates improved survival at 6 wk in those who were HIV-positive by polymerase chain reaction (63). In a randomized placebo-controlled trial in HIV-infected pregnant women, a daily multivitamin resulted in significant reductions in clinical HIV disease progression, improvements in CD4 and CD8 counts and HIV viral loads, and a reduction in HIV-related mortality (64, 65).

  85. #85 Dr. PS Duke
    July 1, 2007

    On June 30 at 6:42, Apy said (in reference to others claiming that a court of law should decide whether or not HIV is harmless):
    ===
    It would certainly be nice if a layman could spend 20 minutes listening to both sides adn be educated enough to make a decision about which side is correct but that is not the case. You are free to make your mind up either way but eventually you are relying on trusting what someone has said in order to form your opinion. I don’t see how a jury of millions of laypeople would change this at all. Let’s say the entire world decides to come to a majority rules verdict. In the end it comes down to how many people believed one side over the other and their verdict is not guranteed to be correct just because a majority agree to it.
    ======

    What is missing in this line of reasoning, is the fact that at least in USA courts of law, there are rules and regulations about telling lies, presenting evidence to back up claims, etc. There are very good reasons why Duesberg et al restrict their comments about the “gay lifestyle” being the cause of AIDS to web sites, and do not enter courts of law with them.

    Recently, the Perth Group entered a legal arena with their rhetoric about lack of proper isolation of HIV, but they were careful not to enter during the trial, where perjury laws were in effect. Instead, they tested the waters in an appeal hearing where there were no laws against perjury. They could say whatever they liked, and not risk penalty if they were caught lying.
    http://www.courts.sa.gov.au/judgments/Judgments2007/0427-SASC-143.htm

    The other point to be made is that scientific peer review is another type of jury system. It too has rules and regulations, and penalties for breaking those rules. While anyone can set up a web site claiming that all gays who get AIDS are drug abusers, if one wished to publish that type of statement in a peer-reviewed journal, they would have to have data to back the claim up. Duesberg has in fact published a few papers in journals, but often in letters or commentary sections where peer review is not done. He has some data on drug use in the USA and data on AIDS cases in the USA, but has never bothered to check to see if the individuals who use the drugs are the same individuals who get AIDS. In fact others have done so, and found that HIV and not drug use, is the factor that correlates with development of AIDS.

  86. #86 noreen Martin
    July 1, 2007

    Independence Day, you hit the nail right on the head? Selenium is important to health, in the states the areas with the lowest naturally occurring selenium in the soil have the highest cancer rates. In Africa, places with low selenium have high AIDS cases. Many vitamins and supplements have been proven to contribute to health. At the height of my sickness, I was taking 50 vitamins, supplements, herbs, good eating habits along with the medicines, which all assisted in my recovery. I believe in using all that is available to the patient to get well. I never said that the meds did not help, only that they should not be used for persons without symptoms or for long term use, then they become the next problem of the patient.

  87. #87 Chris Noble
    July 1, 2007

    Again, the use of two toxic drugs for the placebo arm and three toxic drugs for the drug arm of a study is NOT a placebo controlled study. It is a charade and a disgrace to science and humanity. For a real placebo controlled study see reference number 3 below in which a simple nontoxic mineral that costs a nickel performed better than any HIV drug study.

    Suppression of Human Immunodeficiency Virus Type 1 Viral Load With Selenium Supplementation, A Randomized Controlled Trial, Barry E. Hurwitz, PhD Arch Intern Med. Jan 27, 2007;167:148-154.

    Errr. The majority of patients (~75%) in this study were taking “toxic drugs”. By your logic the study must be invalid.

    You also neglect to mention that the patients taking ART had much lower viral load measurements than those not taking ART. This effect was much bigger than the effect of selenium supplementation.

    You also forgot to answer my question.

    What does the “dissident” theory predict will happen to two groups that take
    a) Drugs A, B and a placebo C
    b) Drugs A, B and C

  88. #88 noreen Martin
    July 1, 2007

    Why isn’t studies being done to settle this arguement? There are too many unanswered questions and things that just don’t add up to accept only the current theory. There has to be many avenues, which leads a person to AIDS. What do I have in common with gay men, who seem to have the majority of cases? I never took drugs except what was over-prescribed by doctors, smoked pot. etc. and probably some of them didn’t either. If the AIDS cases were equally divided between the sexes, then I could entertain that HIV had something to do with it, but it is not.

  89. #89 David Marjanović
    July 1, 2007

    Tara,

    you write that the ‘evolution deniers’ debate has already taken place ‘in the literature’, but ‘hasn’t withstood the test.’

    I see a debate ongoing, spilling into the public sphere, gaining momentum and a great deal of ink spilled in the press.

    LOL. I see a debate in the popular media of the USA and Turkey, and that’s it (with the rest of the world laughing at it). Anywhere else there’s no debate on whether evolution happens, most importantly not in the scientific literature. The proverb applies here:

    Debate is whatcha put on de hook to catch de fish.

    I am familiar with the historical debates, reaching back to Ernst Mayr, I know of no serious scientist who would claim any debate to be over because of putsch-like arguments forwarded by a medical elite.

    There are debates within evolutionary biology, like precisely how fast evolution can happen under which circumstances (or rather how common those circumstances are). Ernst Mayr participated in such debates. The debate on whether evolution happens ended in the late 19th century, and I’m quite surprised you didn’t know that.

    and I am agnostic on most evolutionary claims

    Then read more. :-)

    although I reject the neo-Darwinian simplification of descent as a means and natural selection – ie sexual congress – as the means for speciation.

    So you don’t know what natural selection is.

    Some inheritable traits lead to more surviving and fertile offspring (in a given environment). Over time, the frequency of these traits in a population will therefore increase (if the environment stays stable). That’s natural selection.

    You don’t need sex for it. Give me ten million Escherichia coli on a petri dish, a few microliters of a suspension of a suitable bacteriophage, and a day or two on 37 °C: a few of the bacteria will acquire a mutation that happens to make them resistant against the virus, and so you’ll see circular patches of bacterial lawn appear in the petri dish that is otherwise covered by plaque. (I’ve done that experiment several times at the university; it’s part of introductory courses in molecular biology.) The trait is resistance, and the environment is the virus. There you have natural selection. It’s very simple.

    The symbiogenicists are much further along the right path, in my opinion.

    Symbioses, too, are subject to natural selection. Sure they are important, and sure they were overlooked too much before a few decades ago, but they are merely a special case, not something new that mutation and selection couldn’t explain. It’s like how you can’t predict biology from quantum electrodynamics and the theory of gravity, even though these are enough to explain (in hindsight) every detail that happens in biology, and even though they don’t make the big picture impossible.

    Science is always an opinion.

    You are entitled to your own opinions, but not to your own facts. No matter what the postmodernists say, there is such a thing as reality, and there is such a thing as an observable fact.

    The rest is opinion — but it’s testable. If there’s no way it could possibly be falsified by observation, it’s not science, by definition! As long as you can answer the question “If I were wrong, how would I know?”, you are doing science.

  90. #90 David Marjanović
    July 1, 2007

    What do I have in common with gay men, who seem to have the majority of cases?

    They did AFAIK have the majority of cases around when I was born in 1982. That was because they changed their partners most frequently.

    Those times are over. The vast majority of cases nowadays are heterosexual people of both sexes in southern Africa. Excuse me, don’t you know anything?

    You get HIV by blood contact; tiny wounds suffice. Sex (including oral, BTW) is enough to create such wounds. That’s the most important way AIDS keeps spreading.

    And if you don’t live in a sterile environment while the virus destroys your helper T cells and thus your immune system, you will get the full range of AIDS symptoms from getting moldy alive, or from a mutation that would otherwise have been kept under control by the immune system but now leads to Kaposi’s sarcoma, or from the common cold, and your years will be numbered.

    (There, incidentally, we have the “cofactors” that make AIDS “more complicated than HIV”.)

  91. #91 noreen Martin
    July 1, 2007

    I do know that the majority of AIDS cases in the states is not equal, which you avoided addressing. What is your explantion for that? KS was on the planet long before HIV was implimented with AIDS but let’s just keep on adding more and more unrelated conditions to the AIDS defining diseases as soon it won’t matter what an HIV-Positive person has, it will be blamed on HIV.

    And I do know how to live with AIDS naturally as you see no one is ever allowed to be cured of AIDS. Even cancer patients get a reprieve after 7 years. They cannot let go of the AIDS numbers or else their statistics would crash. Do you not find it odd that these statastics are counted cumulatively, to make it look worse than it is? Why is HIV and AIDS lumped together in the counting, to hide the truth?

  92. #92 noreen Martin
    July 1, 2007

    I know what it feels like to be sick and dying, not to make make it to the bathroom and have accidents in the house. I know what if feels like not be able to eat anything and vomitting one’s gut up. I know how it feels not to be able to get off the couch or even have the strength to fix Christmas bulbs on a tree. I know what if feels like to drop weight and have hair fall out and to look like death warmed over. I know how odd it feels not to be able to remember simple things like a grocery list or phone numbers. I know how painful thrush is in one’s mouth and fearing that it might be cancer. I know how anemia feels and adds to one’s tiredness, how a fast heart beat feels and having heavy breathing and not being able to breath. I’m sure that I have forgotten things and I know how arterial, blood gas tests, spinal taps, IV’s and bone biopsies feel. Most of you talk about theories and papers but I have been there and know what works for me, whether you agree with me or not.

  93. #93 Pope
    July 1, 2007

    They [gays] did AFAIK have the majority of cases around when I was born in 1982. That was because they changed their partners most frequently.
    Those times are over. The vast majority of cases nowadays are heterosexual people of both sexes in southern Africa. Excuse me, don’t you know anything

    Mr. David,

    Was there ever a time when the vast majority of cases in South Africa were not heterosexual people of both sexes (hint, hint perhaps when the apartheid regime was in place).

    Does this mean that before it was homosexuals who changed partner most often, but now that the South Africans are left to their own devices, they are the ones who change partner most frequently?

    Perhaps you mean that there are more AIDS cases in South Africa nowadays than in the rest of the world?

    And if you don’t live in a sterile environment while the virus destroys your helper T cells and thus your immune system, you will get the full range of AIDS symptoms.

    Thats quite a mouthful, david, the full range of AIDS symptoms is pretty extensive. In fact you get the opportunistic diseases that are prevalent in the area or subpopulation you are part of, even if you live in a sterile environment while the virus destroys your helper T cells, since some opportunistic infections are already lying dormant in your body.

    Don’t you know anything?

  94. #94 Pope
    July 1, 2007

    PS

    David writes “southern Africa”. That of course makes it possible that he is educating us about the conditions not in South Africa, but in what Dr. Noble and Mr. Jefferys would refer to as “subsaharan Africa”.

  95. #95 Patriot Games
    July 1, 2007

    This is a very important paper, dicussing the probable mechanism of disease, i.e. selenium depletion caused by HIV.

    It is well known that selenium depletion leads to immune system failure. There are many studies such as this one showing selenium supplementation to have a beneficial effect. This is non-toxic and inexpensive, so it is ignored by conventional medicine which gives toxic drugs causing liver failure, lipodystrophy and stevens johnson exfoliation.

    This paper also explains the long term non-progressors who have HIV and don’t get sick. They have excellent nutrition and don’t get selenium depleted.”Dietary deficiencies that are common in chronically ill, impoverished, and drug-using populations can lead to oxidative stress and alter a viral genome such that a normally benign or mildly pathogenic virus can become highly virulent.44 ”

    Suppression of Human Immunodeficiency Virus Type 1 Viral Load With Selenium Supplementation

    This study is, to our knowledge, the first double-blind, randomized, placebo-controlled trial in a community-based cohort of HIV-infected men and women to demonstrate that daily supplementation with 200 μg of selenium for 9 months elevates the serum selenium level and suppresses the progression in HIV-1 viral load.

    The selenium supplement resulted in no adverse events, suggesting that it may be administered safely at the dosage used, a finding consonant with that of previous oncological clinical trials.13

    The treatment effects were independent of subject-related factors, including age, sex, ethnicity, income, education, and past and current drug use. In addition, the findings remained significant after correcting for the effects of disease-related factors, including ART regimen and adherence, HIV disease stage and duration, and HCV coinfection.

    The study showed that the induced change in serum selenium concentration significantly predicted change in the HIV-1 viral load. Moreover, there is strong evidence that the primary selenium effect was on the viral burden. In contrast, the observed benefit of treatment on the CD4 cell count was indirect via the treatment effect on the viral load.

    Although no previous studies have examined the relationship of serum selenium level with HIV-1 viral load, previous HIV studies have shown a relationship between a lower serum selenium level and a lower CD4 count,28-30 more opportunistic infections,31 faster disease progression, and greater HIV-related mortality.6-7 The only other randomized controlled trial of selenium supplementation (200 μg/d) in HIV-infected individuals found a significant decrease in hospital admission rates and CD4 counts declining below 50 cells/μL for those treated with selenium.32 Thus, selenium supplementation appears to have beneficial effects on HIV disease severity and progression.

    The literature indicates that, throughout HIV disease progression, micronutrient and trace element deficiencies are prevalent and may result from malabsorption, altered metabolism, gastrointestinal tract infection, and altered gut barrier function.8

    The exact mechanism by which selenium exerts its effect on HIV-1 viral replication is not known, although the literature suggests several possibilities. One prominent hypothesis has been that diminished antioxidant function may be a contributing factor. The HIV virion is a powerful polyclonal activator and, in turn, stimulates high levels of proinflammatory cytokines and enhanced reactive oxygen species formation, the consequence of oxidative metabolism.38

    The excessive reactive oxygen species formation, when in imbalance with antioxidant capacity, is termed oxidative stress. Excessive reactive oxygen species formation can damage cells and essential biological molecules, resulting in greater expression of proinflammatory cytokines that can further exacerbate oxidative stress.39-40

    Selenium is required for the formation of glutathione peroxidase,41 which acts in the destruction of hydrogen peroxide and organic hydroperoxides, thereby reducing the further propagation of free radicals and cytotoxic agents.

    The HIV-1 virus may require selenium to produce its own selenoenzymes, thereby depleting selenium resources.42-43

    Dietary deficiencies that are common in chronically ill, impoverished, and drug-using populations can lead to oxidative stress and alter a viral genome such that a normally benign or mildly pathogenic virus can become highly virulent.44

    In particular, HIV-1 replication in vitro is facilitated by exposure to oxidative stress.45 In contrast, antioxidant multivitamin supplementation has been observed to diminish oxidative stress and HIV-1 viral burden.46 These findings support the notion that selenium may act on the HIV virus indirectly.

    The cellular actions of selenium are also linked to the redox regulation of genes. Others have provided evidence that the HIV-1 virion encodes homologues of selenoproteins that influence immune-related genes that regulate cytokine production, cellular proliferation, and apoptosis.47-48 Therefore, the selenoprotein is posited to act directly on the HIV-1 virion to suppress its replication. However, supporting evidence for this hypothesis remains to be obtained. Therefore, benefits derived from selenium supplementation may be due to its indirect and direct effects, but may also be related to another, as yet unidentified, chemopreventive activity.

  96. #96 noreen Martin
    July 1, 2007

    For the what’s it worth department, many HIV-Positives take much higher doses of selenium, 1000mcg or eating 10 brazil nuts is the equivalent. As was mentioned above, it is easy to get selenium, Vitamin D and other nutrient levels tested. However, infectious disease doctors don’t routinely test for these. I found it difficult to get them interested in any supplements whatsoever. They stay focused on “viral loads” and CD4 counts.

  97. #97 Alan Kellogg
    July 1, 2007

    …young Thomas Paine like myself…

    Cooler,

    I knew Thomas Paine. Thomas Paine annoyed the crap out of me. You, sir, are no Thomas Paine.

  98. #98 Pope
    July 1, 2007

    Sir Kellog,

    I was just admiring the genius of your literary style (I suppose these are your sharp analyses, since one arrives on them when clicking your name). It’s truly marvelous how your artful figures of speech distinguish you from the likes of Tara, Noble and Jefferys. It was a difficult choice, I deny it not, but I think this representative piece of prose poetry more than anything bespeaks your originality:

    You ever notice how alike denialists sound? We could be talking about creationists, holocaust deniers, sasquatch skeptics, HIV deniers, terrorism deniers, global warming deniers, or even flat earthers, and you’ll get the same rhethoric with only the details changed.

    One caveat, Sir Kellog, a mere factual correction if you don’t mind, since your style and pitch are truly perfect. We denialists have never expressed scepticism about the existence of the sasquatch.

    While we are on the subject of factual corrections:

    The HIV/AIDS connection is not something cobbled together by people with nothing better to do.

    As a matter of fact that’s exactly what it is. Gallo and friends were so-called retrovirologist left with nothing better to do than looking for an HIV-AIDS connection since they had failed so miserably in finding a retroviral explain-all for cancer. Gallo himself had several failed attempts to come up with a pathologically significant retrovirus under his belt before he finally made a useful invention.

  99. #99 cooler
    July 1, 2007

    This myth that science operates in such a pristine manner and that no public scrutiny should be allowed is ridicolous. We are just supposed to take 100 times the safe EPA level of mercury and listen to Frauds like Gallo and not be allowed to ask any questions. Just trust that a vaguely defined group of “scientists” have reached a “consensus”

    We are told the science is too complex to understand……..An 8th grader could understand Koch’s postulates, much like the public can learn about economic policy, abortion, global warming etc and make a desicion based upon informed consent, not by being brainwashed by a “scientific community” thats been either bought off or brainwashed by the CDC, much like many experts in other oppresive societies have being unduly influenced by governmental/corporate propaganda.

    Where are these honest scientific debates taking place when it comes to health issues? They are not taking place at all. If you have a bad hypothesis yet have support from a particular administration or drug company your hypothesis will be accepted regardless of it’s merits in many instances.

    Can someone show me the scientific studies that were designed to test Gallo’s hypothesis? They dont exist, all the studies that came after 1984 were designed with the premise that HIV already caused AIDS, nullifidian, dumbass, they would have been designed much differntly and controlled for confounding factors if they really saught to confirm what he said. The scientists never saught to prove or disprove his claims because if the CDC supported it, In Orwellian fashion It must be true right?

    Where are the original papers that tested the hypothesis that it was ok to put mercury in vaccines? They don’t exist. There is no debate in science, establishment scientists mindlessly beleive anything the CDC says, do you think if Robert Gallo didnt have government support any of us would have ever heard of “HIV.” Probably not.

  100. #100 Dan
    July 1, 2007

    Amongst those who promote the HIV=AIDS hypothesis, I’ve noticed many times they use the words murder, murdering, murderer and murderers.

    Larry Kramer has often said that gays are murdering each other.

    In one of my hometown weeklies, gay writers talk about gays murdering each other at bathhouses.

    Outspoken AIDS activists have called those who question/challenge the hypothesis murderers.

    Are people who question/challenge the HIV=AIDS hypothesis murderers?

    Yes or No.

  101. #101 Nullifidian
    July 1, 2007

    We are told the science is too complex to understand……..An 8th grader could understand Koch’s postulates,

    But can they understand the exceptions to Koch’s postulates, like the fact that Mycobacterium leprae has not been cultured in vitro and understand why that doesn’t matter to knowing that M. leprae is the causative agent of leprosy?

    much like the public can learn about economic policy,

    Can they critique the general equilibrium theory of macroeconomics in light of recent observed trends in globalization? Do they know the general criticisms of globalization, including recent ones in trade theory which show that the benefits of free trade are a special case, and do not apply now?

    abortion,

    Many of the arguments against abortion rest on assumptions which can be exploded by developmental biology, like the oft-repeated claim that fetuses can feel pain by nine weeks, five weeks, seven weeks. Whatever the number is, and it seems to vary far too much for any real observed phenomenon, the actual baseline for even the possibility of sensing pain (or anything) is when the thymus develops at approximately week 25.

    global warming etc

    Can they understand the difference between weather and climate? Could they explain how global warming could lead to local cooling? What is the “hockey stick”? What’s the current scientific consensus on the “hockey stick”?

    People can learn about these things, but true understanding requires a significant investment in one’s background knowledge, and serious mental effort. You don’t want to admit that because you’re lazy, dishonest, or incapable of mental effort, or some combination of all three. Just look at how you react when I ask you to support your claims with evidence and reasoning, in re: explaining how published studies would look different if they were testing the notion that HIV is a causative agent of AIDS.

    nullifidian, dumbass, they would have been designed much differntly and controlled for confounding factors if they really saught to confirm what he said.

    There it is. There’s your support for your claim. You just repeat the same claim over and over again, and call me a “dumbass” apparently for demanding that you adduce some support for your claim. I guess I should just bow down in abject prostration before the Big HIV Denialist Expert who cannot support his claims. Oh well, if he cannot, who cares since he’s so obviously right that the scientific consensus is due to “thought control” rather than an evaluation of the evidence, even if he doesn’t know what the evidence is and is so ignorant as to confuse an autoimmune disase with an immunodeficiency disease.

    And yet somehow I’m the authoritarian precisely because I disdain this argument based on your overweening arrogance and completely illegitimate arguments to authority. Too funny.

  102. #102 Nullifidian
    July 1, 2007

    …when the thymus develops at approximately week 25.

    Of course, I meant to say the thalamus. I really need to start using preview.

  103. #103 Justice is Swift
    July 1, 2007

    Dan said:

    Amongst those who promote the HIV=AIDS hypothesis, I’ve noticed many times they use the words murder, murdering, murderer and murderers.
    Larry Kramer has often said that gays are murdering each other. In one of my hometown weeklies, gay writers talk about gays murdering each other at bathhouses. Outspoken AIDS activists have called those who question/challenge the hypothesis murderers. Are people who question/challenge the HIV=AIDS hypothesis murderers? Yes or No.

    In Nazi Germany, average ordinary doctors were deeply involved assisting the national program of sterilization and medical genocide of the mentally retarded, homosexuals, and any undesirables for that matter, including 6 million undesirable Jews. This average ordinary doctor went to work every day, and looked into the mirror and said to himself, “I am a good person. I am doing my job.”

    And the same mentality and social forces are at work with the iatrogenic genocide of 300,000 homosexuals and drug addicts, the undesirables of our society. This time the drug was AZT, instead of cyclon B, and it was the ordinary doctor in the Medical System, not Nazi doctors that administered the lethal drug. And again, these ordinary doctors are good people who receive community awards for their deeds. Under the Nazi doctors, millions marched to their deaths unwittingly hoodwinked into believing they entered shower rooms. Similarly a quarter of a million undesirables were eliminated with AZT, all the while trusting in the our medical system, our government agencies, the media and their doctors who simply betrayed them with a lethal drug.

    We sometimes forget that the state of Indiana had an active program of sterilization with laws on the books for many years which served as an example for the Germans to follow.

    And again we see these forces at work with sleep walking doctors administering toxic drugs to pregnant mothers with no placebo controlled trial showing efficacy and plenty of studies showing hideous adverse toxicity. All of which is justified by the prevailing social hysteria over HIV /AIDs. Well, the hysteria is over, and people are waking up and opening their eyes for the first time, and those responsible for these crimes will be held accountable. Justice is swift.

    Nazi Nightmares: Medical Killing

    Nazi doctors carried out direct medical killings as part of “life unworthy of life” policy, as well as deathly experiments on concentration camp prisoners. German doctors were forced to do that according to the Nazi medical decisions. There were two racial programs which directed the entire work of the German physicians of that time:

    - coercive sterilization,
    - killing of “impaired” people.

    Euthanasia program alone, the centers of which were in Hartheim, Somnenstein, Grafeneck, Bernburg, Brandeburg and Hademar, has launched into eternity about 100000 mentally and permanently sick people. They were murdered in carbon monoxide gas chambers. The systematic euthanasia procedures began in April 1940 and within three weeks all Jewish patients were to be murdered.

    Along with that, Nazi obsession with an idea of complete erasure of the Jews out of Europe led to the elimination of Jewish physicians and the gradual exclusion and barring of Jews from medical practice altogether. In 1939 an amendment to the Nuremberg Laws nullified the medical licenses of all Jewish doctors. Jewish professors, among them well known authorities, were excluded from the universities and medical schools.

    In June 1933 a sterilization law was introduced. Chronically sick and “asocial” Germans were sterilized. Physicians took part in “Heredity Health Courts” and performed the sterilization surgical procedures. Reliable estimates for the number of sterilizations fall between 200000 and 350000.

    Further on, in their fulfillment of the Reich commands, the Nazi set up a series of pure extermination camps using gas chambers and specially trained personnel. SS doctors also practiced a murderous “epidemiology” sending prisoners with a contagious disease, especially typhus and scarlet fever, to the gas chambers, sometimes with their fellow patients, contagious or not, so that the entire block could be “disinfected”. In the medical blocks, SS doctors ordered and supervised, and sometimes themselves killed debilitated prisoners with phenol injections.

  104. #104 trrll
    July 1, 2007

    Again, the use of two toxic drugs for the placebo arm and three toxic drugs for the drug arm of a study is NOT a placebo controlled study. It is a charade and a disgrace to science and humanity.

    No, this is sheer nonsense. Ethical standards do not permit placebo controlled studies in dangerous or painful diseases when an effective treatment is available. This is not unique to HIV; it applies to ALL diseases, ranging from cancer to arthritis. The effectiveness of first-generation anti-AIDS drugs was established in placebo controlled studies. Once that was achieved, placebo-controlled studies became unethical, and subsequent generations of drugs were tested against known treatments. Again, this is standard practice for all known diseases.

    Referring to the standard regimen as “toxic drugs” is also deceptive. ALL drugs have soem degree of toxicity associated with them, so “toxic drugs” is at best redundant, as well as falsely implying that there is something uniquely bad about this particular combination of drugs.

  105. #105 cooler
    July 1, 2007

    Dumbass,
    It was HIV expert Joel Gallant that said a diffuse immune response that causes immune depletion, not me. When you “experts” change your tune over and over it’s ok, right? Remember it was Gallo who first said HIV is killing the T cells!

    What about those Experts that said “hit hard hit early” in 1996 and gave monster doses of AZT in the 80′s ooops! The experts admitted they were wrong, and now only give treatment late in the disease. Many people died because of this. It was those evil denialists that warned that it was wrong to take high doses AZT early in treatment! How dare them, even though they were right!

    Because there is no animal model, there should be a study that’s desingned to see if HIV positive people without drugs, AZT, coinfections and catastrophic stress die sooner than hiv negative people.

    All those cohort studies on AIdstruth don’t control for confounding factors because they were never designed to test the HIV hypothesis, they assumed it to be true.

    How else is one supposed to prove that your barely detectable/no animal model/10 year window period microbe causes disease, since you have thrown out Koch’s postulates? Using your standards any passenger virus could be said to cause a disease.

  106. #106 trrll
    July 1, 2007

    An 8th grader could understand Koch’s postulates

    Indeed. In particular, an 8th grader would surely know the meaning of the word “postulate,” understanding its meaning as basically similar to “hypothesis,” or “assumption,” and would immediately recognize the foolishness of holding up these 19th century speculations as some sort of absolute standard for identification of an infectious agent. Indeed, Koch himself revised his postulates after finding exceptions, and many other exceptions have been identified since then.

  107. #107 Pope
    July 1, 2007

    However, the use of antiretroviral therapy is NOW associated with a series of serious side effects and long-term complications that may have a negative impact on mortality rates. More deaths occurring from liver failure, kidney disease, and cardiovascular complications are being observed in this patient population.
    http://www.nih.gov/about/researchresultsforthepublic/HIV-AIDS.pdf

    Trrl, since an answer wasn’t forthcoming on the smallpox thread, maybe you can tell me what that “now” means.

    Does it mean that previously there were no problems with serious side effects, that “might have a negative impact on mortality rates”, but now (Oct. 2006) there are?

    Or does it mean, previously we didn’t really want to admit it, but now we can’t afford to ignore the problem any longer?
    The drugs we’re talking about “now” are all part of the new “mild” drugs that were tested against AZT are they not?

    Would you care to point us to all those placebo controlled studies that showed unequivocally that AZT was a good thing to hit hard and early with?

  108. #108 Patriot Games
    July 1, 2007

    nullfidian said

    We are told the science is too complex to understand……..An 8th grader could understand Koch’s postulates, But can they understand the exceptions to Koch’s postulates, like the fact that Mycobacterium leprae has not been cultured in vitro and understand why that doesn’t matter to knowing that M. leprae is the causative agent of leprosy? [snp for brevity]People can learn about these things, but true understanding requires a significant investment in one’s background knowledge, and serious mental effort. You don’t want to admit that because you’re lazy, dishonest, or incapable of mental effort, or some combination of all three. Just look at how you react when I ask you to support your claims with evidence and reasoning, in re: explaining how published studies would look different if they were testing the notion that HIV is a causative agent of AIDS. nullifidian, dumbass, they would have been designed much differntly and controlled for confounding factors if they really saught to confirm what he said. There it is. There’s your support for your claim. You just repeat the same claim over and over again, and call me a “dumbass” apparently for demanding that you adduce some support for your claim. I guess I should just bow down in abject prostration before the Big HIV Denialist Expert who cannot support his claims. Oh well, if he cannot, who cares since he’s so obviously right that the scientific consensus is due to “thought control” rather than an evaluation of the evidence, even if he doesn’t know what the evidence is and is so ignorant as to confuse an autoimmune disase with an immunodeficiency disease. And yet somehow I’m the authoritarian precisely because I disdain this argument based on your overweening arrogance and completely illegitimate arguments to authority. Too funny.

    Nullfidian uses a typical evasive gimmick in his reply to cooler. The science is much too complex for poor illiterate cooler to understand. Its futile trying to explain, so why bother. Sorry Nullfidian, that crap doesn’t pull any weight. Either put up or shut up. It is not up to cooler to support his claims. He doesn’t have any claims to make. He only has questions, and it is up to you and other paid AIDS political activists and drug company reps to answer them in a calm, logical, understandable fashion with a minimum of ad hominems. It is up to AIDS/Inc., Big Pharma to convince us they are worthy of trust. So far they have not done a very good job at it. The 20 minute John Moore video does not help to instill trust, and is in actuallity a large set back in developing credibility and trust, especially when he appears with his lawyer. The two of them make an “odd” couple if you catch my drift, and the pair actually shoot themselves in the foot. The video actually backfires, just like the Rachel Carsen, environemntal book which was bitterly denounced by the chemical industry only making it more popular, creating a groundswell movement called the EPA.

    Put up a rational dialog which explains 1) the mechanism of disease, how HIV causes Aids. Here is your chance to be creative give it a try. 2) The AIDS animal model or lack therof, 3) the absence of expected numbers of occupationally acquired AIDS cases (take Brazil for example, 200,000 AIDS cases and only ONE occupationally acquired case), 4) the gold standard for HIV test kits or lack therof, 5) the lack of proof of efficacy of any HIV drug over a placebo, 6) and explain why anyone in their right mind would trust a medical system that has admitted past mistakes with AZT and the Dr. Ho “Hit Em Hard” policy, killing hundred of thousands, oops, sorry about that ? Here take this nice smiley face drug and you will feel better soon, my sweet goldilocks. 7) Why the main cause of death of AIDS patients is now liver failure which is not an opportunistic infection, it is an adverse side effect of a toxic HIV drug.? 8) and the original cooler question about the articles which followed the 1984 Gallo article which were announced at a Heckler press conference before any peer review. How did these following articles prove Hiv as a cause of AIDS?. Or, as cooler says, they were set up with the pre-supposition that HIV causes AIDS and therfore did not ever actually prove it. Why should anyone in their right mind believe Gallo after he was convicted of scientific misconduct? Unless of course, there were big bucks from the NIH, buckeroos from the drug companies, and HIV test kit sales involved, which there were. Gallo made a nice penny on his HIV test kit patent. The entire field of HIV research reeks of corruption and scientific misconduct tainted by drug compay money and NIH money. Even Africans are willing to pad their numbers to keep the money rolling in. Is that what you stand for nullfidian, padded numbers, and the genocidal elimination of undesirable homosexuals and drug addicts with medically administered AZT? Do you stand for the outrageous proposal that 2 toxic anti HIV drugs represent a placebo and three toxic anti-HIV drugs represents a drug? What do you stand for, nullfidian? Yourself?

    Back to the placebo question for trill (is it actually troll). Thanks for FINALLY coming up with the well known argument that it is UNETHICAL to test a drug against a placebo, once the first drug in its class has been found effective. Guess what, the first AZT drug trial was corrupted, halted early and tested nothing. The drug group was kept alive with blood transfusions, while the placebo group died of whatever they had, hardly a fair comparison. We need to go back to using a REAL placebo,trll, my honorable drug company representative, especially when selenium which is nontoxic and costs a nickel performs better than your toxic drugs which cost a fortune. At this point it is unethical NOT to use a real placebo controlled trial. There are long term non-progressors who never get sick. Why not do a placebo controlled trial on them? Half get killed off in the toxic drug arm, and the other half lives happily ever after in the placebo arm. What are the ethics of this scenario?

    And yes these are toxic drugs, that’s why I use the word toxic. And no, not all drugs are toxic to the point they cause liver failure and stevens johnson sydrome or mitochondrial dysfunction. That’s REAL toxicity, and as John Moore says in his video, quite truthfully, these drugs should not be sprinkled on your morning bowl of cereal.

  109. #109 Nullifidian
    July 1, 2007

    Dumbass,
    It was HIV expert Joel Gallant that said a diffuse immune response that causes immune depletion, not me. When you “experts” change your tune over and over it’s ok, right? Remember it was Gallo who first said HIV is killing the T cells!

    What about those Experts that said “hit hard hit early” in 1996 and gave monster doses of AZT in the 80′s ooops! The experts admitted they were wrong, and now only give treatment late in the disease. Many people died because of this. It was those evil denialists that warned that it was wrong to take high doses AZT early in treatment! How dare them, even though they were right!

    Because there is no animal model, there should be a study that’s desingned to see if HIV positive people without drugs, AZT, coinfections and catastrophic stress die sooner than hiv negative people.

    All those cohort studies on AIdstruth don’t control for confounding factors because they were never designed to test the HIV hypothesis, they assumed it to be true.

    How else is one supposed to prove that your barely detectable/no animal model/10 year window period microbe causes disease, since you have thrown out Koch’s postulates? Using your standards any passenger virus could be said to cause a disease.

    I’m looking, and not seeing any statement which explains what a virology study which attempted to show that HIV is a causative agent of AIDS would be different from the wealth of studies done so far, even though it is still being alleged that the studies done simply assume the link between HIV and AIDS and that somehow renders them illegitimate. Of course, those of us who actually practice science for a living know that if a foundational assumption is wrong, then hypotheses generated from that assumption are more likely to be falsified in experiment and observation.

    So I ask again, O Masterful Expert on Experimental Design, how would the literature be different if they were testing the hypothesis that HIV is a causative agent of AIDS?

  110. #110 Nullifidian
    July 1, 2007

    Nullfidian uses a typical evasive gimmick in his reply to cooler. The science is much too complex for poor illiterate cooler to understand.

    Wow, and where did I say that?

    If I were to say anything in regards to cooler, it would be, as I have asserted before, that he already knows that the facts do not support him and doesn’t care, which is why he’s so enamoured of the idea of the “public debate” where he and his heros can scam the unsuspecting public.

    Of course, so do you, Troll of 1,000 Identities, so why should I bother jumping through yours or his hoops when neither of you are honest enough to address my questions?

  111. #111 Pope
    July 1, 2007

    Nullfidian: So I ask again, O Masterful Expert on Experimental Design, how would the literature be different if they were testing the hypothesis that HIV is a causative agent of AIDS?

    DUESBERG 2003:

    The chemical AIDS hypothesis could be readily refuted
    by any of the following experiments:
    (i) Demonstrate that in two matched groups, differing
    only with regard to HIV infection, HIV-positives develop
    AIDS but HIV-negatives do not (above the low, longestablished
    risk of AIDS defining diseases in the general
    population). HIV antibody-positive and negative recruits
    from the US Army, which tests routinely for HIV, would
    be ideal for this experiment since their health, lifestyles
    and age are closely matched.
    (ii) Demonstrate that in two matched groups of intravenous
    drug users, differing only in the presence of HIV,
    only the HIV-positives develop AIDS diseases.
    (iii) Demonstrate that in two matched groups of HIVpositive
    humans, differing only in the addiction to recreational
    drugs, both groups have the same incidence of
    AIDS-defining diseases.
    (iv) Demonstrate that in two matched groups of HIV-free
    humans or animals, differing only with regard to the
    addiction to or treatment with recreational drugs, neither
    group would develop AIDS defining diseases over time.
    (v) Demonstrate that in two matched groups of HIVpositives,
    differing only in the treatment with anti-HIV
    drugs, the untreated group develops AIDS long before the
    treated group.
    (vi) Demonstrate that in two matched groups of pregnant,
    HIV-positive mothers, differing only in the now standard
    treatment with AZT during the last two trimesters, those
    treated with AZT are free of abortions and deliver
    healthy babies, but those who are not treated either abort
    spontaneously or deliver babies with AIDS.
    (vii) Demonstrate that in two groups of HIV-positive
    hemophiliacs matched for age and lifetime dosage of factor
    VIII, differing only in anti-HIV treatments, those who
    are untreated have a higher mortality and a higher AIDS
    risk than treated controlsAlthough the controlled studies proposed here follow classical, scientific standards, they are not available in the huge AIDS literature. This is surprising in view of the many AIDS advocacy groups or “activists” reviewing AIDS research for flaws and for new clues. The lack of adequately controlled studies of the long-term effects of recreational drugs and anti-HIV drugs in animals is particularly surprising, because all of these drugs and research funds for AIDS are abundant.

  112. #112 trrll
    July 1, 2007

    Trrl, since an answer wasn’t forthcoming on the smallpox thread, maybe you can tell me what that “now” means.

    Does it mean that previously there were no problems with serious side effects, that “might have a negative impact on mortality rates”, but now (Oct. 2006) there are?

    Or does it mean, previously we didn’t really want to admit it, but now we can’t afford to ignore the problem any longer?

    It means that before antiretroviral therapy was available, there were no side effects from them. With the advent of ARV drugs, the HIV population began to live longer and have reduced AIDS symptoms, but these drugs are not a perfect solution; while patients do much better on ARV therapy than without it, and live longer on the average, these drugs do carry a significant risk of side effects. When HIV infection was a near-term death sentence, ARV side effects were not so much of a concern. Now that ARV therapy is good enough that people with HIV are living much longer, there is more concern for developing improved treatment regimens with reduced side effects.

  113. #113 Chris Noble
    July 1, 2007

    The reason why Duesberg is ignored by the scientific community is because many of these studies have been done despite Duesberg’s protestations to the contrary.

    The following papers deal with several cohorts where it is possible to compare the rates of progression to AIDS and death between HIV+ and HIV- individuals.

    The first set looks at the San Francisco Men’s Health Study that had records going back to the 70s.

    Does drug use cause AIDS? Ascher MS, Sheppard HW, Winkelstein W Jr, Vittinghoff E. Nature. 1993 Mar 11;362(6416):103-4.

    The lack of association of marijuana and other recreational drugs with progression to AIDS in the San Francisco Men’s Health Study. Di Franco MJ, Sheppard HW, Hunter DJ, Tosteson TD, Ascher MS. Ann Epidemiol. 1996 Jul;6(4):283-9.

    The next group is a cohort of homosexual men in Vancouver.

    HIV-1 and the aetiology of AIDS. Schechter MT, Craib KJ, Gelmon KA, Montaner JS, Le TN, O’Shaughnessy MV. Lancet. 1993 Mar 13;341(8846):658-9.

    The last set is from studies of people with haemophilia in the UK

    Comparison of immunodeficiency and AIDS defining conditions in HIV negative and HIV positive men with haemophilia A. Sabin CA, Pasi KJ, Phillips AN, Lilley P, Bofill M, Lee CA. BMJ. 1996 Jan 27;312(7025):207-10.

    Mortality before and after HIV infection in the complete UK population of haemophiliacs. UK Haemophilia Centre Directors’ Organisation. Darby SC, Ewart DW, Giangrande PL, Dolin PJ, Spooner RJ, Rizza CR. Nature. 1995 Sep 7;377(6544):79-82.

    The impact of HIV on mortality rates in the complete UK haemophilia population. Darby SC, Kan SW, Spooner RJ, Giangrande PL, Lee CA, Makris M, Sabin CA, Watson HG, Wilde JT, Winter M; UK Haemophilia Centre Doctors’ Organisation. AIDS. 2004 Feb 20;18(3):525-33.

    Response: arguments contradict the “foreign protein-zidovudine” hypothesis. Sabin CA, Phillips AN, Lee CA. BMJ. 1996 Jan 27;312(7025):211-2.

    The consistent finding is that people with HIV infection suffer progressive loss of CD4 cells and eventual immunesuppression and AIDS. Those people who have the same behaviours such as drug taking and haemophilia that are HIV- do not.

    I am fully aware that Duesberg has replied to these articles. These replies are less than satisfactory. Duesberg unjustly accused Ascher of fabricating data when the truth was that Duesberg had misread the paper.

    Duesberg also claims that the HIV+ groups were given AZT and that is why they suffered CD4 cell loss. The reality is that people were not prescribed AZT until they had either progressed to clinical AIDS or CD4 counts less than 300.

    I’ll go into more detail about Duesberg’s “reanalysis” of the Ascher et al SFMHS study.

    HIV as a surrogate marker for drug use: a re-analysis of the San Francisco Men’s Health Study.

    Duesberg writes: … we found 45 HIV-negative men with AIDS defining conditions (according to the CDC), as listed in Table 1.

    and

    It is important to emphasize that had any of these 45 men been positive for antibod- ies against HIV, they would likely have been recorded as AIDS cases.

    Now If we go through Table 1 Duesberg gives Salmonella as the AIDS defining illness for 18 of the 45. But the CDC clearly state that it must be a recurrent infection to count as AIDS defining. Salmonella is a very common food-borne disease. The CDC estimates 1.4 million cases annually in the US You can do the math to find out how many cases you would expect over 4648 patient years.

    The next biggest group is 14 with transitory CD4 counts less than 200 cells/ml. The CDC is quite clear that repeat testing may be necessary to ensure that CD4 counts are truly reflective. Sheppard et al point out in this letter CD4+ T-Lymphocytopenia without HIV Infection that these CD4 counts were transient low counts amongs a background of normal counts.

    After that Duesberg lists 9 patients with Herpes zoster. I looked in the CDC list of AIDS defining illnesses and couldn’t find Herpes zoster. Now Duesberg does say he is using the CDC definition.

    Next Duesberg lists 6 patients with Thrush/oral candidiasis except the CDC definition clearly states that the cadidiasis must be esophageal or of the bronchi, trachea or lungs. Oral candidiasis doesn’t count it is frequently seen in immunocomptetent persons.

    Immune thrombocytopenic purpura (ITP) is also not in the CDC definition. It is also observed in immunocompetent persons as is TB. Given the incidence of TB in the US at the time was roughly 10 per 100,000 per year it is not unexpected to see one case in 4648 patient years.

    In short there were no HIV-negative AIDS cases in the SFMHS cohort. This has been pointed out to Duesberg before in the literature AIDS data.

    Duesberg was so desperate to produce HIV-negative AIDS cases that he stretches the definition so far that he includes the roughly 1.4 million people in the US that get salmonella food poisoning each year.

    This isn’t someone arguing from the evidence. He twists the evidence to match his own preconceived ideas.

  114. #114 trrll
    July 1, 2007

    The chemical AIDS hypothesis could be readily refuted
    by any of the following experiments:

    Essentially all of these “experiments” would require withholding antiretroviral therapy from HIV infected individuals. Such Tuskegee style experiments are considered highly unethical, and would not be approved by any Human Subjects committee.

  115. #115 trrll
    July 1, 2007

    Guess what, the first AZT drug trial was corrupted, halted early and tested nothing. The drug group was kept alive with blood transfusions, while the placebo group died of whatever they had, hardly a fair comparison. We need to go back to using a REAL placebo,trll, my honorable drug company representative

    The test was halted early because there was a big difference in how well the treatment groups were doing. This is standard procedure and is ethically required, as in the recent Vioxx study by Merck that was terminated early because one group had a much higher incidence of cardiac events. In the AZT study, the placebo group had a much higher rate of AIDS symptoms. Note that it was a double blinded study, so prior to the termination of the study, the doctors did not know which group was AZT and which was placebo. This is done precisely so as to make it impossible to treat the groups differently.

    Oh, and for the record, I do not work for the drug industry, nor do I receive any income from AIDS treatment or research.

  116. #116 cooler
    July 1, 2007

    Actually since HIV progresses so slowly, there really would not be much risk, if the people really got around 200 tcells they could opt to be on ARV’s if they wanted to, there is no risk. A Much bigger risk is telling people there is 100% chance of death when you dont have the evidence to say that, that alone could kill them.

    Its the only way to test a hypothesis of microbe causation when there’s no reliable animal model and where the microbe is only present in a tiny fraction of the cells its said to kill, according to Gallo in 1990 its 1 in 10,000, according to the fool John Moore its like 1 in 100.

    A matched study between hiv postives and negatives where the both dont use AZT/drugs/coinfections/catastropic stress. This is how the study should be conducted, the Cohort studies on AIDStruth were not designed to test the hypothesis, so they didn’t control for these things, a new study would.

  117. #117 David Marjanović
    July 1, 2007

    Was there ever a time when the vast majority of cases in South Africa were not heterosexual people of both sexes (hint, hint perhaps when the apartheid regime was in place).

    Does this mean that before it was homosexuals who changed partner most often, but now that the South Africans are left to their own devices, they are the ones who change partner most frequently?

    Perhaps you mean that there are more AIDS cases in South Africa nowadays than in the rest of the world?

    I did not mean South Africa, as you found out. Concerning the rest of my claims, I can only repeat: the times when most people with AIDS were male are long over. AIDS is established in the population of large parts of Africa (and to a lesser degree many other places in the world), not just in some fringes.

    And if you don’t live in a sterile environment while the virus destroys your helper T cells and thus your immune system, you will get the full range of AIDS symptoms.

    Thats quite a mouthful, david, the full range of AIDS symptoms is pretty extensive. In fact you get the opportunistic diseases that are prevalent in the area or subpopulation you are part of, even if you live in a sterile environment while the virus destroys your helper T cells, since some opportunistic infections are already lying dormant in your body.

    Don’t you know anything?

    Sorry for being imprecise. If you had already lived in a sterile environment before getting HIV, you wouldn’t get AIDS except for Kaposi’s sarcoma and the like (which is a probability and not a certainty), of course. If you have dormant infections, you’ll get those when you’ve lost your helper T cells.

  118. #118 Pope
    July 1, 2007

    David, my question had nothing to do with which part of Africa you were talking about. The AIDS ‘epidemic’ started in Africa. Was it at any point a predominantly male disease there?

  119. #119 David Marjanović
    July 1, 2007

    This myth that science operates in such a pristine manner and that no public scrutiny should be allowed is ridicolous. We are just supposed to take 100 times the safe EPA level of mercury and listen to Frauds like Gallo and not be allowed to ask any questions. Just trust that a vaguely defined group of “scientists” have reached a “consensus”

    We are told the science is too complex to understand……..An 8th grader could understand Koch’s postulates, much like the public can learn about economic policy, abortion, global warming etc and make a desicion based upon informed consent, not by being brainwashed by a “scientific community” thats been either bought off or brainwashed by the CDC, much like many experts in other oppresive societies have being unduly influenced by governmental/corporate propaganda.

    Where are these honest scientific debates taking place when it comes to health issues? They are not taking place at all.

    They have taken place, long ago. Read them up, and if you come up with anything new, reopen the debate. If a debate gets merely repeated for the 10th time without any new arguments, as seems to be the case here, debate is whatcha put on de hook to catch de fish.

    BTW, the “no animal model” claim is bogus. Some viruses are simply human-specific. You don’t get smallpox outside of humans; cow pox (vaccinia) is closely related, but still a different virus. Similarly, chimpanzees can be successfully infected with HIV, but they don’t get ill. Probably they have adapted to the virus, and vice versa, over a long time. Maybe people should try a gorilla model, if only there weren’t so few gorillas (of both species, eastern and western) left, but the chimps (and bonobos) are more closely related to us than the gorillas are.

    the genocidal elimination of undesirable homosexuals and drug addicts with medically administered AZT?

    What a stupid conspiracy “theory”. The times are long over when only homosexuals and drug addicts carried HIV in the First World, let alone Africa (HIV comes from bushmeat — we even know which subspecies of chimpanzee).

    Go over to ERV’s blog. ERV is an actual virologist who actually works on retroviruses.

  120. #120 Pope
    July 1, 2007

    Trrl,

    Despite the inevitable toxicity of anti-HIV drugs, the over 5000 signatories of the Durban Declaration assert that, “drugs that block HIV replication in the test tube also” (i) “delay progression to AIDS”, and (ii) “have reduced AIDS mortality by more than 80%”.
    However, the authors of the Declaration have not provided a reference for controlled studies in support of their assertion. But, they do acknowledge “That it is crucial to develop new antiviral drugs that . . . have fewer side effects” (The Durban Declaration 2000). Since many doctors share the views of the Declaration, we investigate here the evidence for these claims.
    (i) Controlled studies investigating the ability of anti-HIV
    drugs to “reduce mortality” and “delay progression to
    AIDS”: The licensing study of AZT, performed in 1987 by
    the NIH in collaboration with the drug’s manufacturer
    Burroughs Wellcome in the US, is the primary placebo controlled study set-up to test the ability of AZT to reduce
    the mortality of AIDS (Fischl et al 1987; Richman et al
    1987). The study showed that, after 4 months on AZT, 1
    out of 145 AIDS patients died, whereas 19 out of 139
    died in the placebo group. The study interpreted this result
    as evidence for reduced mortality by AZT. However,
    this interpretation failed to consider that among the 4-
    month-survivors of AZT, 30 could only be kept alive
    with multiple blood transfusions because their red cells
    had been depleted by AZT below survivable levels(Fischl et al 1987; Duesberg 1992). Thus, without lifesaving
    transfusions 30 more AZT-recipients would have
    died from anemia. In addition many AZT recipients had
    developed life-threatening bone marrow suppression, neutropenia, macrocytosis, headaches, insomnia and myalgia,
    that augured poorly for their future survival (Richman
    et al 1987). Indeed, the low mortality of 1/145 reported
    for the first 4 months on AZT, could not be maintained in
    a follow-up study, which found the “survival benefits” of
    AZT rapidly declining after the original 4 months period.
    By 21 months, 42% of the original AZT group had died
    and 35% of the control group, which by then had also
    received AZT for 12 months on a “compassionate” basis
    (Fischl et al 1989). Thus the placebo-controlled, licensing
    study did not prove that AZT “reduces AIDS mortality by
    more than 80%” compared to the untreated control.

    The ability of AZT to “delay the progression to AIDS”
    was investigated in 1994 by the largest, placebo-controlled
    study of its kind, the British-French Concorde study
    (Seligmann et al 1994). This study investigated 1749
    HIV-positive, mostly male homosexual subjects divided
    into untreated and AZT-treated subgroups for the onset
    of AIDS and death. The Concorde study found in 1994
    that AZT is unable to prevent AIDS and increases the
    mortality of recipients by 25%. In view of this it concluded, “The results of Concorde do not encourage the early use of zidovudine (AZT) in symptom-free HIV-infected
    adults.” (Seligmann et al 1994). Thus there is no controlled
    evidence that anti-HIV drugs “reduce the mortality of
    “or “delay progression to AIDS”.

    But, in the absence of untreated control groups, the
    effects of the new anti-HIV drugs on the morbidity and
    mortality of HIV-positive recipients can not be determined
    scientifically from the results of these surveys.
    However, the average annual AIDS mortality of all HIVpositives on this planet [including the minority that is on anti-HIV drugs (The Durban Declaration 2000)] can be
    estimated for 2000, the year that falls in between the two
    surveys, based on data provided by the WHO and the
    Durban Declaration: The WHO and the Declaration report
    in 2000 34×3 million “living with HIV”, and the WHO
    reports 471,451 AIDS cases for 2000 (World Health
    Organization 2001b) (obtained by subtracting the WHO’s
    cumulative total of 1999 from that of 2000, see also table
    4). Thus, even if we assume that all AIDS cases were
    fatal in 2000, the resulting global mortality rate of HIVpositives would only be 1×4% – and thus 4 to 6 times
    lower than the 6×7-8×8% mortality rate of HIV-positives
    treated with anti-HIV drugs in the US and Canada.
    Therefore, the claims that anti-HIV drugs reduce the
    mortality of, and delay progression to AIDS are at odds
    with the AIDS facts reported by the Durban Declaration
    and the WHO.

    (i) Diseases and death in HIV-positives treated with anti-HIV drugs: A sudden 10-fold increase in the mortality of HIV-positive British hemophiliacs, right after the introduction of AZT in 1987, made scientific headlines in
    1995, because the increased mortality was attributed to
    HIV by the authors of the study, i.e. Darby et al (1995),
    as well as by the editor of Nature, “More conviction on
    HIV and AIDS” (Maddox 1995). Even the editor of the
    Lancet wrote an editorial asking, “Will Duesberg now
    concede defeat” (Horton 1995)? Darby et al based their
    conclusion on the sudden 10-fold increase of the hemophiliacs’ mortality in 1987, shown in figure 5, on the
    facts that the increased mortality was restricted to HIVpositive hemophiliacs and that the increase was independent of the degree of hemophilia (which is inversely
    proportional to the life expectancy of the patient). But, by 1987 transfusions of blood and factor VIII had
    already infected most hemophiliacs for a long time. Most
    of them were already infected before 1984 (about 75% in
    the US), because all blood supplies with HIV antibodies
    were banned after the introduction of the HIV-antibody test in 1984 (Duesberg 1995c, 1996a). Moreover, the
    mortality of hemophiliacs was steadily decreasing since
    the 1970s until 1987 – despite the presence of HIV
    (Duesberg 1995c)! Thus the only new risk of mortality,
    in and after 1987, was not HIV, but AZT.

    According to researchers from the NIH, AZT also increased
    the mortality of US hemophiliacs 2×7 times and
    their AIDS risk 4×5 times compared to untreated controls
    (Goedert et al 1994; Duesberg 1995c).

    http://duesberg.com/papers/chemical-bases.html

  121. #121 cooler
    July 1, 2007

    I thought the denialists were nuts until i saw the video Hiv Fact or fraud last summer. Its pretty rude that many reputable scientists have questioned the hiv hypothesis, and have been insulted by many. Here is the video I saw last Year.

    http://video.google.com/videoplay?docid=5064591712431946916

    Keep in mind that most scientists who question hiv have no conflicts of interest, unlike John Moore.

    People question HIV because there is no reliable animal model (virtually every animal injected does not die of aids) and there is not much virus present, (its only in a small fraction of T cells) Like 1 in a hundred or so.

    Many take the middle road, Like Luc montagnier the discoverer of HIV, Who in his book “virus” in 2000 still stresses the need for co factors, specifically shyh ching Lo’s mycoplasma penetrans. This microbe causes disease and death in every animal injected as lo showed. DR. Nicolson has found this microbe via pcr in CFS, ALS, GWI and you can see his research here.

    http://www.aegis.com/pubs/atn/1990/ATN09501.html

    Garth Nicolsons new book must be read about mycoplasma and Gulf war Syndrome.

    http://www.projectdaylily.com

    Im not saying that HIV does or Does not cause AIDS but there needs to be more study, and scientists who questioned should be debated publicly, not insulted personally

  122. #122 Patriot Games
    July 1, 2007

    Nullifiddian said;

    I’m looking, and not seeing any statement which explains what a virology study which attempted to show that HIV is a causative agent of AIDS would be different from the wealth of studies done so far, even though it is still being alleged that the studies done simply assume the link between HIV and AIDS and that somehow renders them illegitimate. Of course, those of us who actually practice science for a living know that if a foundational assumption is wrong, then hypotheses generated from that assumption are more likely to be falsified in experiment and observation.

    So I ask again, O Masterful Expert on Experimental Design, how would the literature be different if they were testing the hypothesis that HIV is a causative agent of AIDS?

    Duesberg placed into the record the studies you are asking for 20 years ago in his 1987 book, Inventing the AIDS Virus, and again in his 2003 paper as posted above by Pope which can be found at this link:

    The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition

    J. Biosci. Vol. 28 No. 4 June 2003 PETER DUESBERG, CLAUS KOEHNLEIN and DAVID RASNICK.

    Over time, more and more of Duesberg’s ideas originally published 20 years ago, which had been, rejected are now being accepted by the weight of the evidence. He was right about AZT, he was right about HAART, he was right about the absence of believable series of occupationally acquired AIDS cases in the peer reviewed literature. He was right about the lack of correlation between CD4 cell count and HIV viral load, which means that he was right about the fact that HIV does not directly kill T cells in vivo. He was right about no animal model. He was right about long term non progressors who have HIV and dont get sick, which means HIV is a benign passenger virus (at least in this group). Is he right about everything? Nobody is. But one thing is as sure as night following day, in the end, he will be right, and you and your drug company sponsored associates, and your paid political AIDS activist brown shirts will be wrong.

    There will come a day of reckoning when those responsible for poisoning pregnant mothers with toxic drugs will be held accountable.

    for more information: reviewingaids dot com

  123. #123 Chris Noble
    July 1, 2007

    According to researchers from the NIH, AZT also increased
    the mortality of US hemophiliacs 2×7 times and
    their AIDS risk 4×5 times compared to untreated controls
    (Goedert et al 1994; Duesberg 1995c).

    This is one misrepresentation that is difficult to characterise as anything other than a lie.

    Duesberg fails to distinguish the findings of the researchers from the delusions of his twisted imagination. AZT was given preferentially to people that either had clinical AIDS or who had already suffered sever CD4+ cell depletion. Unless AZT can travel backwards in time then it is not possible for it to cause something that occurred before it was administered.

    It’s like saying that insulin injections cause diabetes.

  124. #124 Justin Moretti
    July 1, 2007

    What I am seeing from the HIV/AIDS denialists is ad-hominem attacks, name-calling, viciousness and a failure to understand some rather simple concepts that their opponents have put forth time and time again.

    1) We aren’t doing randomized placebo-controlled trials any more; we’re doing randomized controlled trials of new agents against proven therapies, because to deny a patient an effective therapy is unethical. What part of this do people not understand?

    2) “We need to go back to using a REAL placebo” says “Patriot Games”, whilst appearing to misrepresent why the trial was stopped (do you have justification for your very serious allegation, and if you do, why aren’t you in court with it?). Randomized controlled trials (whether placebo or not) are stopped early for either of two reasons: First, because the trial arm is doing so much better than the placebo/standard-therapy arm that it is unethical to withhold the drug from the placebo (what happened with AZT). Second, because the trial arm is doing significantly WORSE and must be discontinued for the patients’ safety (as happened with Flecainide, IIRC, for the treatment of some cardiac rhythm abnormalities).

    3) If you would like to put your money where your mouth is, denialists, why don’t you sign up to receive a transfusion of blood from an HIV-positive person, then deny yourself antiretroviral agents and see what happens? Since HIV does not, in your view, cause AIDS, you ought to be safe.

    4) There is no animal model for HIV-AIDS for the same reason that there is no human model for a range of animal diseases – some diseases do not cross species barriers.

  125. #125 Patriot Games
    July 1, 2007

    The honorable Dr Chris Noble said

    This is one misrepresentation that is difficult to characterise as anything other than a lie. Duesberg fails to distinguish the findings of the researchers from the delusions of his twisted imagination. AZT was given preferentially to people that either had clinical AIDS or who had already suffered sever CD4+ cell depletion. Unless AZT can travel backwards in time then it is not possible for it to cause something that occurred before it was administered. It’s like saying that insulin injections cause diabetes.

    You have already demonstrated that you are untrustworthy, so why should anyone trust your appeal to authority without even a quote from your source, not even a link to your reference. Very impolite and inconsiderate of you Dr. Noble to deprive your readers of the proof behind your words. Until then your words are empty shells waiting to be filled. Lets not fill them with colonic contents like last time.

    We have posted ample links to AZT effects on mitochondria. AZT essentially killed all the hemophilacs and homosexuals given the drug, whether HIV or not. Ariel Glaser and Elizabeth Glaser were both sacrificed to AZT toxicity, and betrayed by the medical system, and government agencies they trusted. This is as plain as day from the descriptions posted on the Michael Glaser web site.

    AZT was a horrendous toxic mistake by the medical system. Or was it really a mistake?. Perhaps Dr. Noble is one of those who feels that it is right to eliminate the undesirables of our society as was the state program in Indiana and in Nazi Germany? Is that your opinion Dr. Noble? Iatrogenic Genocide is OK with the noble Dr. Noble? Let’s have your answer to this please.

  126. #126 Chris Noble
    July 1, 2007

    You have already demonstrated that you are untrustworthy, so why should anyone trust your appeal to authority without even a quote from your source, not even a link to your reference. Very impolite and inconsiderate of you Dr. Noble to deprive your readers of the proof behind your words. Until then your words are empty shells waiting to be filled. Lets not fill them with colonic contents like last time.

    How exactly have I demonstrated that I am untrustworthy. Maniotis has fabricated two quotes. He has repeatedly cited papers that have the opposite conclusions from his own spin. You’re calling me untrustworthy? Is this some kind of silly game?

    Caroline Sabin responded to Duesberg’s assertion that the AIDS in people with haemophilia was actually caused by AZT in this article.

    Response: Arguments contradict the “foreign protein-zidovudine” hypothesis

    Patients are given zidovudine because they are ill

    It is not true that most British haemophilic patients infected with HIV have been given zidovudine since 1987. Initially patients were given zidovudine after the development of AIDS. Subsequently, since around 1989, patients have been given zidovudine once their CD4 count has fallen below 0.2×109/l or after the development of symptomatic disease. Similar recommendations are made for pentamidine or co-trimoxazole as prophylaxis against Pneumocystis carinii pneumonia. Consequently, by the time patients begin zidovudine and pentamidine they have low CD4 cell counts and are usually symptomatic.

    Observational studies often show that patients given zidovudine have a worse prognosis than untreated patients.7 Patients receiving zidovudine are selectively treated because they are ill. The interpretation of findings from these studies should not therefore be that zidovudine increases the risk of AIDS. Of the nine patients developing AIDS in our study, seven received zidovudine only after an initial AIDS diagnosis when immunological deterioration had already occurred. There is no possibility, therefore, that either zidovudine or pentamidine had a causal role in the initial development of symptomatic disease in these patients.

    How many times does this need to be pointed out to the acolytes of Duesberg?

  127. #127 Patriot Games
    July 1, 2007

    Justin Moretti said:

    If you would like to put your money where your mouth is, denialists, why don’t you sign up to receive a transfusion of blood from an HIV-positive person, then deny yourself antiretroviral agents and see what happens? Since HIV does not, in your view, cause AIDS, you ought to be safe.

    Your experiment entitled, “inject HIV into a primate, and observe the primate come down with AIDS” has already been done and has been a collossal failure in both chimp-primates and human-primates. The Yerkes primate lab closed down the chimp experiments because they don’t get AIDS after injection with HIV. Not only that, chimps and all primates in the wild have HIV naturally and don’t get AIDS from it.

    What about the human primate experiments? Who did that and where is it published? Our human primates are the health care workers who have been punctured with HIV laden needle sticks for the last 20 years, with no convincing series of occupational AIDS in health care workers ever published in the peer reviewed literature. In Brazil, they had 200,000 cases of AIDS treated in hospitals over 16 years, and not one single case of occupationally acquired AIDS. (until 2000, when one single one was reported and the link has been posted here).

    Don’t accept that do you? OK, what about the other human HIV experiment going on right now? That is the long term non-progressor, elite controller human primate group who have HIV and don’t get AIDS. Don’t have to inject them with HIV cause they already have HIV. They don’t get sick. They dont get AIDS. Your experiment is a collossal failure multiple ways.

    Can’t inject another human with HIV, no IRB would ever approve it, its unethical. Besides who would want a blood transfusion Hiv or not? Nobody.

    So in spite of all that, what if I agreed to your experiment and was injected with HIV, and we waited 10 years and nothing happens. Well, we would have to wait 20 more years. What if I finally die of a heart attack at the age of 72. Oh well, you will say, he must have been a long term non-progressor, lets go inject some one else and keep doing it until we find somebody who dies of AIDS from it. That’s what they did to the chimps, and they didn’t get AIDS unless you kill them with AZT, now that looks exactly like AIDS.

    For more information see reviewing aids DOT com

  128. #128 noreen Martin
    July 1, 2007

    Dr. Noble, you are right that many times the patient has already progressed to AIDS and then are given the antiretrovirals with CD4 decline. Nevertheless, how can one have CD4′s under 100, be sick and dying prior to the medcines and later again have CD4′s under 100 and be healthy as a horse without the antiretrovirals? What is going on here?

  129. #129 Chris Noble
    July 1, 2007

    Our human primates are the health care workers who have been punctured with HIV laden needle sticks for the last 20 years, with no convincing series of occupational AIDS in health care workers ever published in the peer reviewed literature.

    You have been given a peer-reviewed paper describing 57 case of occupationally acquired HIV infection. 26 of these had at that time progressed to AIDS.

    You may not be convinced by this but this tells us more about your ability to maintain your delusional state that the existence of the evidence.

  130. #130 cooler
    July 1, 2007

    Im sure they were given monster doses of AZT and were terrified with a diagnosis of death which can probaly kill you much more than a virus thats in like 1 of 100 cells, nuetralized by antibodies and doesnt kill 99.9 % of animals injected with it.

  131. #131 noreen Martin
    July 1, 2007

    Cooler, you may helped to answer my question as having low CD4′s has never bother or frightened me. Therefore, I didn’t stress out no matter what they were but like the EverReady Battery, I just keep on going.

  132. #132 gwangung
    July 1, 2007

    Im sure they were given monster doses of AZT and were terrified with a diagnosis of death which can probaly kill you much more than a virus thats in like 1 of 100 cells, nuetralized by antibodies and doesnt kill 99.9 % of animals injected with it.

    Oh, good science there….

    Feh.

  133. #133 cooler
    July 1, 2007

    Its common sense dope, but I’m sure you think monster doses of AZT, chemotherapy in a pill, is good for you!

  134. #134 Michael
    July 1, 2007

    Hey Justin.

    You made four wonderful “points” or suggestions up above.

    In response to your first and second “points”, if they could be called such, wherein You claim: “1) We aren’t doing randomized placebo-controlled trials any more; we’re doing randomized controlled trials of new agents against proven therapies, because to deny a patient an effective therapy is unethical. What part of this do people not understand”?

    Justin, are you testing our patience? The ONLY HIV drug that was ever placebo controlled was the original and only four month long, corrupted AZT trial that was run, conducted by, and overseen by the drugs manufacturer. Many of The “lucky winners” of this trial had blood transfusions during the 4 month trial, and ALL ended up dead within 1-1/2 years!!!

    You are simply admitting that it is still currently a situation of more recent non placebo-controlled and fast tracked drug trials that have been done against other non placebo controlled fast tracked trials. And every one of these trials was designed and operated and paid for by the drug company that stood to benefit. And NOT EVEN ONE of these drugs has had the followup long term trials finished that were required by the FDA and promised to in order to market them. Can you say “Conflict of interest”? What part of this do YOU not understand?

    Your third “point”, if you want to call it that:

    “3) If you would like to put your money where your mouth is, denialists, why don’t you sign up to receive a transfusion of blood from an HIV-positive person, then deny yourself antiretroviral agents and see what happens? Since HIV does not, in your view, cause AIDS, you ought to be safe”.

    Hey Justin, how many years would we “denialists” who get such a transfusion have to wait before you admit that you are mistaken? 2? 5? 10? 20? 50? And if we got a cold or flu or herpes or pneumonia or whatever common illness 20 years after such a transfusion, would you be jumping up and down cheering and telling us we now have AIDS from the transfusion?

    Not only that, but in your own ignorance, you are certainly overlooking the FACT that ALL BLOOD TRANSFUSIONS INTERFERE WITH THE IMMUNE SYSTEM!

    See: http://www.med.unipi.it/patchir/bloodl/deleterious.htm

    Blood transfusions are also associated with reduced cancer survival, and a multitude of other problems.

    The only thing getting sick after any blood transfusion gotten from someone HIV positive or negative would prove, is that the dissidents are quite correct that many of the so called AIDS cases were caused by the transfusions themselves! How come hetero hemophiliacs diagnosed as HIV/AIDS never came down with the Number One AIDS Defining Gay Disease of Kaposis Sarcoma????

    Even Ryan White’s death certificate showed he did NOT DIE of anything viral, but due to blood loss and a failed liver from his AZT!

    In your fourth point: “4) There is no animal model for HIV-AIDS for the same reason that there is no human model for a range of animal diseases – some diseases do not cross species barriers”.

    Well I got news for you Justin. Chimpanzees get ABSOLUTELY EVERY SINGLE DISEASE that humans get, except for ONE? Three guesses what supposedly human infectious agent does NOT CAUSE ANY DISEASE IN CHIMPS, and the first two guesses don’t count! And I will even give you a hint: It has three letters and is spelled HIV!

    You know what Justin, if you refrained from posting ignorant posts like the last one you did, you would not have to worry about ad hom attacks, such as being called an ignoranimus or a damned fool! Perhaps you are a young know-it-all that has no room to learn anything new, or perhaps you are naive, or perhaps you are just intentionally playing dumb because you are starved for attention?

  135. #135 Patriot Games
    July 1, 2007

    Dear drug company representative doctor noble,

    Your reference is a government CDC surveillance report which starts off by telling us they found nearly 24,000 AIDS cases among health care workes. This is not a report from the peer review literature (its from the CDC), of course, but GREAT!! This is exactly what we wanted to prove that HIV cause AIDS. 24,00 cases !!.

    Problem is that all these 24,000 cases were not occupationally acquired AIDS. These were the bad boy gay heathcare workers who had outside activities, IV drug users, gay, minorities and others who got their AIDS from something other than occupationally acquired from needle sticks.

    Of these 23,951 AIDS cases in healthcare workers, there were only 26 cases of documented occupational exposure, and this is from the CDC, and we know that nobody would ever lie to the CDC , and the CDC would never lie to us. Right?

    There were also 122 AIDS cases in healthcare workers who were “possible occupationally acquired HIV infection”, And another 51 healthcare workers claiming to have occupationally acquired AIDS with no history of any recognized risk related to occupational or non-occupational exposure.

    Does this report prove that Hiv causes AIDS in our primate experiment? remember that’s the experiment where we inject HIV into chimps and they don’t get AIDS. Does this CDC report contradict the chimp experience, and show that in human primates injected with HIV occupationally, they get AIDS? No. Not enough clarity in the data set to unequivocally say that AIDS is tranmissible from patient to health care worker. You want to believe go ahead. You are paid to believe it.

    Healthcare Workers With AIDS

    Through December 2001, 23,951 cases of AIDS among healthcare workers were reported to the CDC, representing 5% of the 469,850 adults or adolescents with AIDS for whom information on healthcare employment was indicated on the surveillance case report form used in the HIV/AIDS Reporting System. Information on healthcare employment was missing or unknown for 337,225 reported adult or adolescent cases of AIDS. Most (91%) of the healthcare workers with AIDS reported non-occupational risks for HIV infection (eg, sexual contact, injection drug use, or transfusion). The remaining 9% includes healthcare workers with AIDS who had documented occupationally acquired HIV infection (n = 26), possible occupationally acquired HIV infection (n = 122), or no history of any recognized risk related to occupational or non-occupational exposure (n = 51); the investigation to identify risk exposures is ongoing for 1,410 and is incomplete for 640 healthcare workers (due to special circumstances such as death, loss to follow-up, or declining participation in the investigation).

    Lets try to answer this question by looking at Brazil, the highest number of AIDS cases in the world.

    In Brazil, there were 200,000 AIDS patients treated in hospitals and not ONE SINGLE occupationally acquired AIDS case until the year 2002 when this report appeared in the literature.

    Brazilian Journal of Infectious Diseases vol.6 no.3 Salvador June 2002

    The first case of AIDS due to occupational exposure in Brazil

    If anyone is delusional it is the noble doctor noble who wants to believe a problematic cdc report of “26″ out of 24,000 AIDS cases which are “retrospectively occupationally acquired”.

    Take a look at the rest of the WORLD AIDS literature, and what do you find? Duesberg is right. One case of occupationally acquired AIDs in Brazil after caring for 200,000 patients does not cut the mustard as far as I am concerned. If this satisfies your criteria for transmission of AIDS from patient to health care worker, then you are deluded my noble doctor noble, peddler of HIV drugs and AIDS activist politico.

    Oh I forgot, you are the one who believes that 2 toxic HIV drugs equals a placebo, while one toxic HIV drug equals a drug. Right? No wonder. That explains how you can still believe there is plenty of occupationally acquired AIDS in Brazil. After all, dogma is key, and all AIDS drug peddlers and political activists must believe, right?

  136. #136 Patriot Games
    July 1, 2007

    Noble said

    Caroline Sabin responded to Duesberg’s assertion that the AIDS in people with haemophilia was actually caused by AZT in this article.

    My dear Dr. Noble, you obviously have not read Professor Peter. Duesberg’s very thoughtful reply to Sabin’s earlier hemophilia AIDS study which contains all the information rebutting her later comments.

    Your quote is not really accurate, and you are guilty of the crime you accuse others, the misquote. The correct quote is here, by Dr. Duesberg.

    “Patients with haemophilia treated with commercial factor VIII and zidovudine are at risk of developing AIDS defining immunodeficiency diseases like pneumonia, candidiasis, and toxoplasmosis but not Kaposi’s sarcoma or dementia. Their risk of these diseases is proportional to their lifetime dosages of factor VIII and cytotoxic DNA chain terminators like zidovudine.”

  137. #137 Michael
    July 1, 2007

    Hey Patriot Games. Doctor Noble, if you want to call him that, is not a drug company rep. He is much more dangerous than that. Reality is stranger than fiction they say, and he is certainly evidence of this.

    He is a computer animation programmer down under in Australia with his “doctorate” in computer programming.

    And this is true! A few years ago, he helped work on a cartoon animation job model of an HIV drug supposedly destroying the evil HIV.

    I think that after having been lauded for his animation job, it seems to have gone straight to his overactive imagination and seems to interfere with his grasp on reality. Happens to a lot of programmers. They confuse their computer programs for reality. Perhaps because he thought the animation of a drug destroying HIV was reality and he also thought for sure that he had helped saved the world from the evil HIV by programming the drug to destroy it!

    Ever since helping to make that cartoon, he has become an all knowing “expert” in virology, HIV, and HIV drugs. He is not about to let a little reality pointed out by you or anyone else get in the way of his mission to save the world from his cartoons of the evil and brilliant genius HIV running amok in his mind!

  138. #138 Chris Noble
    July 1, 2007

    My dear Dr. Noble, you obviously have not read Professor Peter. Duesberg’s very thoughtful reply to Sabin’s earlier hemophilia AIDS study which contains all the information rebutting her later comments.

    Duesberg makes a number of claims here that are rebutted by Sabin in the comment that I posted. Duesberg argues that it must have been the AZT that caused the AIDS in these patients with haemophilia. However, as Sabin points out the patients were given AZT after they had progressed to AIDS.

    Simply repeating Duesberg’s initial false assertion does not make it any more true. Try to explain to me how the AZT travelled back in time to cause AIDS before it was taken.

    Your quote is not really accurate, and you are guilty of the crime you accuse others, the misquote. The correct quote is here, by Dr. Duesberg.

    What are you talking about? You’re going to have to be a bit more specific if you are going to accuse me of dishonesty.

  139. #139 Michael
    July 1, 2007

    Hey Patriot Games. See what I mean? “Doctor” Noble is not about to let reality interfere with the cartoon playing over and over in his head.

  140. #140 Michael
    July 2, 2007

    Patriot, Justin is not the only one who overlooks what I posted about blood transfusions. Even pseudo animation doctors are susceptible to ignoring the hazards of blood transfusions.

    For the Second Time:

    YOU are certainly overlooking the FACT that ALL BLOOD TRANSFUSIONS INTERFERE WITH THE IMMUNE SYSTEM!

    See: http://www.med.unipi.it/patchir/bloodl/deleterious.htm

    Blood transfusions are also associated with reduced cancer survival, and a multitude of other problems.

    The only thing getting sick after any blood transfusion gotten from someone HIV positive or negative would prove, is that the dissidents are quite correct that many of the so called AIDS cases were caused by the transfusions themselves! How come hetero hemophiliacs diagnosed as HIV/AIDS never came down with the Number One AIDS Defining Gay Disease of Kaposis Sarcoma????

    Even Ryan White’s death certificate showed he did NOT DIE of anything viral, but due to blood loss and a failed liver from his AZT!

  141. #141 Michael
    July 2, 2007

    Noninfectious Serious Hazards of Transfusion

    Although there has been a 10,000-fold reduction in the risk to patients from transfusion-transmitted infectious diseases in recent decades, there has been little progress in reducing the risk of noninfectious hazards of transfusion. As a result, patients today are harmed from noninfectious serious hazards of transfusion at a rate that exceeds infectious hazards by 100-fold to 1000-fold.

    American Association of Blood Banks – ASSOCIATION BULLETIN , June 14, 2001

    Serious hazards of transfusion (SHOT) initiative: analysis of the first two annual reports. Over 24 months, 366 cases were reported, of which 191 (52%) were “wrong blood to patient” episodes. Analysis of these revealed multiple errors of identification, often beginning when blood was collected from the blood bank. There were 22 deaths from all causes, including three from ABO incompatibility. There were 12 infections: four bacterial (one fatal), seven viral, and one fatal case of malaria. During the second 12 months, 164/424 hospitals (39%) submitted a “nil to report” return.
    BMJ 1999;319:16-19 ( 3 July )

    Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. We conclude that TRALI may be more frequent than previously recognized, and patient susceptibility, product age, and increased levels of bioactive lipids in components may predispose patients to TRALI. TRALI, like the acute respiratory distress syndrome may be a two-event phenomenon with both recipient predisposition and factors in the stored units playing major roles.
    Blood. 2002 Sep 5

    Transfusion-related alloimmune neutropenia: an undescribed complication of blood transfusion. Alloimmune neutropenia in neonates is rare. We describe severe and persistent neutropenia in a 4-week-old neonate, which arose within 2 h of a transfusion of blood that contained about 28 mL of plasma and in which strong antibodies against human neutrophil antigen 1b (HNA-1b) were subsequently identified. The infant was positive for HNA-1b. No other likely cause of neutropenia was discovered. We believe this complication of blood transfusion to be a previously unrecognised one, and have called the condition transfusion-related alloimmune neutropenia (TRAIN).
    Lancet. 2002 Oct 5;360(9339):1073.

    Transfusion in premature infants impairs production and/or release of red blood cells, white blood cells and platelets. Forty-eight hours after red blood cell transfusion to premature infants, there is an absolute decrease in red blood cell precursors, immature white blood cells and platelets, probably due to erythropoietin-suppression.
    J Paediatr Child Health. 2002 Jun;38(3):265-7.

    Influence of storage on red blood cell rheological properties. Serious hemorrheological disorders, including the decrease in RBC deformability secondary to shape abnormalities, acidosis, and the decrease of blood clotting, start already at the second week of storage and progress up to the end of the storage period. Transfusion of packed RBC older than 7 days may contribute to hemorrheological disorders in critically ill patients.
    J Surg Res. 2002 Jan;102(1):6-12.

    Immunological aspects of blood transfusions.
    Almost all identified acute and/or severe immunological reactions towards blood transfusions, reported by surveillance systems such as SHOT (Severe Hazards of Transfusion) in the UK are mediated by allo-antibodies. In contrast, the clinical effects of transfusion-induced cellular immunity are virtually unknown. Although alterations in lymphocyte responses and natural killer cell functions after blood transfusion has been reported in many publications, the relevance of these in vitro assays for in vivo immunity are lacking. Even for clinically obvious immunomodulatory effect of blood transfusions, such as the mitigation of renal graft rejection, no uniform in vitro explanation has been identified. In the laboratory animal it has been shown that when two antigenic stimuli are given simultaneously, the response to one of these antigens is often decreased. Blood transfusions introduce a multitude of foreign antigens. Indeed, immunostimulation and suppression by blood transfusions have both been found. Systematic studies on immunological side-effects of blood transfusions are hardly available. Since the UK and France introduced a transfusion vigilance system, severe immunological side-effects such as haemolytic reactions, TRALI (acute lung injury), PTP (post-transfusion purpura) and graft vs. host disease are registrated in these countries and their incidence can be estimated based on the national number of transfusions. However, every blood transfusion interferes with the immune system of the recipient. The available evidence of harm from immune responses not leading to severe transfusion reactions will be discussed.
    Transpl Immunol. 2002 Aug;10(2-3):183-90.

    Stored blood products stimulate cancer growth. During storage, blood products become proangiogenic stimulating both cancer cells and endothelial proliferation in vitro. These findings may have clinical significance in terms of the detrimental effects blood products contribute to cancer patients survival.
    British Journal of Surgery Volume 89 Issue s1 Page 19 – June 2002

    Effect of blood transfusion on long-term survival after cardiac operation. We found that blood transfusions during or after coronary artery bypass operations were associated with increased long-term mortality.
    Ann Thorac Surg. 2002 Oct;74(4):1180-6.

    The Association Between Preoperative Concentration of Soluble Vascular Endothelial Growth Factor, Perioperative Blood Transfusion, and Survival in Patients with Primary Colorectal Cancer Preoperative blood transfusion may be associated with high preoperative concentrations of soluble vascular endothelial growth factor (sVEGF) in patients with colorectal cancer. Transfusion during or after the operation is associated with poor survival in patients with Dukes stage A, B, and C rectal cancers.
    Eur J Surg 2001 Apr;167(4):287-92

    Impact of allogenic packed red blood cell transfusion on nosocomial infection rates in the critically ill patient. Transfusion of packed red blood cells is associated with nosocomial infection. This association continues to exist when adjusted for probability of survival and age. In addition, mortality rates and length of intensive care unit and hospital stay are significantly increased in transfused patients.
    Crit Care Med. 2002 Oct;30(10):2249-54.

    Red blood cell transfusions in critically ill patients. If RBC transfusions increase the risk of death, as suggested by the results of the study by Vincent et al and by the TRICC study, it is possible that several factors related to the processing and storage of blood products may have important clinical consequences. For example, decreasing the number of leukocytes using leukofiltration by an order of 4 logs in packed units of RBCs prior to storage may have significant clinical ramifications. As a second example, there is limited information establishing the efficacy of RBCs after prolonged storage. One of the first clues to the disturbing possibility of harm associated with transfusion of older vs newer RBCs was an association between RBCs older than 15 days and gut ischemia measured using gastric tonometry. Both examples illustrate the need for further research regarding the clinical consequences of blood transfusions.
    JAMA. 2002 Sep 25;288(12):1525-6.

    Blood transfusions correlate with infections in trauma patients in a dose-dependent manner. In summary there is a clear dose-dependent correlation between transfusions of pRBCs and the development of infection in trauma patients. Multivariate analysis further demonstrated that pRBCs were an independent risk factor for the development of infections. Although transfusions are frequently indicated, they should be administered appropriately and with no more pRBCs than absolutely necessary.
    Am Surg. 2002 Jul;68(7):566-72.

    Increased Rate of Infection Associated With Transfusion of Old Blood After Severe Injury. Transfusion of old blood is associated with increased infection after major injury. Other options, such as leukocyte-depleted blood or blood substitutes, may be more appropriate in the early resuscitation of trauma patients requiring transfusion.
    Arch Surg. 2002 Jun;137(6):711-717.

    Association of bacterial infection and red blood cell transfusion after coronary artery bypass surgery. RBC transfusions were independently associated with a higher incidence of post-CABG bacterial infections. The risk of infection increased in proportion to the number of units of RBC transfused.
    Ann Thorac Surg 2002;73:138-142

    Transfusion of Blood Components and Postoperative Infection in Patients Undergoing Cardiac Surgery The administration of blood derivatives, mainly RBCs, was associated in a dose-dependent manner with the development of severe postoperative infection, primarily nosocomial pneumonia.
    Chest. 2001;119:1461-1468

    Emerging infectious disease issues in blood safety. In recent years, numerous infectious agents found worldwide have been identified as potential threats to the blood supply. Several newly discovered hepatitis viruses and agents of transmissible spongiform encephalopathies present unique challenges in assessing possible risks they may pose to the safety of blood and plasma products.
    Emerg Infect Dis. 2001;7(3 Suppl):552-3.

    West Nile virus infection transmitted by blood transfusion. Seroconversion of a symptomatic donor, the presence of viral genetic material in an associated whole-blood retention segment, and recovery of WNV from an associated component provides compelling evidence for transfusion-acquired infection. This report has important implications for blood safety.
    Transfusion. 2003 Aug;43(8):1018-1022.

    Transmission of prion diseases by blood transfusion Transmission of BSE to a single animal using this approach was reported recently. This study confirms this result with a second transmission of BSE and four new cases of transmission of natural scrapie. Positive transmissions occurred with blood taken at pre-clinical and clinical stages of infection. Initial studies indicate that following such infection by the i.v. route, deposition of the abnormal prion protein isoform, PrP(Sc), in peripheral tissues may be much more limited than is seen following oral infection. These results confirm the risks of TSE infection via blood products and suggest that the measures taken to restrict the use of blood in the UK have been fully justified.
    J Gen Virol. 2002 Nov;83(Pt 11):2897-905.

    A prospective study of blood transfusion history and liver cancer in a high-endemic area of Japan. A history of blood transfusion carried a significant risk of developing liver cancer in the study region. The people with a history of transfusion should be monitored more aggressively for viral infections and liver disease, as they may not report the infection or they may be unaware that they are infected
    Transfusion Medicine 2002 Oct; 12:297-302

    Rethinking blood shield statutes in view of the hepatitis C pandemic and other emerging threats to the blood supply.
    Researchers have identified at least twenty-five pathogens that can be transmitted through blood transfusions. Four percent of patients who receive the average amount of blood during a transfusion are at risk of being infected with a contaminated unit, and exposed to the danger of serious adverse reactions, including future debilitating conditions.
    J Health Law 2001 Summer;34(3):419-58

  142. #142 trrll
    July 2, 2007

    Over time, more and more of Duesberg’s ideas originally published 20 years ago, which had been, rejected are now being accepted by the weight of the evidence.

    This rewrites the history rather drastically. I’ve been reading the AIDS/HIV literature since the early days when it was merely an unusual cluster of cases of Kaposi’s sarcoma, and I remember that when originally published, Duesberg’s ideas were originally taken quite seriously by many scientists. Over the years, as more and more evidence accumulated supporting the HIV hypothesis, scientists one by one discarded Duesberg’s claims. Today, Duesberg is left virtually alone, still doggedly hanging onto his own pet hypothesis while the scientific community has moved on, still trying with increasing desperation to nitpick away the flood of results that do not support his hypothesis.

  143. #143 Chris Noble
    July 2, 2007

    This rewrites the history rather drastically.

    Duesberg: KS is caused by poppers.

    Duesberg: KS is caused by poppers.

    Duesberg: KS is caused by poppers.

    Duesberg: KS is caused by poppers.

    Evidence: KS is caused by HHV-8

    Duesberg: See I told you KS wasn’t caused by HIV.

    PS. Evil totalitarian Tara was censoring this relevant post with lots of links

  144. #144 Chris Noble
    July 2, 2007

    Here is another Maniotism.

    The A, B, C’s of AIDS Denialism

    But AIDS denialists at the Red Cross published statistics recently indicating that (31):

    “among “non-risk” blood donors, the current estimate of incidence out of 37,164,054 units screened, 12 were confirmed to be positive for HIV-1 RNA – or 1 in 3.1 million donations – and only 2 of which were detected by HIV-1 p24 antigen testing.”

    2 or 12 out of 37,164,054 can in no way account for the near 1 million infections said to afflict Americans, so this is AIDS denialism.

    ….

    13 Stramer et. al. “Detection of HIV-1 and HCV Infections among Antibody-Negative Blood Donors by Nucleic Acid-Amplification Testing”, New England Journal of Medicine, Volume 351:760-768; August 19, Number 8, 2004.

    The “quote” is manufactured by Maniotis. This is not what Stramer et al report. Even a brief look at the title would give you a clue. Stramer et al looked at how many extra HIV infected units were picked up by testing units from antibody-negative donors.

  145. #145 Pope
    July 2, 2007

    In their predictably weak and selective response to Duesberg’s long (but by no means exhaustive http://aras.ab.ca/azt-sicker_n_deader.html) list of nails in the AZT coffin, we equally predictably find the centre piece argument that AZT was only administered to patients already sick and dying of AIDS, hence the poor record.

    Even the words of Goedert et al. themselves contradict this:

    Sujects who had started AZT had an increased risk [4.5 times]of AIDS, probably because Zidovudine was administered first to those whom clinicians considered to be at highest risk (Lancet 1994)

    Please note the “we don’t really give a shit” probably, then note the wording “increased risk of AIDS”, meaning the patients didn’t have AIDS yet. Clinicians may very well have decided through CD4 counts, clairvoyance or some other means that some patients were more likely to progress from mere HIV+ to fullblown AIDS and administered AZT preferentially to those. Regardless, the intervention was A SPECTACULAR FAILURE BY ANY STANDARD.

    When Duesberg mentions that something akin to a nuclear device hit haemophiliacs in 1987 and increased deaths tenfold after years of decrease, the only new factor was AZT:

    Thus the only new risk of mortality,
    in and after 1987, was not HIV, but AZT

    http://scienceblogs.com/aetiology/2007/06/introduction_to_hiv_and_hiv_de.php#comment-485409

  146. #146 DT
    July 2, 2007

    Patriot Games said:

    “My dear Dr. Noble, you obviously have not read Professor Peter. Duesberg’s very thoughtful reply to Sabin’s earlier hemophilia AIDS study which contains all the information rebutting her later comments.

    Dr Noble has responded quite comprehensively to this. But I wondered if you really read the Duesberg analysis yourself? As you seem to speak for him, can you explain why he says the following:

    “The HIV hypothesis predicts the same pattern of AIDS diseases in haemophilia as in other AIDS patients, but Kaposi’s sarcoma and dementia were not observed in the haemophilic patients studied by Sabin et al (table 2).”

    First I’d like a reference to a paper stating that the “HIV hypothesis” predicts the same pattern of diseases in hemophiliacs. There must be a published prediction somewhere.
    Where is it?

    Obviously to claim this is nonsense – there is no such prediction because it is patently false. What infections/OIs/conditions someone gets is dependent upon current and previous exposure to opportunists.

    Hemophiliacs do not get Kaposi because…….. they do not use poppers (only joking!). We all know it is because they have very low infection rates with HHV8 which causes KS (as opposed to gay men/heterosexuals). The relevant point here is that HHV8 is sexually transmitted, so is prevalent in those with high rates of partner change / history of other STIs.

    Duesberg just doesn’t understand STIs – he never has and never will.

  147. #147 DT
    July 2, 2007

    Michael, thank you for your long (and irrelevent) spamoid post detailing the problems that can arise with blood transfusion. It is much appreciated as evidently medical science must have previously been totally unaware of these problems.

    However, among all the references, I think I may have missed the crucial one that shows that blood recipients without HIV infection develop AIDS-defining illnesses.

    Blood transfusion is common, many hundreds of thousands of recipients should now be wasting away with “AIDS”. Can we see one paper that reveals the extent of this devastation somewhere (anywhere?). Extra brownie points are awarded if this is in a country which has been screening blood for HIV since 1983.

    And while you are at it, could you provide any paper showing, as denialists claim, that hundreds of thousands of HIV negative drug users have got PCP?

  148. #148 DT
    July 2, 2007

    Pope, the fact remains that in the Goedert hemophilia study those who are more ill, who already had AIDS or who were more likely to get AIDS are preselected as the ones who were given AZT.

    The study was actually designed to assess the impact of factor 8 purity on progression of HIV, and not to look at the impact of AZT. In science one cannot twist study design around and jump to totally invalid conclusions. The study methodology correctly controls for the different independent variables (including AZT use) for the study variable of Factor 8 purity.

    If a study was designed to assess the impact of AZT then it would have been completely different, and controlled for variables such as duration of infection, CD4 count and clinical stage of disease. This was not done, since this is not what the study was about.

    In typical fashion, denialists have taken a single line out of a table in a paper, reinterpreted it’s significance to promote their own agenda, and falsely claim that the overall study suddenly supports their spurious claims. They ignore the context of the study, ignore relevant parts of the text which explain why sick patients were given AZT, and dispense with all conventional scientific protocol concerning trial methodology and analysis.

  149. #149 Pope
    July 2, 2007

    Pope, the fact remains that in the Goedert hemophilia study those who are more ill, who already had AIDS or who were more likely to get AIDS are preselected as the ones who were given AZT

    DT, That was a probably, not a “fact”. the fact, according to the wording in the paper, is that HIV+ patients given age had a 4.5 times higher risk of AIDS.

    That this particular study, like every other study, with perhaps a handful exceptions, is not designed to test the “HIV=AIDS, and the drugs are great” party line does not change that.

    Perhaps you have noticed that Duesberg does not cite this study as other than a piece of corroborating evidence, just a little something that should give drug reps a pause for thought before touting their goods?

    Other, more direct, evidence is given, which you can choose not to ignore.

  150. #150 Pope
    July 2, 2007

    My “£%$£” computer, probably programmed By Dr. Noble, chose for some, I’m sure very logical, reason to change ‘AZT’ into ‘age’.

  151. #151 DT
    July 2, 2007

    Aside from your handwaving Pope, I see little that actually answers any of the substance of my post.

    This was NOT a study looking at the impact of AZT. If it were then the methodology would have used completely different variables, and been presented in a different way. Since the analysis did not do this, you cannot conclude that AZT was given or not given to groups of patients with similar duration of HIV infection, CD4 counts and similar clinical correlates for advanced HIV.

    Like we said, AZT was just becoming generally available back then. It was earmarked for those with advanced disease or AIDS (as is suggested in the text of the paper). The fact that those who actually got it had a high mortality means nothing in the context of determining if AZT could affect outcome.

    And yes, other more direct evidence is available, which supports the orthodox view (Sabin’s paper for starters) which Duesberg misinterprets and in which Sabin, in response to Duesberg’s misrepresentation, conclusively demonstrates that AZT was given to those who already had AIDS or whose counts dropped below 200.

    Like Dr Noble said, you can’t blame insulin for giving people diabetes (or to relate this more specifically to what you claim, you can’t blame insulin for “killing diabetic patients” when insulin is only given to the diabetics with the worst glucose control who have high predicted mortality anyway)

  152. #152 Patriot Games
    July 2, 2007

    The noble doctor noble is back to his “quote picking”

    maniotis said:
    But AIDS denialists at the Red Cross published statistics recently indicating that (31): “among “non-risk” blood donors, the current estimate of incidence out of 37,164,054 units screened, 12 were confirmed to be positive for HIV-1 RNA – or 1 in 3.1 million donations – and only 2 of which were detected by HIV-1 p24 antigen testing.”
    ….
    2 or 12 out of 37,164,054 can in no way account for the near 1 million infections said to afflict Americans, so this is AIDS denialism.
    ….
    13 Stramer et. al. “Detection of HIV-1 and HCV Infections among Antibody-Negative Blood Donors by Nucleic Acid-Amplification Testing”, New England Journal of Medicine, Volume 351:760-768; August 19, Number 8, 2004.

    noble said;
    The “quote” is manufactured by Maniotis. This is not what Stramer et al report. Even a brief look at the title would give you a clue. Stramer et al looked at how many extra HIV infected units were picked up by testing units from antibody-negative donors.

    The quote is not “manufactured”. It is very correct, as anyone can easily see.

    Detection of HIV-1 and HCV Infections among Antibody-Negative Blood Donors by Nucleic Acid-Amplification Testing Volume 351:760-768 August 19, 2004 Number 8 NJM, Susan L. Stramer, Ph.D.,

    Background Testing of blood donors for human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) RNA by means of nucleic acid amplification was introduced in the United States as an investigational screening test in mid-1999 to identify donations made during the window period before seroconversion.
    Methods We analyzed all antibody-nonreactive donations that were confirmed to be positive for HIV-1 and HCV RNA on nucleic acid-amplification testing of “minipools” (pools of 16 to 24 donations) by the main blood-collection programs in the United States during the first three years of nucleic acid screening.
    Results Among 37,164,054 units screened, 12 were confirmed to be positive for HIV-1 RNA — or 1 in 3.1 million donations — only 2 of which were detected by HIV-1 p24 antigen testing.
    For HCV, of 39,721,404 units screened, 170 were confirmed to be positive for HCV RNA, or 1 in 230,000 donations (or 1 in 270,000 on the basis of 139 donations confirmed to be positive for HCV RNA with the use of a more sensitive HCV-antibody test). The respective rates of positive HCV and HIV-1 nucleic acid-amplification tests were 3.3 and 4.1 times as high among first-time donors as among donors who gave blood repeatedly. Follow-up studies of 67 HCV RNA-positive donors demonstrated that seroconversion occurred a median of 35 days after the index donation, followed by a low rate of resolution of viremia; three cases of long-term immunologically silent HCV infection were documented.
    Conclusions Minipool nucleic acid-amplification testing has helped prevent the transmission of approximately 5 HIV-1 infections and 56 HCV infections annually and has reduced the residual risk of transfusion-transmitted HIV-1 and HCV to approximately 1 in 2 million blood units.

    This following paragraph is not a quote, rather is a comment, and it is clear as day that the point of the comment is quite correct.

    2 or 12 out of 37,164,054 can in no way account for the near 1 million infections said to afflict Americans, so this is AIDS denialism.

    Yes, my honorable noble doctor noble, your very astute interpretation of the title of this article is quite correct.

    The topic of the paper concerns the techniques used by the blood bank to screen donor samples for HIV, especially for antibody negatve samples which might harbor HIV which is missed.

    About 1% of the blood donor samples are discarded because of a serologically positive result to HIV antibodies (ELISA) which, as we all know, is overly very sensitive, producing false positives.

    In 1999 DNA amplification testing for HIV was introduced, and all blood donor samples were also tested using this method in which 16 samples are pooled as a cost saving measure.

    The Stramer paper is concerned with establishing the validity of doing the DNA amplification test. Stramer looked at the data and found that 12 of the blood donor samples were postive for HIV by DNA amplification, yet were negative by HIV antibody serology. This is good news, because our blood supply is safer by picking up these 12 cases of HIV by which would have been missed, and Stamer is doing a good job.

    Dr. Stramer then explains that these 12 HIV positives, which were HIV antibody negative, were explained as window period cases. This means these 12 cases are new HIV infections ocurring in the window period before antibody production starts, so the antibody test is still negative. Eight of these 12 had follow up and all seroconverted, or developed a positive antibody test after about 20-40 days days or so, when their natural antibody production kicked in. We assume the other 4 lost to follow up would have done the same.

    Getting back to the validity of the comment,

    2 or 12 out of 37,164,054 can in no way account for the near 1 million infections said to afflict Americans, so this is AIDS denialism.

    Lets give you the benefit of the larger number 12, and Stramer is telling us that there are 12 cases of new infection window periods detected when testing a pool of 37 million Americans. Assuming the CDC number of ONE million HIV infectd Americans annually, is this enough new infection to maintain a pool of 1 million HIV infections annually? Perhaps an AIDS mathematican like Dr. Rebecca Culshaw should answer this question.

    It appears obvious that 12 cases of new infection window periods detected in 37 million americans doesn’t seem hardly enough to maintain our epidemic, does it? Let’s ask kevin, cooler, noreen, Pope, Michael, Adele and Raven what they think.

    So in conclusion, my noble doctor noble, not only are you incorrect in your accusation about the misquote which was exactly correct. You are also demonstrated your interpretive failure to understand the comment below the quote. Of course this is nothing unusual for the noble doctor noble, as we have seen this repeatedly in your past comments. The noble doctor noble’s ability to actually understand what he reads is similar to the ability of a robot. Try to do better next time, if there is one.

    For more information see reviewing aids DOT com

  153. #153 Adele
    July 2, 2007

    Forty Mules playing Patriot Games on the Fourth of July,

    Are you familiar with the concept, self-selected group?

    HEre’s a story for you. Back in 1985 they started testing people who applied for the military for HIV. If you have HIV or some other things they don’t take you. In 1985 most infected people hadn’t been tested and didn’t know. People applied and got rejected. Word got around. Also public education got ramped up and people learned more about HIV and AIDS and testing. Fast forward to 1995 and alot more HIV positive people knew they were positive and didn’t apply for the military. ANd all those people who apply and got rejected couldn’t apply again. If you graph all this data it looks like HIV rates go down over time.

    Problem is, your having a population that’s self selecting. Against drug use, HIV positive, homosexuality etc. ANd a population who’s knowledge about the policies and HIV changes over time. You can’t take it to the whole country. Unless your a complete idiot like that guy at Virgina Tech what’s his name?

    SAme with any of these other groups like blood donors. Last time I gave blood they asked me some questions like where I had been traveling and who I had sex with. Obvious, if I was HIV+ the last time they wouldn’t have taken me too. Blood donors self select and get screened too. THey’re not the general population.

    Even when Maniotis gets his quote right he’s taking it out of context and lying about what it means. What a pathetic man.

  154. #154 apy
    July 2, 2007

    In that HIV Facts movie, Duesberg says that if you have HIV antibodies then that means your body is controlling the virus and killing it off. He says this is how it is for all known viruses.

    It also says all retroviruses have something like 6 genes and there is nothing in the genetic structure that should make it act like it supposedly does.

    I don’t know enough about retroviruses to comment would anyone mind informing me? Thank you.

  155. #155 Patriot Games
    July 2, 2007

    Adele said

    Are you familiar with the concept, self-selected group? (snipped for brevity)

    Oh, sure the blood donors are self selected. That’s why 1 per cent (15,000 to 40,000 bags) of donated blood are discarded every year because of a positive serology. These 15-40,000 donors must have forgot to un-selfselect.

    Don’t forget we are looking for window period cases who don’t know they are HIV positive because their serology is still negative. How can a blood donor person self select when they are still HIV negative?

    Handwaving Adele?

    Again I pose the same question with you have evades or ignored. Are 12 cases of “window period” new HIV infections out of tesing 37,000 samples enough to maintain ONE MILLION HIV infections in America annually?

    While you are thinking about that, why not post the links to your HIV electron micrographs with the gold labeled antibody tags?

    Even when Maniotis gets his quote right he’s taking it out of context and lying about what it means. What a pathetic man.

    Compared to your idol John Moore who is a repulsive snake, Andy Maniotis is an angel. I have demonstrated Andy’s quote to be correct, and his comment to be correct as well, and you still cast ad hominems? Your ill will towards Maniotis is misplaced and reflects poorly on you Adele.

    Happy Fourth of July.

  156. #156 Sensor
    July 2, 2007

    I’m down for a review of the unanswered question –

    what is the gold standard? The purified, particulate reference standard?

    Anyone?

  157. #158 Sensor
    July 2, 2007

    I went to the page and this is what’s there. There is no purified particulate standard for HIV tests. There is a grabass of garbage from every experiment on people you nazis say has clinical Aids.

    Where is the particulate standard?:

    The Source of Critical HIV Research Materials
    Almost twenty-three years ago, the National Institutes of Health realized the need for a source of critical research materials involving HIV and other pathogens for the scientific community. This led to the establishment of the NIH AIDS Research and Reference Reagent Program. Created by the National Institute of Allergies and Infectious Diseases [NIAID], this year marks the nineteenth year of this vital and growing program.

    What’s New >> Reagent News
    Cell Lines
    Rev-CEM (#11467)
    CEM-SS cells were infected with a Lentivirus pNL-GFP-RRE(SA), [cat# 11466]. Clones were isolated and selected for HIV-dependent GFP expression. Order #11467 here.
    Cloning Vectors
    pNL-GFP-RRE(SA) (#11466)

    pNL-GFP-RRE was first constructed by complete deletion of all HIV ORFs of pNL4-3 by replacing the 8.1 kb BssHII-BlpI fragment of the HIV-1 genomes with an insert containing the GFP ORF and the HIV-1 Rev-responsive element (RRE) including the HIV-1 sequence immediately following the BssHII site and the first 336 nucleotides of the gag ORF (the gag reading frame was disrupted by a frame shift mutation at the ClaI site by blunt end ligation), the GFP ORF was derived from pIRES-hrGFP-1a (Stratagene) by PCR amplification. pNL-GFP-RRE-(SA) was constructed by insertion of a PCR fragment into the NotI-SmaI site of pNL-GFP-RRE, in front of the GFP ORF. The insert carries the HIV-1 A5 splicing acceptor and D4 donor. GFP is expressed from the HIV-1 LTR promoter in HIV infected cells when Tat and Rev are present. Order #11446 here.
    Expression Vectors
    pEGFP-Vpr (#11386)

    The Vpr coding region was amplified using PCR, from a full-length pNL4-3 clone. The 5′ oligonucleotide contained a HindIII restriction site that allowed fusion of the eGFP open reading frame with that of Vpr. The 3′ oligonucleotide contained a stop codon as well as an Xbal restriction site. The mammalian coding sequences include humanized GFP (eGFP) fused with Vpr under control of a CMV-IE promoter and a neomycin resistance gene under the control of an SV40 promoter. Order #11386 here.
    pcRev (#11415)
    Derived from pBC12/CMV/IL-2 (cat#11416) by cleavage with Hind III and Xho I followed by insertion of a Rev cDNA from the HXB3 strain of HIV-1 IIIB. Order #11415 here.
    pQE30T gly-met SDF-1a/CXCL12 (#11435)
    The pQE30 plasmid from QIAGEN was modified to contain a tobacco etch virus (TEV) protease cleavage site following the hexa-histidine tag and preceding the multiple cloning site. The DNA encoding mature SDF-1a was cloned into the BamHI (5′) and HindIII (3′) sites. Subsequently, site directed mutagenesis was used to modify the TEV protease site from ENLYFQGS to ENLYFQGM. This results in the DNA coding for modified TEV protease site preceding the DNA coding for mature SDF-1a. Since mature SDF-1a protein has no Met residues, SDF-1a expressed with this vector can be subjected to CNBr cleavage to remove the hexa-histidine tag. This leaves mature SDF-1a with a native N-terminus. XL-1 blue E. coli should be used for propagation or production of more plasmid. SG 13009 E. coli with pREP4 should be used for expression. Order #11435 here.
    pcDNA3.1-APOBEC3DE-V5-6xHIS – (#11433)
    The cloning insert was obtained from Open Biosystems (Huntsville, AL). Insert for human AID was cloned into mammalian expression vector pcDNA3 with a V5 epitope tag from SV5 paramyxovirus and a polyhistidine epitope at the C terminus. Plasmid DNA was transfected into 293T cells and expression of human APOBEC3DE was detected with a monoclonal anti-V5 antibody. Expression of human APOBEC3DE is driven by the CMV promoter. Order #11433 here.
    pMM310 (#11444)
    A PCR fragment containing full-length env and rev genes was derived from the genomic DNA of infected PBMC. The original virus (HIV-1 BaL) was obtained from NIH AIDS Research & Reference Reagent Program (cat #510). The env/rev cassette was cloned into pcDNA3.1D/V5-His TOPO© expression vector by a directional cloning approach. A single transformed ampicillin resistant E. coli colony was selected and expanded. Recombinant plasmid carries resistance genes for ampicillin and neomycin. Order #11444 here.
    HIV-1 clone BaL.01 (#11445)
    A PCR fragment containing full-length env and rev genes was derived from the genomic DNA of infected PBMC. The original virus (HIV-1 BaL) was obtained from NIH AIDS Research & Reference Reagent Program (cat #510). The env/rev cassette was cloned into pcDNA3.1D/V5-His TOPO© expression vector by a directional cloning approach. A single transformed ampicillin resistant E. coli colony was selected and expanded. Recombinant plasmid carries resistance genes for ampicillin and neomycin. Order #11445 here.
    HIV-1 clone BaL.26 (#11446)
    A PCR fragment containing full-length env and rev genes was derived from the genomic DNA of infected PBMC. The original virus (HIV-1 BaL) was obtained from NIH AIDS Research & Reference Reagent Program (cat #510). The env/rev cassette was cloned into pcDNA3.1D/V5-His TOPO© expression vector by a directional cloning approach. A single transformed ampicillin resistant E. coli colony was selected and expanded. Recombinant plasmid carries resistance genes for ampicillin and neomycin. Order #11446 here.
    pGag-EGFPt (#11468)
    The insert consists of Rev-independent HIV-1 Gag coding sequences [pCMV55M1-10 obtained from Dr. George Pavlakis, NCI (Schwartz et al (1992) J. Virol. 66: 7176-7182] fused in frame to EGFP. The clone was constructed as follows: 1) Rev independent Gag was amplified by PCR. The 5′ primer contained a Kpn I site and overlapped with the start of the coding region of Gag. The 3′ primer contained a Bam HI site, linkers that removed the Gag STOP codon, and bases that overlapped with the 3′ end of Gag. 2) The PCR product was digested with Kpn I and Bam HI and ligated into KpnI/BamHI cut pEGFP-N1 (Clontech). Note that the protein product contains a linker of 10 amino acids (NRNGDPPVAT) between the end of Gag and the beginning of EGFP.. Order #11468 here.
    Molecular Clones
    pAncCgp120-op (#11397)
    Derived from the pAncCgp160-opt clone (cat#11399). The env gene was truncated by introducing a stop codon immediately after the cleavage site (REKR). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 490aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11397 here.
    pAncCgp145-opt (#11398)
    Derived from the pAncCgp160-opt clone (Cat#11399). The env gene was truncated by introducing a stop codon immediately after the transmembrane domain (SIVNR). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 686 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11398 here.
    pAncCgp160-opt (#11399)
    A full-length subtype C ancestral env reconstructed from alignments of full-length subtype C env sequences available in the 2001 Los Alamos HIV Sequence Database. The ancestral env was inferred from maximum likelihood phylogenetic analyses and represents the most likely sequence at the interior node of the subtype C cluster (Gaschen et al. Science 296:2354-2360, 2002). For this construct, the env gene was artificially reconstructed by substituting original viral codons with those of highly expressed human genes (Andre et al. J. Virol 72:1497-1503, 1998). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The env amino acid sequence was not changed. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 842 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11399 here.
    pConBgp120-opt (#11400)
    Derived from the pConBgp160-opt clone (cat#11402). The env gene was truncated by introducing a stop codon immediately after the cleavage site (REKR). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the XbaI and BamHI sites. The size of the translated Env protein is 505 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11400 here.
    pConBgp145-opt (#11401)
    Derived from the pConBgp160-opt clone (cat#11402). The env gene was truncated by introducing a stop codon immediately after the transmembrane domain (SIVNR). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 701 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11401 here.
    pConBgp160-opt (#11402)
    A full-length subtype B consensus env gene reconstructed from alignments of full-length subtype B env sequences available in the 2001 Los Alamos HIV Sequence Database. The consensus env was generated by selecting the most common amino acid at each position in the protein alignment. For this construct, the env gene was artificially reconstructed by substituting original viral codons with those of highly expressed human genes (André et al. J. Virol 72:1497-1503, 1998). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The env amino acid sequence was not changed. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 850 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11402 here.
    pConBgp160-201NS-opt (#11403)
    Derived from the pConBgp160-opt clone (cat#11402). The envelope cleavage site was generated by altering the potential N-linked glycosylation site at AA position 201 (201N/S). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 850 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11403 here.
    pConBgp160-UNC-opt (#11404)
    Derived from the pConBgp160-opt clone (cat#11402). The envelope cleavage site was removed by altering the primary cleavage site (REKR?SEKS). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 850 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11404 here.
    pConCgp120-opt (#11405)
    Derived from the pConCgp160-opt clone (Cat#11407). The env gene was truncated by introducing a stop codon immediately after the cleavage site (REKR). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 490 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11405 here.
    pConCgp145-opt (#11406)
    Derived from the pConCgp160-opt clone (Cat#11407). The env gene was truncated by introducing a stop codon immediately after the transmembrane domain (SIVNR). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 686 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11406 here.
    pConCgp160-opt (#11407)
    A full-length subtype C consensus env gene reconstructed from alignments of full-length subtype C env sequences available in the 2001 Los Alamos HIV Sequence Database. The consensus env was generated by selecting the most common amino acid at each position in the protein alignment. For this construct, the env gene was artificially reconstructed by substituting original viral codons with those of highly expressed human genes (André et al. J. Virol 72:1497-1503, 1998). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The env amino acid sequence was not changed. The final construct was ligated into pcDNA3.1(-) expression vector using the EcoRI and BamHI sites. The size of the translated Env protein is 842 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11407 here.
    pWITO4160.27 gp160-opt (#11408)
    Derived from pWITO4160 clone 27. For this construct, the env gene was artificially reconstructed by substituting original viral codons with those of highly expressed human genes (André et al. J. Virol 72:1497-1503,1998). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The env amino acid sequence was not changed. The final construct was ligated into pcDNA3.1(-) expression vector using the XbaI and BamHI sites. The size of the translated Env protein is 849 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11408 here.
    pWITO4160.27 gp160-rev (#11409)
    A PCR fragment containing full-length env and rev genes was derived from plasma virion-associated RNA from a subject acutely infected with a clade B virus by reverse transcription and nested PCR amplification. The env/rev cassette was cloned into the pcDNA3.1/V5-His©TOPO® expression vector and screened to ensure correct orientation with the CMV promoter. A single transformed ampicillin-resistant E. coli colony was selected and expanded. The size of the translated Env protein is 849 aa. Order #11409 here.
    pCAAN5342.A2 gp160-opt (#11410)
    Derived from pCAAN5342 clone A2 (Cat#11038). For this construct, the env gene was artificially reconstructed by substituting original viral codons with those of highly expressed human genes (André et al. J. Virol 72:1497-1503, 1998). A Kozak sequence GCCGCCGCC was introduced upstream of the ATG start codon. The env amino acid sequence was not changed. The final construct was ligated into pcDNA3.1(-) expression vector using the XbaI and BamHI sites. The size of the translated Env protein is 852 aa. A single transformed ampicillin-resistant E. coli colony was selected and expanded. Order #11410 here.
    pWT/BaL (#11414)
    This vector contains a Full-length HIV-1 provirus. This consists of the backbone of the HXB-3 strain of HIV-1 IIIB containing 2687bp Sal I to Bam HI fragment from strain BaL, i.e. the BaL Tat, Rev, Vpu and gp120 sequences plus part of Vpr and gp41. Order #11414 here
    p81A-4 (#11440)
    This clone is a full length HIV-1 infectious molecular clone containing the V1-V3 envelope regions of Ba-L in an NL4-3 background. The vector encodes beta-lactamase. Cloning is described in Virology 213:70-79, 1995. Order #11440 here
    p21-85 (#11441)
    This clone is a full length HIV-1 infectious molecular clone containing the V2-V3 envelope regions of Ba-L in an NL4-3 background. The vector encodes beta-lactamase. Cloning is described in Virology 79:4828-4837, 2005. Order #11441 here.
    p20-36 (#11442)
    This clone is a full length HIV-1 infectious molecular clone containing the V3 envelope region of Ba-L in an NL4-3 background. The vector encodes beta-lactamase. Cloning is described in Virology 79:4828-4837, 2005. Order #11442 here.
    p49.5 R5-Tropic Molecular Clone (#11389)
    This clone is a full-length HIV-1 infectious molecular clone containing the V3 envelope region of Ba-L in an NL4-3 background. This vector encodes beta-lactamase. Cloning is described in J. Virol. 65:5782-5789, 1991; J. Virol. 66:6547-6554, 1992; Virology 213:70-79, 1995. Order #11389 here.
    Monoclonal Antibodies
    D50 MAb anti-gp41 (642-665) (#11393)
    Affinity purified from ascites fluid by Protein A/G chromatography. Recognizes gp41 (642-665). MAb D50 binds to the C-heptad but is not neutralizing. D50 MAb was generated during a study of the influence of the oligomeric structure of Env in determining the repertoire of the antibody response. ELISA titer against HIV-1 lysate (200ng/well) is 1:1000-1:10,000. Order #11393 here.
    Anti-human DC-SIGN (9E9A8) MAb (#11422)
    Does not cross react with DC-SIGNL. Use at 20 µg/ml for blocking, or at 0.5 µg/ml for FACS.. Order #11422 here.
    Anti-human DC-SIGN/DCSIGNL (14EG7) MAb (#11423)
    Cross reacts with DC-SIGN. Use at 20 µg/ml for blocking, or at 0.5 µg/ml for FACS. Order #11423 here.
    Polyclonal Antibodies
    Chicken polyclonal antibody to APOBEC3F#157 (IgY) (#11425)
    Chicken polyclonal antibody raised against human APOBEC3F (NP_660341.2) using a synthetic peptide specific for N-terminal amino acids (CYEVKTKGPSRPRLDAK). Affinity purified against immunizing peptide. The APOBEC3F antibody can be used for western blot detection of recombinant APOBEC3F protein from E. coli or Baculovirus, etc., at a 1:250-1:1000 dilution. NOTE: Reagent will not easily detect human APOBEC3F derived from human cells by western blot. Order #11425 here.
    Chicken polyclonal antibody to APOBEC3F#162 (IgY) (#11426)
    Chicken polyclonal antibody raised against human APOBEC3F (NP_660341.2) using a synthetic peptide specific for C-terminal amino acids ((C+)KYNFLFLDSKLQEILE). Affinity purified against immunizing peptide. The APOBEC3F antibody can be used for western blot detection of recombinant APOBEC3F protein from E. coli or Baculovirus, etc., at a 1:250-1:1000 dilution. NOTE: Reagent will not easily detect human APOBEC3F derived from human cells by western blot. Order #11426 here.
    Rabbit Anti-Human APOBEC3F (C-18) (#11474)
    Rabbit polyclonal antibody raised against human APOBEC3F using a synthetic peptide specific for C-terminal amino acids (C-GLKYNFLFLDSKLQEILE). Affinity purified using peptide antigen. The APOBEC3F (C-18) antibody works well at 1/1000 for immunoblotting, and readily detects APOBEC3F expressed in transiently transfected cell lines such as 293T, but has not been shown to detect endogenous APOBEC3F present in primary human T-cells. Order #11474 here.
    Proteins
    HIV-1 Nef Protein (#11478)
    A cDNA sequence encoding HIV-1 Nef, Gly 3-Asp 205 (Accession #AAL12764), was fused to His-tag (MASTTHHHHHHDTDIPTTGGGSRPDDDDKH) at the N-terminus and expressed in E. coli. Order #11478 here.
    Viruses
    HIV-1 CC 1/85 (#11394)
    R5 primary virus which became R5X4 by 7/86 during the course of infection in patient “C”. Order #11394 here.

  158. #159 Sensor
    July 2, 2007

    Is this how you convince yourselves that your donig science? By doing all this lab voodoo, cloning scraps in bacteria? There’s no purified particulate reference standard.

    There is no stand-alone particle in the list above, only scraps that you’ve anvilled together, most of them you constructed by following academic models of what you think you should find.

    Is this how you convince yourself? Because its’ so dense and complicated?

    There is no purified particulate reference standard. It’s not there. That is why the tests always say the same thing, like, Don’t use this test to diagnose, and if you do, then use another too, and another, and then don’t use any test, but use this one, but only for peopel in risk groups.

    Isn’t that it? The risk grop makes the test work, because the test is bullsh**.

    Thank yoyou you answered my question.

    Seriously dude, thanks. You’ve been a big help. You sick pucks.

    No, serously, You just answered my question, thanks.

    SensOR.

  159. #160 Pope
    July 2, 2007

    And on top of that Bush just commuted Libby’s sentence – no jail time.

  160. #161 ElkMountainMan
    July 2, 2007

    Senor Sensor is not exactly helping the case of those very few whom I would consider “honest denialists.”

    Which also raises the question, have the career denialists ever truly cared, or in the words of the sophomorically Bialyesque Sensor, “iven a gats rass,” about those with HIV and AIDS?

    The behavior of dishonest denialists (Maniotis, Duesberg), depraved and deranged denialists (Bialy, Jensen), or out-and-out ready-for-the-institution freaks (JD and Sensor, assuming these are not any of the above-mentioned) prompts me to ask why Noreen Martin takes what they say so seriously. I commend her for distancing herself from “Sensor’s” hatred and encourage her to reexamine what these people say, not simply how they convey it.

    Truly, all of the scientific arguments presented by the various level-headed debaters on this page, as convincing as they are, do not hurt denialism so much as the inexplicably sociopathic behavior of most of its own practitioners.

  161. #162 Sensor
    July 2, 2007

    Elkmountaingoat,

    What is the singular purified particulate reference standard for hiv tests?

    There, is that “Hate-free” enough for you?

    Simple question, sensitive one, answer it simply.

  162. #163 cooler
    July 2, 2007

    Some people snap when they percieve an injustice and are constantly mocked by big pharma/cdc sycophants, some don’t. Im not saying whats right or wrong but thats probably the philosophy behind it.

  163. #164 Sensor
    July 2, 2007

    ElkMountainMAN,

    What you don’t get is, if this “””SCIENCE””” is Wrong, and it sho nuff is, then millions of po folk is getting murdered on drugs and going without good water food and medicine.

    Simple enough Mountain Friend? So feelings can run, ya know, a little HIGH After 20 years of bein all sweet and nice.

    So, I’ll give it to you nice, one mo time:

    What is the singular purified particulate reference standard for “HIV TESTS”?

    SenSor SenSes ALL

  164. #165 noreen Martin
    July 2, 2007

    Elkmountainman, you make some valid points and sometimes some of the denialists seem to be nuttier than a fruitcake. That being said, we cannot ignore some of the questions that these people or level-headed “rethinkers,” I like that term better, bring up. If some of these questions had been satisfactory answered, I would not be a rethinker myself. But direct questions deserve direct answers and direct proof. I have asked my doctors over and over, I see alot because I go to a training hospital, where is the document that unequivocally proves that HIV cause AIDS? This is a fair question to ask and expect an answer too. But all I ever get is that it is somewhere in PubMeb. That’s not good enough. I would hope that these doctors should be able to quote the reference just like a preacher could quote scripture. They tell me that they will get back with me, which means three more months and they never cross that bridge again with me. This is only one issue, there are many more. And you folks on the other side wonder why we are rethinkes?

  165. #166 Dan
    July 2, 2007

    Slooowwww down there, Sensor.

    Just because this bunch of folks couldn’t lead you to that singular purified particulate reference standard for HIV tests, doesn’t mean it doesn’t exist now…does it?

  166. #167 Pope
    July 2, 2007

    ElkMountainMan,

    To show you that we in the HIV resistance movement have our hearts in the right place, I have linked the one and only incontrovertible picture of the purified, particulate HIV just for you.

    http://www.reviewingaids.com/awiki/index.php/Image:ObjectAndSubject.jpg

    That and the good news about Libby should make your Independence Day.

  167. #168 Old Glory
    July 2, 2007

    Sensor said,

    Elkmountaingoat,What is the singular purified particulate reference standard for hiv tests?There, is that “Hate-free” enough for you? Simple question, sensitive one, answer it simply.

    ElkMountaineerGoatMan would probably say (if he could);

    The gold standard for HIV tests; Don’t you know this is 2006 and science has advanced since 1984. We don’t need a gold standard for the HIV tests. Besides we have DNA tests now and we know they are always right 100% of the time, so who needs a gold standard?

    Proof that HIV causes AIDS; How HIV causes AIDS is proven and published somewhere in pubmed. Exactly where is not important. We know it is in there somewhere. Just ask Google or Wikipedia, they will tell you that its there somewhere. Anybody who asks where, is a “denialist”, gets cut off from NIH funding and drug company money.

    Animal model for AIDs. We have an animal model. One chimp got AIDS and died after we injected some blood into it. Exactly what we injected is published in the paper, so go look it up stupid.

    Occupational AIDS. Hundreds or thousands of doctors and nurses got AIDS from needle stick injuries from their AIDS patients. This is a fact. They were too embarassed to let any body know about it. After all getting AIDS is a bad thing, so they hid this information. That’s why there are no reports in the medical literature, they were embarassed to tell anyone.

    Aids drugs are safe and have saved millions of lives. You didn’t now this? Yes its true. How do we know. Well we did PLACEBO controlled studies and showed this. Yes placebo controlled. A cocktail of HIV drugs is a perfectly good placebo. All HIV patients who die on these drugs died of AIDS, while all patients who lived, lived because of the miraculous healing powers of the drugs. Yes, destroying the mitochonria actually heals the cells. Its unhealthy to have too many mitochondria, you know.

    The HIV AIDS vaccine; Just because there is no vaccine for HIV does not one small iota detract from the fact that HIV causes AIDS, or the need to spend billions of dollar over the next 20 years doing research to find a vaccine. A vaccine is just around the corner. Another 100 billion dollars, and AIDS will be cured saving billions of lives on the planet. Nobel prizes will be awarded for the vaccine discovery. It will be glorious.

    HIV drugs for pregnant HIV MOMs and kids. The benefits are so great and the adverse side effects so miniscule, it is hard to actually give out these life saving drugs without breaking out in tears and cry with joy at how many lives are saved from each pill.

    AIDs in Africa. Yes the Indianapolis Star is correct. There is AIDS in Africa and its getting worse every day. We had AIDS in gay drug addicted America and we cured it with the life saving drugs, so AIDS escaped and went to Africa because Africans are not too careful, if you catch my drift. We may never cure Aids in Africa because they don’t listen to us when we tell them to stop having sex. They just keep doing it. Go figure.

  168. #169 Old Glory
    July 2, 2007

    Sensor said,

    Elkmountaingoat,What is the singular purified particulate reference standard for hiv tests?There, is that “Hate-free” enough for you? Simple question, sensitive one, answer it simply.

    ElkMountaineerGoatMan would probably say (if he could);

    The gold standard for HIV tests; Don’t you know this is 2006 and science has advanced since 1984. We don’t need a gold standard for the HIV tests. Besides we have DNA tests now and we know they are always right 100% of the time, so who needs a gold standard?

    Proof that HIV causes AIDS; How HIV causes AIDS is proven and published somewhere in pubmed. Exactly where is not important. We know it is in there somewhere. Just ask Google or Wikipedia, they will tell you that its there somewhere. Anybody who asks where, is a “denialist”, gets cut off from NIH funding and drug company money.

    Animal model for AIDs. We have an animal model. One chimp got AIDS and died after we injected some blood into it. Exactly what we injected is published in the paper, so go look it up stupid.

    Occupational AIDS. Hundreds or thousands of doctors and nurses got AIDS from needle stick injuries from their AIDS patients. This is a fact. They were too embarassed to let any body know about it. After all getting AIDS is a bad thing, so they hid this information. That’s why there are no reports in the medical literature, they were embarassed to tell anyone.

    Aids drugs are safe and have saved millions of lives. You didn’t now this? Yes its true. How do we know. Well we did PLACEBO controlled studies and showed this. Yes placebo controlled. A cocktail of HIV drugs is a perfectly good placebo. All HIV patients who die on these drugs died of AIDS, while all patients who lived, lived because of the miraculous healing powers of the drugs. Yes, destroying the mitochonria actually heals the cells. Its unhealthy to have too many mitochondria, you know.

    The HIV AIDS vaccine; Just because there is no vaccine for HIV does not one small iota detract from the fact that HIV causes AIDS, or the need to spend billions of dollar over the next 20 years doing research to find a vaccine. A vaccine is just around the corner. Another 100 billion dollars, and AIDS will be cured saving billions of lives on the planet. Nobel prizes will be awarded for the vaccine discovery. It will be glorious.

    HIV drugs for pregnant HIV MOMs and kids. The benefits are so great and the adverse side effects so miniscule, it is hard to actually give out these life saving drugs without breaking out in tears and cry with joy at how many lives are saved from each pill.

    AIDs in Africa. Yes the Indianapolis Star is correct. There is AIDS in Africa and its getting worse every day. We had AIDS in gay drug addicted America and we cured it with the life saving drugs, so AIDS escaped and went to Africa because Africans are not too careful, if you catch my drift. We may never cure Aids in Africa because they don’t listen to us when we tell them to stop having sex. They just keep doing it. Go figure.

  169. #170 Chris Noble
    July 2, 2007

    Compare

    “among “non-risk” blood donors, the current estimate of incidence out of 37,164,054 units screened, 12 were confirmed to be positive for HIV-1 RNA – or 1 in 3.1 million donations – and only 2 of which were detected by HIV-1 p24 antigen testing.”

    with

    “Among 37,164,054 units screened, 12 were confirmed to be positive for HIV-1 RNA — or 1 in 3.1 million donations — only 2 of which were detected by HIV-1 p24 antigen testing”

    Quotation marks are meant to indicate a direct quote. Unless you check the references you are relying on Maniotis to correctly report the findings of the paper. The fabricated parts of the quote do accurately describe the findings of the paper. The donors were not “non risk” they were antibody negative. The “incidence” was actually a prevalence (Denialists never seem to understand the difference) and not in the total population of blood donors but in the subpopulation that were antibody negative. Blood donors are also not a good indictaion of the general population because they are already screened.

  170. #171 No More Evasion
    July 2, 2007

    OK, noble doctor noble, enough of your obsessive compulsive rituals and answer the simple question posed. Are 12 HIV acute infection window cases out of 37 million blood tests sufficent to maintain One Million HIV infections in the America annually? Lets have it yes or no. Stop your evasion and spit it out, or you dont get to peddle any more toxic drugs to unsuspecting Africans.

  171. #172 Chris Noble
    July 2, 2007

    OK, noble doctor noble, enough of your obsessive compulsive rituals and answer the simple question posed. Are 12 HIV acute infection window cases out of 37 million blood tests sufficent to maintain One Million HIV infections in the America annually? Lets have it yes or no. Stop your evasion and spit it out, or you dont get to peddle any more toxic drugs to unsuspecting Africans.

    The “simple question” is not simple. It is based on false premises. The prevalence of HIV detected in blood units is around 300 times higher than the value that Maniotis implies. You are not allowed to donate blood if you have previously tested HIV positive or are in a high risk group. The people that donate blood are not the same group that are responsible for infecting people. The prevalence of HIV in blood donors is about 30 times lower than the prevalence of HIV in the total population.

  172. #173 Red White and Blue
    July 2, 2007

    The noble Doctor noble said:

    The “simple question” is not simple. It is based on false premises. The prevalence of HIV detected in blood units is around 300 times higher than the value that Maniotis implies. You are not allowed to donate blood if you have previously tested HIV positive or are in a high risk group. The people that donate blood are not the same group that are responsible for infecting people. The prevalence of HIV in blood donors is about 30 times lower than the prevalence of HIV in the total population.

    excuse me for asking, but what is the “prevalence” of HIv in donated blood samples? Providing a number here would sufficent.

    What prevalence number is Dr. Maniotis implying?

    How do you have this knowledge that the people who are HIV positive and donate blood which is discarded are not the people who infect others? Did you ask them? Or did you read this in a publication somewhere, reference please.

    The prevalence of HIv in blood donors is 30 times lower than the prevalence of HIv in the population

    What is this prevalence number and list the reference for your statement please.

    Why do you first say 300 then say 30. Typo?

    How many acute window period HIV infections would you estimate are needed to maintain one million HIV infections annually? How about a million? Does that work for you? To many? How about 100,000 does that work for you. Still too many? How about 10,000? Does that work for you? Still too many, How about 12 ? does that work for you? good, because that is exactly the number that was detected after testing 37 million blood samples for HIv and discarding the ONE PER CENT (37,000) positives for HIV serology. After discarding the chronic HIV cases, they found 12 acute window period HIV infections. The magic number is 12. TWELVE. TWO times SIX. Count the fingers on both hands and add two.

    That’s why Stramer is a denialist;

    2 or 12 out of 37,164,054 can in no way account for the near 1 million infections said to afflict Americans, so this is AIDS denialism.

    Starting to see the light now, noble doctor noble?

  173. #174 Chris Noble
    July 2, 2007

    excuse me for asking, but what is the “prevalence” of HIv in donated blood samples? Providing a number here would sufficent.

    One of the adavntages of reading the papers that Maniotis cites rather than relying on his misinterpretation is that you can learn something.

    Reference 15 of the paper is Current prevalence and incidence of infectious disease markers and estimated window-period risk in the American Red Cross blood donor population.

    The observed prevalence of HIV in the donated blood units was 9.7 per 100,000 this is about 300 times higher than that implied by Maniotis.

    It is also about 30 times lower than the overall prevalence in the US population (around 1 million per 300 million).

    Considering that you have to fill out a questionairre with a long list of questions such as “Have you had sex with a HIV+ person” before you donate blood it is no wonder that the prevalence amongst blood donors is lower than the national average.

    There also aren’t 1 million new infections per year. That is the estimate for prevalence. The estimate for incidence is about 40,000.

    Starting to see the light now, noble doctor noble?

    No.

  174. #175 trrll
    July 2, 2007

    It also says all retroviruses have something like 6 genes and there is nothing in the genetic structure that should make it act like it supposedly does.

    To a biologist, this is an amazingly dumb argument. It is simply not possible to inspect the genome of any organism, no matter how small, and predict with any reliability what it will do once introduced into the body. Moreover, there is no minimum number of genes required to produce selective toxicity to a particular cell type. There are some bacterial proteins, made by a single gene, that are highly toxic only to one specific type of cell in the body.

  175. #176 Pope
    July 3, 2007

    Trrll,

    I’m glad we got that straight. I’ve always thought that the idea of specific suppressor and activator (AIDS) genes to explain HIV’s unpredictably long latency periods must sound amazingly dumb to any real biologist.

  176. #177 Adele
    July 3, 2007

    Well, I’m a biologist masters not PhD, I’m not a kickboxer. So maybe I’m not as qualified as Pope Claus Jensen to talk about transcription regulation of HIV.

    If Claus thinks transcriptional regulation is funny maybe he should talk to his pal Bialy who used to research that stuff in the sixties and seventies. If Claus is right then Bialy’s whole career is a failure not just the past thirty years of it.

    But Claus is wrong. But it’s ok it’s easy to make a mistake like saying “real biologist” thinks transcription is “amazingly dumb” when you don’t have a clue what your talking about.

  177. #178 Gold Tagged Antibody Man
    July 3, 2007

    Hey Adele,

    How about those links to the EM photos of HIV with the gold tagged antibody labels?

    Please?

  178. #179 Adele
    July 3, 2007

    How do you get on here if you don’t have access to internet? Just type in immunogold and HIV or SIV or FIV or virus.

    But I can help out too. Since you all are stuck in 1975 itcan be a shock to bring you up to 2007 too fast. So here’s an old review with 85 references and a few images too.

    Nakai M GotoT, J Electron Microsc (Tokyo). 1996 Aug;45(4):247-57 “Ultrastructure and morphogenesis of human immunodeficiency virus.”

    When you’ve read it and the references you’ll know enough about the subject to learn what happened the last ten years espcially with computer aided things. Get back to me then.

    PS two really cool papers from this year not exactly what you’re asking for but related

    Wright E et al “Electron cryotomography of immature HIV-1 virions reveals the structure of the CA and SP1 Gag shells” EMBO J. 2007 Apr 18;26(8):2218-26. Epub 2007 Mar 29

    Arhel N et al “HIV-1 DNA Flap formation promotes uncoating of the pre-integration complex at the nuclear pore” EMBO J. 2007 Jun 20;26(12):3025-37. Epub 2007 Jun 7

  179. #180 Adele
    July 3, 2007

    Maybe after you read the review you can send your friend Etienne a mail and ask him why he doesnt keep up with his old field. Too busy being a quack I guess.

  180. #181 DT
    July 3, 2007

    Since using pubmed or even google seems beyond the denialists grasp, perhaps a direct link to a couple of other papers with HIV ems might help…
    http://jvi.asm.org/cgi/content/full/72/5/4403
    http://jvi.asm.org/cgi/content/full/77/9/5439

    In fact, the journal of virology is packed with similar papers. But I guess some only see what they wish to see.

  181. #182 Patriot Games
    July 3, 2007

    Adele said Maybe after you read the review you can send your friend Etienne a mail and ask him why he doesnt keep up with his old field. Too busy being a quack I guess.

    As you know Peter Duesberg was the original retro-virologist, and there never was even the faintest question about the existence of retro-viruses in any of his publications.

    Etienne’s objections related to purification of materials for a gold standard, and I believe his issues have never been addressed properly. So, if asking a few unanswered questions is your definition of a quackery, then you definitely picked the right century and the right country for it. Welcome to 1984.

  182. #183 Chris Noble
    July 3, 2007

    As you know Peter Duesberg was the original retro-virologist, and there never was even the faintest question about the existence of retro-viruses in any of his publications.

    Have you asked Stefan Lanka? See there is no scientific consensus!
    If you ever manage to convince Stefan Lanka that the retroviruses that Duesberg studied actually exist then I’ll believe you.

    Etienne’s objections related to purification of materials for a gold standard, and I believe his issues have never been addressed properly.

    Duesberg has addressed these issues.

  183. #184 Gold Tagged Antibody Man
    July 3, 2007

    Dear Adele,

    Thanks loads for the links to the gold labeled HIV Electron micrographs. I have been reviewing them as well as others using your helpful suggestions and found them quite interesting.

    The HIV cone shaped cores, lateral bodies and surface knobs are well demonstrated, and I can see the small gold particles as well, indicating the HIV is labeled with the gold antibodies.

    Sorry to bother you with this, but I was wondering if you could direct me to the paragraphs where the host cell death is imaged on the electron micrographs. So far, plenty of the EM studies show HIV in various stages of the life cycle, but none of the EM photograms show any damage to the host cell. Perhaps I am missing this paragraph, and could you please point it out to me? Which article and page specifically?

    While you are at it, would you please point out in this schematic of the retroviral life cycle, at which step the HIV does damage to the host cell? As you can see, this diagram does not specfically mention that the host cell is being damaged by the viral replication, so please indicate at which step this is ocurring.

    Thanks in advance.

  184. #185 Michael
    July 3, 2007

    Gold.

    Of course Adele cannot point out the step wherein HIV does damage to the host. The reason is simple. The step at which HIV does damage to the host is the very moment it is believed in, and beliefs are invisible as they are but the vibrations of energy within the cells when the belief is activated.

    Notice that the life cycle picture you shared is not an actual picture of what goes on in a cell, but is a very clear and accurate picture of what goes on in a human mind. It is actually a diagram showing how the HIV belief enters into the ear of a human, enters the mind and is chewed up, freaked out over, and regurgitated right back out of the mouth with very slight mutations to the belief and directly into the ear of the next believer who then does the same. This HIV stuff is absolutely the most infectious belief that humankind has ever dreamed up. There may be no salvaging the infected. Perhaps it would be better to administrate immediate high dosage AZT and put them all out of their misery (and we can blame the effects on the HIV, haha).

  185. #186 cooler
    July 3, 2007

    Nobody knows how HIV escapes antibody protection, and how it kills cells, when it only infects a very small % of t cells. But scientists have reached a “consensus”, which is what you’d expect if the government supports a particular theory, therefore anyone questioning the “consensus” is a “denier”

  186. #187 Chris Noble
    July 4, 2007

    Nakai M GotoT, J Electron Microsc (Tokyo). 1996 Aug;45(4):247-57 “Ultrastructure and morphogenesis of human immunodeficiency virus.”

    That’s a bit too far past 1970 for people suffering from Denialist Time Warp syndrome.

    How about this one from 1987?

    Fine structure of human immunodeficiency virus (HIV) and immunolocalization of structural proteins.

  187. #188 trrll
    July 4, 2007

    Sorry to bother you with this, but I was wondering if you could direct me to the paragraphs where the host cell death is imaged on the electron micrographs. So far, plenty of the EM studies show HIV in various stages of the life cycle, but none of the EM photograms show any damage to the host cell.

    This doesn’t make sense. EM is well suited for imaging physical structures like virus particles, but is not capable of imaging biochemical phenomena like cell death. Particularly since the process of preparing tissue for EM kills the cells anyway.

    To study biolchemical processes like cellular damage, one primarily uses the methods of biochemistry and cell biology.

  188. #189 Pope
    July 4, 2007

    Well, I’m a biologist masters not PhD, I’m not a kickboxer. So maybe I’m not as qualified as Pope Claus Jensen to talk about transcription regulation of HIV.
    If Claus thinks transcriptional regulation is funny maybe he should talk to his pal Bialy who used to research that stuff in the sixties and seventies. If Claus is right then Bialy’s whole career is a failure not just the past thirty years of it.

    Adele, since you have a Masters in biology, I would have thought you had read and understood that qualifying word I put in the parentheses in front of (AIDS) “gene”. I was obviously not referring to ‘ordinary’ transcriptional regulation or ‘ordinary’ late gene expression.

    But you can stop me laughing by producing that specific AIDS gene for Jensen and Bialy, whoever they are.

  189. #190 Pope
    July 4, 2007

    Thanks loads for the links to the gold labeled HIV Electron micrographs. I have been reviewing them as well as others using your helpful suggestions and found them quite interesting.

    I don’t think anyone doubts there are plenty of pictures of gold tagged things. The question is what they show apart from the gold tags.

    Funny thing Dr. Noble should mention Dr. Lanka. Has Dr. Noble forgotten that Dr. Lanka obtained an admission in his petition to the German Bundestag via Federal Ministry of Health that there exists no EM of HIV from patient plasma or serum?

  190. #191 Gold Tagged Antibody Man
    July 4, 2007

    Gold Tagged said;
    Sorry to bother you with this, but I was wondering if you could direct me to the paragraphs where the host cell death is imaged on the electron micrographs. So far, plenty of the EM studies show HIV in various stages of the life cycle, but none of the EM photograms show any damage to the host cell.

    Trill said;

    This doesn’t make sense. EM is well suited for imaging physical structures like virus particles, but is not capable of imaging biochemical phenomena like cell death. Particularly since the process of preparing tissue for EM kills the cells anyway. To study biolchemical processes like cellular damage, one primarily uses the methods of biochemistry and cell biology.

    Trill comments are very obviously wrong, as anyone with the slightest knowledge of the field knows that electron microscopy shows a number of changes which take place indicative of injury leading to cell death: distention of cisternae of endoplasmic reticulum, detachment of ribosomes from rER with increase in free cytoplasmic ribosomes, swelling of mitochondria, formation of blebs in the plasma membrane, segregation of fibrillar and granular components of the nucleolus.

    Yes, of course, the cell are fixed with glutaraldhyde and imaged in a vaccum which kills the cells. The point is that the changes in the cells in vivo, are FIXED, so even though the cells are dead from fixation, the EM images are what the cells looked like while alive at the time of fixation. (artifacts can occur of course).

  191. #192 DT
    July 4, 2007

    Perhaps Trll is taking you too literally, GTAM.
    You had asked “Sorry to bother you with this, but I was wondering if you could direct me to the paragraphs where the host cell death is imaged on the electron micrographs. So far, plenty of the EM studies show HIV in various stages of the life cycle, but none of the EM photograms show any damage to the host cell. Perhaps I am missing this paragraph, and could you please point it out to me? Which article and page specifically?”

    Well, as you say, EMs can indicate cell damage, and they do in HIV. And contrary to the assertion of dissidents, HIV DOES damage cells.
    Here is a good paper for starters:
    http://www.nature.com/cdd/journal/v12/n1s/full/4401582a.html
    This gives over a hundred references to HIV-induced cell damage, so get reading if you need more details.

    The dissident MO is to throw around broad statements as though they represent solid fact (eg “There are no EMs of HIV”). In response, we then point them towards EMs.

    The dissident MO then takes us down one of 2 paths, either to dispute that the EMs show HIV at all (and drag readers into an abtruse detailed discussion about microvesicle constructs), or to qualify their original statement by saying “Ah, but what I actually meant was there are no EMs of HIV inducing cellular damage“.

    The response again is to point them towards just such papers (and then the whole cycle can begin again).

    Employing these techniques we soon arrive at a point where the dissidents are arguing “Ah, but I still haven’t seen evidence that Nef activates P21-activated kinase (PAK) proteins or Rho GTPase exchange factor Vav in T cells. Usually well before this point the dissident has lost all sense of direction completely and is just arguing for the sake of it, and hoping to hell that random viewers of the bloated thread will be so overwhelmed by detail that they are unable to see how wrong they are. The initial refuted assertion that “There are no EMs of HIV” has been left gathering cobwebs deep in the infancy of the exchange.

    To give them credit, this MO works usually quite well. It does however equally well expose their intellectual bankrupcy.

  192. #193 Gold Tagged Antibody Man
    July 4, 2007

    Well, as you say, EMs can indicate cell damage, and they do in HIV. And contrary to the assertion of dissidents, HIV DOES damage cells.Here is a good paper for starters:

    nature DOT com/cdd/journal/v12/n1s/full/4401582a.html

    This gives over a hundred references to HIV-induced cell damage, so get reading if you need more details.

    My dear drug company representatives and AIDS political activists,

    Thanks for agreeing that EM is capable of showing cell organelle damage and findings leading to cell death as was DENIED by your fellow AIDS apologist.

    Also thanks for pointing us to the 100 refences which you say shows EM images of gold tagged HIV particles producing cell damage and death.

    However, I am still having difficulty locating the exact EM image showing cell organelle damage and cell death. Perhaps you might be of assistance?

    For example, the fifth reference article of the 100 or so is this one. The title sound very promising. This is what we wanted to know, the behavior of HIV in living cells.

    Visualization of the intracellular behavior of HIV in living cells

    by David McDonald1, et al The Journal of Cell Biology, Volume 159, Number 3, 441-452

    The authors correlated EM with LM with a green fluorescent tag on the HIV genome to study the lifecycle and movement of HIV into and out of cells.

    To track the behavior of human immunodeficiency virus (HIV)-1 in the cytoplasm of infected cells, we have tagged virions by incorporation of HIV Vpr fused to the GFP. Observation of the GFP-labeled particles in living cells revealed that they moved in curvilinear paths in the cytoplasm and accumulated in the perinuclear region, often near the microtubule-organizing center. Further studies show that HIV uses cytoplasmic dynein and the microtubule network to migrate toward the nucleus. By combining GFP fused to the NH2 terminus of HIV-1 Vpr tagging with other labeling techniques, it was possible to determine the state of progression of individual particles through the viral life cycle. Correlation of immunofluorescent and electron micrographs allowed high resolution imaging of microtubule-associated structures that are proposed to be reverse transcription complexes. Based on these observations, we propose that HIV uses dynein and the microtubule network to facilitate the delivery of the viral genome to the nucleus of the cell during early postentry steps of the HIV life cycle.
    .
    Our observations of the composition and trafficking of intracellular HIV complexes suggests the following scenario. After entering the cytoplasm, the HIV genome uses some aspect of the actin cytoskeleton to move within the peripheral regions of the cell. This is consistent with evidence that actin can be used to gain access to the microtubule network (Taunton, 2001). It is also supported by previous reports that an intact actin cytoskeleton is necessary for efficient infectivity (Bukrinskaya et al., 1998). The infectious viral particle must next make its way to the microtubule network, where it can initiate reverse transcription even before losing the majority of its capsid protein. At some point after interaction with the microtubule network, the conical capsid dissociates, yet the RTC maintains its interaction with microtubules. This interaction is likely mediated by tethering with a cellular motor complex which has both minus end- and plus end-directed motor activities, as is proposed for Ad-2. Minus end-directed movement of the RTC along the microtubule network ultimately leads to the microtubule organizing center, very near the nuclear membrane, where the mature RTC can then enter through nuclear pore complexes in order to integrate into the host DNA.

    Although this article deals with a very advanced technique with simultaneous Light Microscopy with Green Flourescent tags and Electron Microscopy of the HIV particles in living cells, nowhere in their observations of the composition and trafficking of intracellular HIV complexes did the authors show EM or LM images of damage to cell organelles or death of host cells by the tagged HIV particles they observed.

    If this is incorrect, allow me to apologize in advance, and then point us to the figure number for the EM image, the paragraph and page which shows the HIV particles causing cell damage or cell death.

    Sorry to be a bother about it, but, this is the second or third time I have asked for a link which shows the gold tagged HIV particles damaging the cell organelles.

    Please dont say, just go to pubmed. Thats not very polite, is it? And please don’t list a hundred refences and say, it’s in there somehere. That not very polite either is it?

    So far, your assertion that there are plenty of EM photos showing damage and cell death caused by the gold tagged HIV particles, has not been backed up by producing those images. Why the delay?

    A whole series of EM papers were already listed above. Why not use one of those and merely give us the page and figure number that shows the HIV particles damaging cell organelles ?

    Thanks in advance for your thoughfulness.

  193. #194 Pope
    July 4, 2007

    The dissident MO then takes us down one of 2 paths, either to dispute that the EMs show HIV at all (and drag readers into an abtruse detailed discussion about microvesicle constructs), or to qualify their original statement by saying “Ah, but what I actually meant was there are no EMs of HIV inducing cellular damage”.

    There is as simpler path which you forgot to mention: to qualify by saying “a picture of HIV directly from a patient’s serum or plasma”.

  194. #195 Roy Hinkley
    July 4, 2007

    GTAM and Pope,

    How about this.

    http://www.pnas.org/cgi/reprint/85/10/3570

    Figure 4 the electron micrograph of HIV infected T4 cells releaseing HIV particles, panels “(D and E) Cells actively producing virus. Note degenerative ultrastructure that follows virus release.”

  195. #196 Gold Tagged Antibody Man
    July 4, 2007

    Roy Hinley said

    GTAM and Pope, How about this.
    www DOT pnas.org/cgi/reprint/85/10/3570
    Figure 4 the electron micrograph of HIV infected T4 cells releaseing HIV particles, panels “(D and E) Cells actively producing virus. Note degenerative ultrastructure that follows virus release.”

    Dear Roy, when did they let you out?

    Seriosly, thanks for the link to,

    Cytopathic effect of human immunodeficiency virus in T4 cells is linked to the last stage of virus infection by REGINE LEONARD, DANIEL ZAGURY, ISABELLE DESPORTES, JACKY BERNARD, JEAN-FRANCOIS ZAGURY, AND ROBERT C. GALLO, Proc. Nat. Acad. Sci. Vol. 85, pp. 3570-3574, May 1988

    Yes, I can see that figure 4 demonstrates cells with “degenerative ultrastructurw following virus release”, just as you say. Great. Now we all know that CD4 cell damage (and also cell death) occurs when HIV particles are released from the host cell. HIV kills CD4 cells at particle release when (as in Figure 2 schematic), the host cell wall is ruptured. Therefore, this means that Duesberg is wrong and Gallo is right. But wait a minute. One thought just ocurred to me. And that is this, it’s been 19 years since this publication, so there has been plenty of time for others to replicate and confirm these findings. I don’t remember anybody else mentioning host cell wall rupture upon particle release. Seems to me that if this was true, the whole debate over HIV would have been long finished in 1988. None of the more recent EM papers showed cell wall rupture upon particle release. As a matter of fact, they all showed “budding” of particles from the outer cell membrane which DOES NOT CAUSE CELL RUPTURE. Maybe I just missed it. Have these findings of host cell wall rupture after HIV particle release been repeated and confirmed by others? You know, that’s what science is all about.

    Let’s ask all the other AIDS political activists, and drug company reps, and everybody else, Adele, andy, Raven, franklin, Pope, kevin, Patriot Games, cooler, Tara and Michael on the thread if they agree that Figure 4 and also the schematic Figure 2 have been verified by subsequent research.

  196. #197 DT
    July 4, 2007

    Sometimes these debates can become rather surreal. It seems that dissidents who either deny the existence of HIV or deny its primary role in causing immunodeficiency quite like to indulge in their pastime of intellectual masturbation.

    I can imagine the equivalent arguments with someone who vehemently denies that planes can fly. Their strategy is to as quickly as possible sidetrack the main argument into a discussion about the minutiae of drag coefficients with rounded versus straight winglet tips, and claim that unless evidence is forthcoming that the former is superior to the latter, that this will undermine the entire concept of aerodynamics and send the paradigm of heavier-than-air flight tumbling from the skies.

    Why on earth are the dissidents seeking such specific information about EM demonstrable ultrastructural damage to organelles in the cell from HIV? So far, whenever evidence for anything has been demanded, it has been provided. But what is the dissidents’ purpose? Provision of the information will not shake their denial – they have stated before that this is too deeply entrenched to change. And if the few posters here who represent the orthodox scientific viewpoint fail to provide a particular reference, what difference would this make? Could one of the dissidents tell us what their conclusion would be if say GFP-Vpr-labeled HIV was not shown to move along a particular microtubule when another researcher had previously said it was?

  197. #198 Gold Tagged Antibody Man
    July 4, 2007

    Does that mean you agree or disagree with Figure 2 and Figure 4 of the PNAS paper cited by Roy Hinckley? A simple yes or no would be sufficient, with your reasons for the answer.

  198. #199 DT
    July 4, 2007

    “Let’s ask all the other AIDS political activists, and drug company reps, and everybody else, Adele, andy, Raven, franklin, Pope, kevin, Patriot Games, cooler, Tara and Michael on the thread if they agree that Figure 4 and also the schematic Figure 2 have been verified by subsequent research.”

    Aww! I’m feeling left out now!

    Firstly, direct CPE/lysis is only one of several ways in which HIV can impair T cell function/deplete their numbers.

    Secondly, the Gallo paper is further work building on earlier work from their group – so the work has been replicated/confirmed.

    Thirdly, there are other papers referring to HIV CPEs – 20 seconds on Pubmed threw up this:
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1527842
    No doubt there are others. So there is verification of this point. But you are wrong to think that because this is so the whole debate about HIV should be over. Firstly there will always be a scientific debate- science doesn’t stand still and there is still a lot to learn about this virus and how it does what it does, and secondly there will always be plonkers like yourself indulging in a pseudo-debate, imagining that it is somehow important and people of importance are taking any notice of what you say.

  199. #200 Chris Noble
    July 4, 2007

    Let’s ask all the other AIDS political activists, and drug company reps, and everybody else, Adele, andy, Raven, franklin, Pope, kevin, Patriot Games, cooler, Tara and Michael on the thread if they agree that Figure 4 and also the schematic Figure 2 have been verified by subsequent research.

    There is a thing called Science Citation Index. Use it.

    Several people have shown good will by giving you references to support their arguments.

    What have you provided other than multiple aliases, accusations of being pharmashills and hot air?

    Funny thing Dr. Noble should mention Dr. Lanka. Has Dr. Noble forgotten that Dr. Lanka obtained an admission in his petition to the German Bundestag via Federal Ministry of Health that there exists no EM of HIV from patient plasma or serum?

    That is dishonest on two counts. It was not an admission. There are thousands of electronmicrographs of HIV from plasma and serum. The viral titer is relatively low in the peripheral blood except during acute infection and hence viral culture is used. Contrary to “dissident” claims controls are used and HIV does not magically appear in non-infected cultures.

    If you really have a hang-up about culture (which you shouldn’t) there are electronmicrographs of HIV in lymphoid tissue without culture.

    HIV infection is active and progressive in lymphoid tissue during the clinically latent stage of disease

  200. #201 Pope
    July 4, 2007

    Dear Robodoc. Noble,

    Are you programmed to write ‘dishonest’ at regular intervals or what’s wrong with you? Are you paid extra for using certain words?

    If you don’t like ‘admission’, then use ‘confirmation’ or whatever you’re comfortable with for heaven’s sake. you’ll have to forgive me for smiling, but I don’t think this qualifies as an honesty issue.

    I say “no EMs directly from serum or plasma”. You say “dishonest! there are thousands of EMs from culture. My dear, dignified friend, how is it dishonest to be precise?

    The German Federal Ministry for Health say that the ‘viral concentration’ would only be high enough for EM directly from serum or plasma during initial ‘burst stage’ infection or ‘advanced AIDS stage’- which begs some familiar questions about pathogenesis. However, they admi… I mean confirm that these pictures had by 2001 never been taken.

  201. #202 Chris Noble
    July 4, 2007

    I say “no EMs directly from serum or plasma”. You say “dishonest! there are thousands of EMs from culture. My dear, dignified friend, how is it dishonest to be precise?

    The post I was replying to did not have that caveat.

    The German Federal Ministry for Health say that the ‘viral concentration’ would only be high enough for EM directly from serum or plasma during initial ‘burst stage’ infection or ‘advanced AIDS stage’- which begs some familiar questions about pathogenesis.

    If you has read the article that I linked you would have realised that it has been known for quite some time that the major reservoirs of HIV are in lymphoid tissue where the vast majority of the CD4 cells are. This is where the pathogenesis of HIV disease occurs. Only a small percentage of CD4 cells are in peripheral blood.

    Duesberg is like a second rate magician tring to distract his audience with his right hand while he bends a spoon with his left hand and the chair leg.

    However, they admi… I mean confirm that these pictures had by 2001 never been taken.

    I have just given you a link to a paper from 1993 that shows HIV in uncultured lymphoid tissue. What is your ad hoc pretense for ignoring this evidence?

  202. #203 Pope
    July 4, 2007

    I say “no EMs directly from serum or plasma”. You say “dishonest! there are thousands of EMs from culture. My dear, dignified friend, how is it dishonest to be precise?

    The post I was replying to did not have that caveat.

    Dr. Noble, you absolutely rock!

    And you are quite right, I didn’t use the word ‘directly’ in my first formulation. I didn’t use the word ‘culture’ either. Since I’m not a virologist, I wasn’t aware that if I don’t specifically point out that the serum or plasma hasn’t been tinkered with in all sorts of ways I am misleading people.

    I have just given you a link to a paper from 1993 that shows HIV in uncultured lymphoid tissue. What is your ad hoc pretense for ignoring this evidence?

    Dr. Noble, I have 2 equally poor excuses.

    1. We were talking about HIV in plasma and serum.

    2. When I followed your link I didn’t immediately end up on a picture of anything. In view of ’1′, I admit I was too lazy to do more about it.

    Contrary to “dissident” claims controls are used and HIV does not magically appear in non-infected cultures.

    I do confess I have a hard time believing that controls always are being carried out (when they are being carried out) in a fraudulent manner. Perhaps I’m a little less hard nosed than Dr. Lanka after all?

    However, I followed Dr. PS Duke’s (aka Harvey Bialy I suspect) exciting link and came upon this good old denialist classic, courtesy of our friend Dr. Maniotis:

    The 1997 DIADS Official “HIV” Culturing Manual also exhibits evidence of AIDS denialism. Under quality control,” Section VI, page 45, the DAIDS manual
    warned “HIV” cell culturists: “Do not use PHA stimulated PBMC older than 3 days post stimulation” when
    testing them for the absence of “HIV” from your healthy donor source In non-technical language, DAIDS claimed that the way to make sure control cultures (healthy donor source) were indeed not infected with “HIV,” was to quit
    watching the control cultures after 3 days. Perhaps DAIDS simply followed Montagnier’s and Gallo’s AIDS denialism, and accepted that it was PHA, and not “HIV” that could, after 3 days, induce the same effect on T-cells not incubated with “HIV” (A), as it did with infected cultures (2-9)? Nevertheless it is denialism, because they warn culturists to terminate control cultures after 3 days, and thus control cultures are NOT terminated at the same times as the “HIV” infected cultures.

  203. #204 Pope
    July 4, 2007

    Ok, that quotation got a little bit muddled. Since I don’t want to be the cause of further allegations against Dr. Maniotis for manipulating his quotes let me make clear this is the main quotation from DIADS:

    “Do not use PHA stimulated PBMC older than 3 days post stimulation” when testing them for the absence of “HIV” from your healthy donor source”

    Following that is Dr. Maniotis’ commentary

  204. #205 Pope
    July 4, 2007

    This part is possibly not a verbatim quote:

    “when testing them for the absence of “HIV” from your healthy donor source”

  205. #206 Dale
    July 4, 2007

    Oh Pope! What do you suppose happens if you use PHA stimulated PBMCs that are more than 3 days old? It’s not what Andy is trying to imply. It won’t reduce the specificity of the assay but the sensitivity.

  206. #207 Rock of Gibraltar
    July 4, 2007

    Since some of my comments have sparked a new blog, I felt obliged to comment. There are many theories about health such as the Botanic Theory, which believed that health is a perfectly sound mind in a perfectly sound body; different organs performing in an easy and regular manner.

    The Botanic Theory of Health was founded around 1813 by Dr. Samuel Thomson who developed the principle of life from nature and the field of nature for its cures. Dr. Thomson stated that our bodies were composed of four elements – earth, air, fire and water. He believed that a healthy state consisted in the proper balance of these elements and disease occured in their disarrangement. He believed that whatever supported the internal heat and directed the determining powers to the surface, would expel the disease and save the patient.

    He used plants to restore and repair the waste and decay within the body; by removing obstruction, promoting perspiration and restoring the digestive organs by exciting and maintaining a degree of heat and action in the system; he found this to be suited to treat every form of disease.

    Therefore, he believed that the first conditon in health was to have suitable food, being necessary to generate heat and form new cells for growth and to repair worn out tissue.

  207. #208 Rock of Gibraltar
    July 4, 2007

    Posted under wrong category, should be under what is health.

  208. #209 Patriot Games
    July 4, 2007

    Adele gave us some links to EM photos of HIV particles with gold tagged antibody labels, and about 24 hour ago, it was mentioned that none of the images showed injury or damage to the host cella. A request was made for these images.

    The initial reply to this was incorrect, that EM is not capable of showing cell damage, which it is.

    The next reply was a link to an old paper co-authored by Gallo in PNAS from 1988 which says that cell damage from the final step of hiv partical release is shown in Figure 4 page 3574. http://www.pnas.org/cgi/reprint/85/10/3570
    In addition, the page 3472 figure 2 schematic shows cell wall lysis and cell death upon release of the HIV particles.

    The honorable drug company reps and political AIDS Activists were asked if they agreed or not with model proposed by the 1988 PNAS Gallo paper, and the few replies to this question have been, to put is bluntly, stonewalling and evasion.

    So rather than waste time, I will anser this question for noreen, kevin, cooler, adele and raven and others who may be lurking and learning about HIV AIDS for the first time.

    The answer to this question comes from the Robert Koch Institute Dec 1997 entitled, Fine Structure of HIV and SIV by Hans R. Gelderblom Dec 1997,
    Robert Koch-Institut, Nordufer 20, D-13353 Berlin, Germany

    please see figurs 2 thu 6 whch shows HIV particles budding from the outer cell membrane with no damage to the host cell. Nowhere in this review is there any mention of damage to the host cell upon viral particle release or at any other step. In addition to that, the last paragraph says, viral half life for the HIV shed by budding is 30 hours explaining the rapid decay of viral infectivity, and “fine structure data have been collected on EM on viruses grown in culture, the validity of the structural model still has to be proven by EM evaluation of infectious plasma HIV”

    This 1997 review of HIV fine structure contradicts the 1988 PNAS Gallo Figure 2 and Fig 4 proposals. Of course, this is not surprising considering Gallo’s reputation for being wrong on his past proposals, and Gallo’s tainted past history of scientific misconduct.

    For the lurkers here, and other readers learning about HIV AIDS for the first time, I will summarize the conclusions reached so far.

    1) HIV causes AIDS has never been proven in the peer reviewed literature.(unless “go to pubmed” is supposed proof)

    2) The EM and IMF studies show HIV particles, however, these images do not show host cell damage caused by the tagged HIV. EM studies showing fine details of HIV grown in cell culture has never been validated by EM of infectious plasma virus.

    3) There is no gold standard for the HIV antibody test kits.

    4) There have been no placebo controlled testing proving efficacy of highly toxic HIV drugs. (unless you consider two toxic drugs to be a placebo , and three toxic drugs to be a drug). The first AZT phase II trial was fraudulent, and later trials could not be truly placebo controlled because of the accpetance of the fraudulent first AZT trial.

    5) The rationale for using cytotoxic drugs is flawed, since HIV is a genetic sequence in the cellular genome, and this can never be eradicated by toxic drugs.

    6) The proposal that everyone testing positive for HIV will die without HIV drugs is obviously incorrect, as many long term non-progressors are alive and well without ever using toxic HIv drugs for 10 to 15 years.

    for more information see; reviewing aids DOT com

  209. #210 Roy Hinkley
    July 5, 2007

    To the University of Illinois at Chicago, I’ll be forwarding you my CV for consideration for an open faculty position. At least I can read with comprehension.

    Pope, Maniotis has totally misread that section of the document. He has in fact quote-mined a sentence and is telling the unwitting that it says what his delusions would like for it to say rather than what the authors actually said.

    The manual advises against using 3 day post stimulation PBMCs for either a control or as cells to culture HIV on.

    Read section one:

    “I. PRINCIPLE
    Peripheral blood mononuclear cells (PBMC) are isolated from healthy, uninfected donor blood for
    use in various assays and to culture HIV. The PBMC are stimulated with the mitogen
    phytohemagglutinin-P (PHA-P), in the presence of human interleukin 2 (IL-2) for 24-72 hours
    before use to promote blast formation and replication of T-cells.”

    That’s the 3 days the sentence:
    Do not use PHA-stimulated donor PBMC older than 3 days post stimulation.”

    refers to. It’s saying once cells have been stimulated with PHA they must be used within 3 days whether you intend to use them as a negative control, or to be innoculated with the virus.

    It’s a quality control step, in less technical terms it says: “Use cells while they’re still fresh.”

  210. #211 Chris Noble
    July 5, 2007

    “Do not use PHA stimulated PBMC older than 3 days post stimulation” when testing them for the absence of “HIV” from your healthy donor source”

    You’re right it is not a verbatim quote. It’s another Maniotism.

    You could have performed an f..ing google search and discovered this for yourself.

    Virology Manual for HIV Laboratories

    Maniotis is either illiterate, deluded or lying. I’ll leave it for you to choose an option.

    The quote comes form a section that describes the method for preparing PHA-Stimulated uninfected domor PBMCs. These are commonly used for culturing HIV. The protocol warns that you shouldn’t use these more than 3 days after preparing them. Maniotis’s misinterpretation is frankly weird.

    The protocol also says that the PHA-Stimulated uninfected PBMCs should be checked to make sure they really are uninfected. The assay for this is exactly the same one that is used to coculture HIV from the PBMCs of people possibly infected with HIV. The control goes through exactly the same assay.

    If I were Maniotis I would not be sending this ABC of stupidity around the web with his university affiliation on it. He appears to crucify himself.

  211. #212 Pope
    July 5, 2007

    Dear Dr. Noble, Roy Hinkley,

    Heheh… I actually did perform a f..ing google and concluded Maniotis was being a little bit tongue in cheek, but that the quote + paraphrase was basically correct. But then I obviously got nervous and tried to make everything perfect re. the quotes – clumsily and unsuccessfully. I’ll try again.

    Set up a qualitative HIV culture using the newly prepared donor PBMC as “patient cells” to verify that the new donor is HIV culture negative (See – Qualitative PBMC Macrococulture Method.)
    Do not use PHA-stimulated donor PBMC older than 3 days post stimulation.

    So far I think Dr. Maniotis has given us a fair paraphrase.

    He then goes on to interpret the 3 days post stimulation as the recommended max. period in which to watch the negative culture. Assuming that by ” See Qualitative PBMC Macrococulture Method” is meant the following section on
    Qualitative PBMC Macrococulture Assay, there’s these instructions:

    Maintain cultures for 21 days or until culture meets criteria for positivity.

    If this is not the difference Dr. Maniotis meant, and if it is not the correct interpretation of the “Do not use PHA-stimulated donor PBMC older than 3 days post stimulation”, I admit defeat and leave it to Dr. Maniotis to explain himself.

  212. #213 Chris Noble
    July 5, 2007

    So far I think Dr. Maniotis has given us a fair paraphrase.

    Only if fair is a synonym for deceptive.

    He then goes on to interpret the 3 days post stimulation as the recommended max. period in which to watch the negative culture.

    Which is wrong. It means don’t leave the stimulated PBMCs lying around for 3 days before you use them either to culture HIV or as controls. Start with a fresh batch.

    It is very hard not to conclude that Maniotis is deliberately trying to deceive his audience. Close to every single reference he gives is either misquoted (sometimes entirley fabricated) or misrepresented.

    You have demonstrated that you were deceived

    His ABC of AIDS Denial serves one purpose. It is a classic example of pseudoscience and fits the title of the thread rather well.

  213. #214 Patriot Games
    July 5, 2007

    It is typical of AIDS apologists to evade and stonewall, rather than come clean and admit a mistake. That’s because they are paid political activists, drug company reps with NO MORAL or ETHICAL character.

    Since our AIDs Apologists seem to be busy with thir own mental masturbation dealing with technical minutia of PHA and PMBC’s , and are ignoring a recent illustration (above) about their idol Bob Gallo, the inventor of the AIDS Virus, that Bob Gallo was caught in a lie in his 1988 PNAS paper Figure 4 and Fugure 2 in which he deceitfully and falsely told the world that when HIV particles are released from the host cell, there is cell damage and cell wall lysis. This a lie in the peer reviewed medical literature, and this lie is not alone. There are many more similar lies upon which the AIDS dogma is built. This is not science. It is pseudoscience, and those who defend it are the lowest of the low. No wonder people have lost trust in a system that has betrayed them with toxic drugs for a false theory supported with lies like this 1988 PNAS article coauthored by Gallo.

    Adele gave us some links to EM photos of HIV particles with gold tagged antibody labels, and about 24 hour ago, it was mentioned that none of the images showed injury or damage to the host cella. A request was made for these images.

    The initial reply to this was incorrect, that EM is not capable of showing cell damage, which it is.

    The next reply was a link to an old paper co-authored by Gallo in PNAS from 1988 which says that cell damage from the final step of hiv partical release is shown in Figure 4 page 3574. http://www.pnas.org/cgi/reprint/85/10/3570
    In addition, the page 3472 figure 2 schematic shows cell wall lysis and cell death upon release of the HIV particles.

    The honorable drug company reps and political AIDS Activists were asked if they agreed or not with model proposed by the 1988 PNAS Gallo paper, and the few replies to this question have been, to put is bluntly, stonewalling and evasion.

    So rather than waste time, I will answer this question for noreen, kevin, cooler, adele and raven and others who may be lurking and learning about HIV AIDS for the first time.

    The answer to this question comes from the Robert Koch Institute Dec 1997 entitled, Fine Structure of HIV and SIV by Hans R. Gelderblom Dec 1997,
    Robert Koch-Institut, Nordufer 20, D-13353 Berlin, Germany
    http://www.hiv.lanl.gov/content/hiv-db/COMPENDIUM/1997/partIII/Gelderblom.pdf

    please see figures 2 thu 6 whch shows HIV particles budding from the outer cell membrane with no damage to the host cell. Nowhere in this review is there any mention of damage to the host cell upon viral particle release or at any other step. In addition to that, the last paragraph says, viral half life for the HIV shed by budding is 30 hours explaining the rapid decay of viral infectivity, and “fine structure data have been collected on EM on viruses grown in culture, the validity of the structural model still has to be proven by EM evaluation of infectious plasma HIV”

    This 1997 review of HIV fine structure contradicts the 1988 PNAS Gallo Figure 2 and Fig 4 proposals. Of course, this is not surprising considering Gallo’s reputation for being wrong on his past proposals, and Gallo’s tainted past history of scientific misconduct.

    For the lurkers here, and other readers learning about HIV AIDS for the first time, I will summarize the conclusions reached so far.

    1) HIV causes AIDS has never been proven in the peer reviewed literature.(unless “go to pubmed” is supposed proof)

    2) The EM and IMF studies show HIV particles, however, these images do not show host cell damage caused by the tagged HIV. EM studies showing fine details of HIV grown in cell culture has never been validated by EM of infectious plasma virus. Gallo’s 1988 PNAS article lied about this.

    3) There is no gold standard for the HIV antibody test kits.

    4) There have been no placebo controlled testing proving efficacy of highly toxic HIV drugs. (unless you consider two toxic drugs to be a placebo , and three toxic drugs to be a drug). The first AZT phase II trial was fraudulent, and later trials could not be truly placebo controlled because of the acceptance of the fraudulent first AZT trial.

    5) The rationale for using cytotoxic drugs is flawed, since HIV is a genetic sequence in the cellular genome, and this can never be eradicated by toxic drugs.

    6) The proposal that everyone testing positive for HIV will die without HIV drugs is obviously incorrect, as many long term non-progressors are alive and well without ever using toxic HIv drugs for 10 to 15 years or longer.

    for more information see; reviewing aids DOT com

  214. #215 Gold Tagged Antibody Man
    July 5, 2007

    Adele said

    The questions about damage were answered by other people. Our “patriot” can pretend they weren’t or not look at the papers they gave. I guess the goal is, get the “drug company reps” to say slightly different things you can twist and then say falsely we’re all lying to you.

    Dear Adele,

    After reviewing your cited EM studies of images of host cells with labeled HIV particles, th question came up, where is the cell damage from the HIV? None of the images showed any cell damage. Your response is, OH the question has already been answered by somebody else. Well guess what Adele, you are wrong, the question has NOT been answered, and bluntly you appear to be stonewalling and evasive as your AIDS Activists have done.

    This was the reply you are referring to by your AIDS Activist associate

    Well, as you say, EMs can indicate cell damage, and they do in HIV. And contrary to the assertion of dissidents, HIV DOES damage cells.
    Here is a good paper for starters:
    http://www.nature.com/cdd/journal/v12/n1s/full/4401582a.html
    This gives over a hundred references to HIV-induced cell damage, so get reading if you need more details.

    Well, I spent a lot of time looking at the 100 references of this article which SUPPOSEDLY show EM electron micrographs of HIV induced host cell damage, and I can report to you that THIS IS A LIE. None of them show it. If they do, post the page and figure number. Nobody did.

    At this point, only one paper was presented by the Drug Rep alias Roy Hinkley.

    This showed host cell damage, the PNAS 1988 paper coauthored by Gallo,
    http://www.pnas.org/cgi/reprint/85/10/3570

    and this was found to be contradicted by a 1997 review from the Koch Institute.

    http://www.hiv.lanl.gov/content/hiv-db/COMPENDIUM/1997/partIII/Gelderblom.pdf

    The figure 2 and figure 4 in the 1988 PNAS article co-authored by Gallo is a LIE in the peer reviewed literature which was contradicted by the Gelderblom 1997 review.

    Since it was so difficult or impossible for you AIDS activists to come up with a credible paper which shows HIV host cell damage, they then came up with this one:
    Nature 362, 355 – 358 (25 March 1993); doi:10.1038/362355a0 HIV infection is active and progressive in lymphoid tissue during the clinically latent stage of disease Giuseppe Pantaleo*, Cecilia Graziosi*, James F. Demarest*, Luca Butini†, Maria Montroni†, Cecil H. Fox‡, Jan M. Orenstein§, Donald P. Kotler & Anthony S. Fauci*

    However, this discusses HIV in Lymph nodes of the GI tract, and there are no Electron Micrograph images showing HIV induced host cell damage in this letter either. Why do you lie to us and say that this has been answered when it has not? Have you betrayed our trust, Adele?

  215. #216 Adele
    July 6, 2007

    cell damage and cell wall lysis

    So Bob Gallo said HIV kills plant cells?!! Amazing. GTAM, you are a credit to denialists everywhere. Never have so few brain cells lied about so much in so many ways. Probably without even realizing it.

    You don’t understand how puzzling your demands are, patriot plow and now I see I’ll never be able to teach you. Like I told you the only thing you’ll be satisfied with is when we can shrink a electron microscope from truck sized to microscopic and put it in the bloodstream and take pictures of dying cells. Check back in forty or fifty years.

  216. #217 Pope
    July 6, 2007

    In other words, Adele, you cannot produce any relevant EMs. Why didn’t you just say so at first?

  217. #218 Adele
    July 6, 2007

    The original question was for EMs of virions.

    You got EMs of virions.

    Then the question was how do you know they’re not microvesicles.

    I sent the review including image and links to other immunogolds.

    Then you want virions in the act of killing cells.

    Claus Jensen, do you understand what EMs are for? Do you understand why you sometimes use a light microscope and why you use EM?

    I hope your a better kickboxer than logician. Otherwise why would you live in Thailand don’t they have enough kickboxers there already?

  218. #219 Pope
    July 6, 2007

    In other words you don’t have the relevant EMs, which is fair enough. Antibody Man’s request was too tall an order. Is it so illogical to ask why you didn’t just say so at first, without your weird comments about Thai kickboxers? Are you sure you are well?

  219. #220 Adele
    July 6, 2007

    Just saying Claus Jensen from Barnesworld is a kickboxing instructor in Thailand not a scientist or EM technician. Richard Jefferys did identify you as Claus Jensen if you remember. I think you also sometimes go by McDonald don’t you.

  220. #221 Pope
    July 6, 2007

    hahaha… You may be stupid enough to believe Jefferys when he comes out with something like that, but are you now telling me you believe those lying homophobics on Barnesworld?

    Is that how you do science Adele?

    At least there’s a picture of an almost purified supposed me in vivo. http://barnesworld.blogs.com/barnes_world/2007/05/views_from_the_.html

    That’s more than you can say for your pet supposed virus.

  221. #222 Adele
    July 6, 2007

    Yeah, but do you have a photo of yourself taken from the Hubble Space Telescope? Or an EM of you at your computer?

    Didn’t think so.

  222. #223 Pope
    July 6, 2007

    What do I know? Big Brother and Jefferys are obviously watching me from somewhere.

  223. #224 Nick Naylor
    July 6, 2007

    Thanks to Chris Noble for linking to the DAIDS Manual, an expose of “trade secrets” that reveals a few of the “inbred” notions of “isolation” from dedicated HIV researchers. And of course we now see him giving his “expert opinion” on cell-culture quality control to an experienced researcher, which no doubt would qualify him in Judge Sulan’s court, but hardly anywhere else. What we need is an opinion formed in light of the relevant sections of the DAIDS manual.

    Chris said: “It means don’t leave the stimulated PBMCs lying around for 3 days before you use them either to culture HIV or as controls. Start with a fresh batch.”

    No, it doesn’t mean that.

    Chris, it’s called refrigeration … do they really need a special standard explicitly stating that cell-cultures shouldn’t be left “lying around?

    Alas, as usual by now, it is the zealotry of the rush to attack that takes over when Chris evaluates a legitimate point. The general point is the likelihood of artifacts when “co-culturing” and assaying so-called HIV-1 antigen as confirmation of “HIV infection” in a “seropositive” patient, on which Dr Maniotis has provided more than enough evidence.

    BTW, his expertise includes cell-culturing which certainly qualifies him in pointing out the obvious flaw in pages 41-50 of the DAIDS Manual. We really have a literacy test at this point. The distinction between “patient” and “donor” cells is critical in order to grasp what’s going on. Why? Because the 3 day “limit” on pg 45 clearly refers to the next section (45-50) where the “new donor” cells become the equivalent of “patient” cells which in turn require another donor’s cells for determination of a negative co-culture. Presumably, “donor” cells are from seronegative persons so an assumption may be that for negative results in accordance with 45-50, there’s no problem. But the culturing is supposed to be an independent verification, which means that possible positive results from a “donor” monoculture needs to be assayed in accordance with the procedures of 45-50, excluding the co-culturing step. This requires “use” or assay for p24 past the 3 day time limit, i.e. “maintain cultures for 21 days or until culture meets criteria for positivity”. Unfortunately, this simple control has been effectively deleted by the “quality control” statement.

    So Dr Maniotis’ point stands.

  224. #225 Adele
    July 6, 2007

    No, it doesn’t stand. Except as a textbook example of a lie.

    And what the hell do you mean by “refrigeration”? Do you think you can just throw cells in the refrigerator and keep it there forever?

    What kind of a chemical engineer are you, Eugene Semon? Go back to watching Fox and Bill O’Reilly. You don’t have anything to contribute here.

  225. #226 Roy Hinkley
    July 6, 2007

    GTAM, 40, Pope, birds of a feather, et al. ad nauseum,

    I was waiting for you and your drawer full of sockpuppets to indicate that you had actually read the Gallo paper. Since you haven’t, and you seem hell-bent on putting your ignorance on display I’ll help you out a little. Mind you, I won’t be able to answer a lot of follow-up questions, you know the ones where you keep changing the issue at hand to try to evade the fact that you’ve been proven wrong yet again…, because I don’t really like to ride the HIV/AIDS denialist merry-go-round. Whenever I do take a ride it’s always the same: A never-ending cycle of illogic and nonsense spinning round and round in a downward spiral towards insanity….

    And then I throw up.

    In other words, you sicken me.

    First, as others have pointed out, nobody would expect to determine the mechanism for cell killing by using electron microscopy. To deamnd such “proof” that HIV kills cells is as idiotic as a tobacco company executive who demands an electron micrograph of cigarette smoke caught in the act of causing widely metastatic lung cancer.

    Second, if you read the Gallo paper you will see that introducing HIV to cultures of growing CD4+ cells causes 10-30% of activated T cells to die. That’s your cell death right there. It happens when HIV is introduced and it does not happen in cell cultures where no HIV is introduced. You do not need an electron micrograph to see devastation on this scale.

    Third, as I’m sure you’ve ignored hundreds of times, HIV kills CD4 cells through several different pathways some are direct, as shown in the Gallo EM I provided, others are indirect. Direct cell killing is not the only mechanism HIV uses to kill CD4 cells, it’s not even the main mechanism. It is the mechanism you asked for, and received, an electron micrograph of though.

    Fourth, you claim that figures 2 through 6 here: http://www.hiv.lanl.gov/content/hiv-db/COMPENDIUM/1997/partIII/Gelderblom.pdf
    Disprove direct cell killing by HIV. I don’t expect you to follow this but just in case someone else is reading this too:

    look at figure 6. See the reference for the figure: “(from Gelderblom et al. 1987b26).“? It refers to reference 26 in the “References”:

    26. Gelderblom, H.R., H. Reupke, T. Winkel, R. Kunze and G. Pauli. 1987b. MHC-Antigens: Constituents of the envelopes of human and simian immunodeficiency viruses. Z. Naturforsch. 42c: 1328-1334

    (You may note that Gelderblom is the same Gelderblom who wrote the original document you cited.)

    Do you see the title? ” MHC-Antigens: Constituents of the envelopes of human and simian immunodeficiency viruses.” This would seem to indicate that Dr. Gelderblom is studying viruses in this work right? He didn’t write a paper called, for instance, “Mechanisms of HIV induced cell death as determined by Electron Microscopy” or something. Rather, he is studying viruses, in particular he is studying the MHC-Antigens which are constituents of the envelope of the virus. To do that it seems reasonable that he will need a source of virus to study, no? Where would be the best place to get those viruses from?

    Dead cells from a line of cells that experience cell death in the presence of the virus?

    Or, living cells from a line of cells that are resistant to the cytopathic effects of the virus and are able to go on producing virus indefinitely?

    My personal preference would be living cells from a resistant line of cells. But your preference may differ from mine, and that’s fine. Why don’t we see which one Dr. Gelderblom preferred for this work?

    You may find the abstract for reference 26 here:
    http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=2452527&dopt=Citation
    in it you will see that Gelderblom used two different CD4+ cell lines: H9 and Molt-3. Guess what? Both are resistant to HIV’s cell killing effects! Look it up if you don’t believe me. Here’s a little something to get you started.
    http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=6200935&ordinalpos=26&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    This is why so much of what you read about HIV science seems mysterious, wrong, and sometimes diabolical to you. It’s because you don’t understand what you’re reading. It’s because, with all due respect, you don’t know your ass from a hole in the ground in regards to biology.

    Now, settle down. Settle down. I know what you’re saying. (It’s time to spin the merry-go-round right?) “Of course they’re resistant to HIV because HIV doesn’t kill cells!”

    To which I’ll refer you to the 10-30% cell-killing when HIV is added to activated CD4+ T cells in the first Gallo EM paper I cited. You can work backwards or forwards through the mountains of evidence that HIV kills CD4+ cells from there if you like.

    Oh! I almost forgot.

    That.

    That one, right there.

    No! Not that one. The other one.

    Yeah that one! That’s it!

    The other one’s just a hole in the ground.

  226. #227 pope-on-a-rope
    July 6, 2007

    The debate tactics here remind me of the great boxer Mohammed Ali and his “rope-a-dope” thing… Lean back and relax, let the other guy get worn out.

    Anyway, for most assays, the protocol would specify to start with fresh reagents, cells or whatever. And it is important for people who are interested in this to know for example, what percentage of cell cultures plus virus will show positive results in 2-to-5 days vs 18-to-21 days. When the protocol says “incubate for 21 days or until positive” it could be interpreted here as meaning either that 21 days is the minimum time or the maximum time.

    In fact, from what I have seen of assays done on an aliquot of each culture ever day over a 3 week time period, is that the level of virus proteins produced is not constant. It ramps up over the first few days, then goes down as the virus kills off the cells. It only goes back up again if the culture is refreshed with new uninfected cells. There are dozens of papers showing this, with many different virus isolates and clones, and with many different cell types.

    Lu W, Andrieu JM.
    Similar replication capacities of primary human immunodeficiency virus type 1 isolates derived from a wide range of clinical sources.
    J Virol. 1992 Jan;66(1):334-40.
    PMID: 1727492

    Dittmar MT, Simmons G, Donaldson Y, Simmonds P, Clapham PR, Schulz TF, Weiss RA.
    Biological characterization of human immunodeficiency virus type 1 clones derived from different organs of an AIDS patient by long-range PCR.
    J Virol. 1997 Jul;71(7):5140-7.
    PMID: 9188581

    Clark SJ, Saag MS, Decker WD, Campbell-Hill S, Roberson JL, Veldkamp PJ, Kappes JC, Hahn BH, Shaw GM.
    High titers of cytopathic virus in plasma of patients with symptomatic primary HIV-1 infection.
    N Engl J Med. 1991 Apr 4;324(14):954-60.
    PMID: 1900576

    Chiodi F, Valentin A, Keys B, Schwartz S, Asjo B, Gartner S, Popovic M, Albert J, Sundqvist VA, Fenyo EM.
    Biological characterization of paired human immunodeficiency virus type 1 isolates from blood and cerebrospinal fluid.
    Virology. 1989 Nov;173(1):178-87.
    PMID: 2683359

    etc…

  227. #228 Frederick Gillet
    July 6, 2007

    For those who might think Adele has the slightest leg to stand on, here are a few links to EM studies of viral induced cell death, illustrating that electron microscopy is a routine tool for examining viral cell damage. This is not an impossible dream as Adele claims, it is a commonplace tool used every day to examine the effect of a virus on host cell structure. Where are the Electron Microscopy studies of HIV induced cell damage? There aren’t any because HIV is a benign passenger virus as Duesberg correctly stated in his landmark 1987 PNAS paper, and in his 1996 book, “Inventing the Aids Virus”.

    http://jvi.asm.org/cgi/content/full/78/9/4884

    Journal of Virology, May 2004, p. 4884-4891, Vol. 78, No. 9

    JC Virus Induces Nonapoptotic Cell Death of Human Central Nervous System Progenitor Cell-Derived Astrocytes Pankaj Seth,1 Frank Diaz,1 Jung-Hwa Tao-Cheng,2 and Eugene O. Major1*

    JC virus (JCV), a human neurotropic polyomavirus, demonstrates a selective glial cell tropism that causes cell death through lytic infection. Whether these cells die via apoptosis or necrosis following infection with JCV remains unclear. To investigate the mechanism of virus-induced cell death, we used a human central nervous system progenitor-derived astrocyte cell culture model developed in our laboratory. Using in situ DNA hybridization, immunocytochemistry, electron microscopy, and an RNase protection assay, we observed that astrocytes support a progressive JCV infection, which eventually leads to nonapoptotic cell death. Infected astrocyte cell cultures showed no difference from noninfected cells in mRNA expression of the caspase family genes or in any ultrastructural features associated with apoptosis. Infected cells demonstrated striking necrotic features such as cytoplasmic vacuolization, watery cytoplasm, and dissolution of organelles. Furthermore, staining for caspase-3 and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling were not detected in infected astrocyte cultures. Our findings suggest that JCV-induced cell death of these progenitor cell-derived astrocytes does not utilize an apoptosis pathway but exhibits a pattern of cell destruction consistent with necrotic cell death.

    http://www.virologyj.com/content/2/1/26

    Ultrastructural studies on dengue virus type 2 infection of cultured human monocytesJesus A Mosquera , Juan Pablo Hernandez ,Virology Journal 2005, 2:26

    http://vir.sgmjournals.org/cgi/content/full/84/12/3305

    The mechanism of cell death during West Nile virus infection is dependent on initial infectious dose J. J. H. Chu and M. L. Ng, J Gen Virol 84 (2003), 3305-3314

  228. #229 Frederick Gillet
    July 6, 2007

    For those who might think Adele has the slightest leg to stand on, here are a few links to EM studies of viral induced cell death, illustrating that electron microscopy is a routine tool for examining viral cell damage. This is not an impossible dream as Adele claims, it is a commonplace tool used every day to examine the effect of a virus on host cell structure. Where are the Electron Microscopy studies of HIV induced cell damage? There aren’t any because HIV is a benign passenger virus as Duesberg correctly stated in his landmark 1987 PNAS paper, and in his 1996 book, “Inventing the Aids Virus”.

    http://jvi.asm.org/cgi/content/full/78/9/4884

    Journal of Virology, May 2004, p. 4884-4891, Vol. 78, No. 9

    JC Virus Induces Nonapoptotic Cell Death of Human Central Nervous System Progenitor Cell-Derived Astrocytes Pankaj Seth,1 Frank Diaz,1 Jung-Hwa Tao-Cheng,2 and Eugene O. Major1*

    JC virus (JCV), a human neurotropic polyomavirus, demonstrates a selective glial cell tropism that causes cell death through lytic infection. Whether these cells die via apoptosis or necrosis following infection with JCV remains unclear. To investigate the mechanism of virus-induced cell death, we used a human central nervous system progenitor-derived astrocyte cell culture model developed in our laboratory. Using in situ DNA hybridization, immunocytochemistry, electron microscopy, and an RNase protection assay, we observed that astrocytes support a progressive JCV infection, which eventually leads to nonapoptotic cell death. Infected astrocyte cell cultures showed no difference from noninfected cells in mRNA expression of the caspase family genes or in any ultrastructural features associated with apoptosis. Infected cells demonstrated striking necrotic features such as cytoplasmic vacuolization, watery cytoplasm, and dissolution of organelles. Furthermore, staining for caspase-3 and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling were not detected in infected astrocyte cultures. Our findings suggest that JCV-induced cell death of these progenitor cell-derived astrocytes does not utilize an apoptosis pathway but exhibits a pattern of cell destruction consistent with necrotic cell death.

    http://www.virologyj.com/content/2/1/26

    Ultrastructural studies on dengue virus type 2 infection of cultured human monocytesJesus A Mosquera , Juan Pablo Hernandez ,Virology Journal 2005, 2:26

  229. #230 Bill O'Reilly
    July 7, 2007

    Adele, I strongly object to your implication that this Eugene is a fan of mine when everyone knows he’s in favor of surrender in Iraq.

    And if you don’t know what refrigeration means … well … I have enough idiots for fans and certainly don’t welcome you or your ilk as new viewers.

  230. #231 trrll
    July 7, 2007

    Trill comments are very obviously wrong, as anyone with the slightest knowledge of the field knows that electron microscopy shows a number of changes which take place indicative of injury leading to cell death: distention of cisternae of endoplasmic reticulum, detachment of ribosomes from rER with increase in free cytoplasmic ribosomes, swelling of mitochondria, formation of blebs in the plasma membrane, segregation of fibrillar and granular components of the nucleolus.

    Yes, EM can identify morphological changes in cells, which may be interpreted as reflecting damage. But morphological changes are not cell death, and the demand was for “where the host cell death is imaged on the electron micrographs.” Cell death is a biochemical phenomenon and cannot be imaged with an imaging method that kills all cells. I’d be more convinced of cell dath by something like failure of Trypan blue exclusion by unfixed cells than by any kind of EM.

  231. #232 Pope
    July 7, 2007

    Trrl,

    Let’s have the EMs of morphological damage then, since it’s long been the way the request was formulated.

  232. #233 Pope
    July 7, 2007

    Now, settle down. Settle down. I know what you’re saying. (It’s time to spin the merry-go-round right?) “Of course they’re resistant to HIV because HIV doesn’t kill cells!”
    To which I’ll refer you to the 10-30% cell-killing when HIV is added to activated CD4+ T cells in the first Gallo EM paper I cited
    .

    Dear Roy, I was more thinking along the line of what is the percent of HIV cell-killing in non-activated cells?

  233. #234 Adele
    July 7, 2007

    One sock puppet or another said,
    electron microscopy is a routine tool for examining viral cell damage. This is not an impossible dream as Adele claims, it is a commonplace tool used every day to examine the effect of a virus on host cell structure

    I didn’t say that. You twist my words like you twist what trrll said. How many people have told you, the electron microscope is not the best tool to use for this? We can take EMs of syncytia but why would you take an EM of that? You can see it in light. The paper you gave above with “watery cytoplasm” and “cytoplasmic vacuolization” why do you need EM to do that? If viruses are all accumulating in one organelle and lysing it, maybe an EM would be nice, try to catch it in the act. But that’s not what HIV does as far as I know so why an EM.

    I think it was Hinkley sorry if I’m confusing him who gave the best analogy to what your asking for, “Where’s the EM of cigarette smoke in the act of causing lung cancer?”

    If you can give us that EM and I mean I want to see the actual cigarette smoke and the actual damage its causing and accompanying biochemical evidence the damage is leading to cancer. Then I’ll find every EM you want or take them myself in the lab if I can’t find them. Until then your a poser like Andrew.

  234. #235 Roy Hinkley
    July 7, 2007

    Gee Pope,

    I thought we made this clear. It’s that one. Right there. The other one is just a hole in the ground.

    Since HIV causes T cell activation in vivo, it really wouldn’t be a valid experiment if we didn’t activate the T cells in vitro.

    But, the very first time a meet a person HIV+ or – who doesn’t experience regular T cell activation, I’ll be sure to give that question the serious consideration it deserves.

  235. #236 Adele
    July 7, 2007

    Claus, claus, claus, pope, can’t you do better than this,
    I was more thinking along the line of what is the percent of HIV cell-killing in non-activated cells

    Do you know what an activated cell is?

    Ok, step back.

    Do you know what a cell is?

    OK. How’s this,

    Do you have access to an immunology textbook there in Thailand?

    Take a break from whatever it is you do and read a few chapters. Laugh at yourself like we all laugh at you. And come back and ask some more intelligable questions.

  236. #237 Adele
    July 7, 2007

    Sorry Roy missed your post!

  237. #238 Roy Hinkley
    July 7, 2007

    If you will actually look at the Gallo paper I think you will see it very nicely answers all of your questions so far.

    You want aberrant morphology? How but the multinucleated syncitial cells in panels F, G, and H of figure 4? nuclear membrane dissolved, chromosomes dispersed throughout the cytoplasm? What’s normal about this?

    Additionally this same paper looked at both in vitro grown virus and virus obtained fresh from the blood of AIDS patients.

    To put it bluntly:

    “Look you stupid bastard, you’ve got no arms left.”
    http://en.wikipedia.org/wiki/Black_Knight_(Monty_Python)

  238. #239 trrll
    July 7, 2007

    Let’s have the EMs of morphological damage then, since it’s long been the way the request was formulated.

    I copied and pasted the the request exactly as it was formulated. Do you need to see it again?

    Sorry to bother you with this, but I was wondering if you could direct me to the paragraphs where the host cell death is imaged on the electron micrographs

    Perhaps you are under the mistaken impression that EM is some sort of gold standard for detecting cell damage. This is quite wrong. As I noted before, preparation for EM kills cells, so by the time that you look at them, they are already quite dead. It is true that sometimes one can observe structural abnormalities that give one an indication that a cell is damaged, and some clue as to what has happened to it, but the converse is not true–i.e. failing to observe structural damage in EM does not mean that a cell is healthy. Moreover, there are artifacts in EM that can sometimes be mistaken for cell damage. To ask whether a cell is healthy or not, the best approach is to use a method that measures its metabolic activity or the integrity of its cell membrane. There are also some histological stains that can detect if a cell has been triggered to die via the apoptotic pathway, in which the cell digests its own DNA. These are in general more reliable than EM for assessing cell health.

  239. #240 Chris Noble
    July 7, 2007

    I can only imagine that after the next moved goalpost the sockpuppet choir will insist that somebody produce an electron micrograph of HIV during sexual transmission.

  240. #241 Pope
    July 7, 2007

    Adele ‘intelligable’ is spelled with 3 ‘i’s, and yet I understood what you meant. You, however, persist in pretending Patriot Games asked for a picture imaging cell death in Trrll’s sense.

    You and Trrll were wrong, you don’t need the Hubble telescope to show a virus doing cell damage. There’s nothing more to it. No big deal, doesn’t mean HIV doesn’t cause AIDS. But you were wrong.

    You (Roy) showed one picture of cell lysis, Patriot accepted that if that was genuine and could be backed up it was what he was looking for. Well can it? You can say ‘no’, ‘yes’ or ‘go screw yourself’. But returning to nitpicking how the request was originally worded/interpreted is just childish. Trrll has now returned 3 times to give us the basic lecture about imaging cell death. Has he anything else to contribute, like a photo?

    I agree with you guys, there’s plenty of pictures of syncytia. Maybe Patriot Games will have to swallow that one. Maybe not. The cell lines used are leukemic no? – that is if one is allowed to ask a simple good faith question without being booed out of the theatre. nobody made fun of the Hubble telescope.

    The same goes for Roy and Adele on the point of activation. Are you saying that the in vitro mitogenic, PHA, IL-2 or what have you activation/stimulation and the absence of antibodies accurately mimics the in vivo conditions? Is that what you’re saying Roy, cuz it sure sounds like it? If you’re gonna pretend you don’t know what I’m talking about here, I’m just gonna have to say you guys are ‘unintelligable’and should go back and do some more reading, or go for a holiday in Thailand, you know take a break from the kids and the other parent.

    In the meantime direct your scorn towards Zagury, Gallo and the Perth Group, who obviously all think different results obtain when you change culture conditions:

    Early in 1986, Zagury, Gallo and their colleagues reported that: “T4 lymphocytes from normal donors infected by HTLV-III in vitro, as well as HTLV-III-infected primary T4 cells from AIDS patients, have been difficult to maintain in culture for longer than 2 weeks, and it has often been assumed that the virus has a direct cytolytic effect on these cells”. However, by avoiding PHA stimulation and by reducing the number of cells per millilitre of culture medium from 105-106 to 103-104, they were able to “grow the infected cells for 50-60 days” without cellular degeneration which, according to them, was due to “the lack of further antigenic stimulation and, presumably, the reduced concentrations of toxic substances released by the mature cells”

  241. #242 Chris Noble
    July 7, 2007

    Where are the Electron Microscopy studies of HIV induced cell damage?

    There are hundreds if not thousands of studies that show HIV induced cell damage in lymphoid organs.

    I’ve already cited one of them in this thread so you have no excuse for your ignorance.

    HIV infection is active and progressive in lymphoid tissue during the clinically latent stage of disease

  242. #243 Pope
    July 7, 2007

    Ok you Sharks, I meant in the absence of an immune system to be precise

  243. #245 Chris Noble
    July 7, 2007

    If you’re gonna pretend you don’t know what I’m talking about here, I’m just gonna have to say you guys are ‘unintelligable’and should go back and do some more reading, or go for a holiday in Thailand, you know take a break from the kids and the other parent.

    The only person that is pretending anything is you when you pretend that you understand what you are talking about.

    Why do you assume that virtually every scientist in the world is stupid? You have yet to demonstrate that you understand even an infinitesimal fraction of the science that you pretend to judge.

    This study is for you.

    http://www.apa.org/journals/features/psp7761121.pdf

  244. #246 Pope
    July 7, 2007

    Dr. Noble, you’re the one who is presuming and judging and cooking up wild accusations. Show me where I judge, or imply that the scientists in question are stupid (regarding the lab stuff we’re talking about), Or shut up, cut back on the drugs for awhile and do some in vivo jerking off instead of merely cyber-abreacting your frustrations.

  245. #247 ERV
    July 7, 2007

    Wow. The ‘PBMC refrigeration’ comment up there. Wow.

    When I do my experiments, I always start with freshly isolated PBMCs or ones frozen back in nitrogen (NOT optimal, but if you dont need all the fresh cells, you save them ‘just in case’). You can keep the cells going in your experiment for months–>years if you keep feeding them and pumping in fresh cells. But you dont just keep PBMCs going in the incubator to use ‘whenever’ like you can with COS1s, TZMs, or 293Ts.

    Thats fantastically stupid, and considering the source, deceptive.

  246. #248 Chris Noble
    July 8, 2007

    Dr. Noble, you’re the one who is presuming and judging and cooking up wild accusations. Show me where I judge, or imply that the scientists in question are stupid (regarding the lab stuff we’re talking about), Or shut up, cut back on the drugs for awhile and do some in vivo jerking off instead of merely cyber-abreacting your frustrations.

    When your arguments are of the form that DAIDS openly state in their reference manual that controls should be treated differently to the standard assay for HIV culture then it is appararent that you think that thousands of scientists are stupid.

    Every single HIV Denialist argument eventually reduces to the implication that every scientist that accepts the overwhelming evidence that HIV exists and causes AIDS is corrupt, ignorant or stupid.

  247. #249 Pope
    July 8, 2007

    Dr. Noble,

    You may remeber that it was not I, but a real credentialed scientist who advanced that argument.

    I mentioned it here, and when you all in an unusally not too condescending and beside the point way informed me it was a based on misreading/misinterpretation, I publicly conceded you might very well be right, as well as own inability to judge the matter.

    However, when the piranhas pounce on one word, “activated”, in what was merely a playful one-liner response to a humorous comment about “denialists”, it invites a sharper answer than “ooppss sorry guys, maybe I misunderstood something, here’s what I meant, please help me understand the issue…” – Especially when it’s obvious that no one’s interested in what I meant or if I know what I’m talking about, only in the fact there was meat in the feeding trough.

    The exact same goes for Nick’s “fridge” comment and countless other examples.

  248. #250 Chris Noble
    July 8, 2007

    You may remeber that it was not I, but a real credentialed scientist who advanced that argument.

    The point was that you were prepared to accept that the credentialled scientists at DAIDS are all inept and stupid. If you don’t understand the science then it boils down to you choosing to believe a tiny fringe of scientists who do no research on HIV of their own over the thousands of scientists that do.

  249. #251 Pope
    July 8, 2007

    Nonono, Dr. Noble, you’re barking up the wrong tree with that Nathan Geffen line. Intelligent laypeople are very well capable of understanding the science with a little bit of explanation. Your new version of the argument from consensus, holding the majority of scientists’s intelligence hostage to your cause, is not valid. The scientists who thought the Earth was flat were not all stupid, they were operating under mistaken assumptions.

    Far be it from me to lecture a science connoiseur like yourself, Dr. Noble, but it is easy to operate within a system made up by facts, beliefs, assumptions that are all rational seen from within that system, but look stupid from without.

    In this debate, I have to test anything the prominent ‘denialists’ say without regard to how stupid it may make certain people look. If you haven’t worked in a testing lab, it is not easy to know what the DAIDS manual translates into in practice, or what Dr. Maniotis meant by his remark, which was part of a larger argument.

    I do find it unlikely that clinicians are instructed to terminate all control cultures after 3 days, but I didn’t concede the point because I find it unlikely or because it might make somebody look stupid, but because I didn’t find enough support in the text or in Maniotis’ consequent explanation.

    In his considered answer, Maniotis did have things to say relating to the tests and the DAIDS manual which do not hinge on this. I fail to understand why you keep revisiting over and over these old already settled very minor points, when new ones have been made for you to sink your teeth into.

    Are your perceived victories so few and far between that you have to keep pulling them out again and again

  250. #252 Chris Noble
    July 8, 2007

    Nonono, Dr. Noble, you’re barking up the wrong tree with that Nathan Geffen line. Intelligent laypeople are very well capable of understanding the science with a little bit of explanation.

    I agree with you wholeheartedly. Science is democratic. The knowledge is freely available to any one that wants to learn. Unfortunately, HIV Denialists start from a position of ignorance and fight tooth and nail to maintain that ignorance. Denialists are not interested in understanding the science they are only interested in finding justifications to continue their Denial. It is transparently simple to see who gets their “knowledge” from Denialist websites and books and who gets it from actually studying the science.

    Your new version of the argument from consensus, holding the majority of scientists’s intelligence hostage to your cause, is not valid. The scientists who thought the Earth was flat were not all stupid, they were operating under mistaken assumptions.

    The idea that scientists thought that the Earth was flat is propagated almost solely by cranks who want to justify why the vast majority of scientists view their crank ideas as pseudoscience.

    In this debate, I have to test anything the prominent ‘denialists’ say without regard to how stupid it may make certain people look. If you haven’t worked in a testing lab, it is not easy to know what the DAIDS manual translates into in practice, or what Dr. Maniotis meant by his remark, which was part of a larger argument.

    The problem is that I see the opinions of the prominent Denialists regurgitated without the slightest picogram of skepticism. If you don’t understand how to read a virology manual then you have to weigh up the probability that the scientists at DAIDS are all amazingly stupid compared to the probability that Maniotis has reading problems.

  251. #253 Pope
    July 8, 2007

    Science is not democratic. It’s an elitist discipline if any, and doesn’t have to obey any democratic consensus or consider anybody’s feeling. Scientific institutions and the scientists that work in them, however, are a very different matter. They should not censor questioning, even the most radical questioning in an oligarchical manner. They are obliged to subject themselves to the scrutiny of those who pay their salaries (and that ain’t the pharma cos) and are all but force-fed their drugs. They should not be their own judges, and they should certainly not be part of a political power apparatus.

    Everybody is interested in what justifies her own point of view, Dr. Noble. As the saying goes, one man’s denialist is another man’s freedom fighter. Some people learn, and perhaps change their points of view, some don’t. The ones that you attract here with every second headline bashing “denialists”, are obviously the people who are going to either pat your back or confront you with the well-known denialist claims. There is no better way to learn about a thing than to confront it with radical critique, and it’s not realistic to expect that everybody who’s not on your side must become expert on virology, epidemiology, immunology, pathology, biochemistry, genomics etc. to participate. If you don’t like it, don’t respond. Or ask Tara to write on something else. Or ask her to require proof of a PhD in a relevant field to join.

    Robodoc Noble, I should have known a red flag would go up when I chose the flat Earth example. I was not implying that denialists are part of a Copernican revolution by mentioning the flat Earth. I was merely saying that many things make sense from within. You can substitute capitalism for flat Earth, if you will. From within the capitalistic system, greed, price gouging, accumulation of obscene wealth and private property seems both rational and ethical. Why it is even compatible with the loftiest Christian ideals if you ask the current prez. Even so, not all Capitalists are stupid or deliberately hypocritical.

    Again Dr. Noble, most people can read a virology manual, just like most people can read and understand a book on horse riding. That doesn’t mean there’s not a lot of blanks to fill in between the page and the saddle, so to speak. Once again, I do not consider what’s stupid or not. I air the idea, running the greatest risk myself of sounding stupid I should think, and abandon it if I find it wanting.

  252. #254 trrll
    July 8, 2007

    Trrll has now returned 3 times to give us the basic lecture about imaging cell death. Has he anything else to contribute, like a photo?

    When you quit making the same basic mistake, I will quit administering the same basic lecture. I’m certainly not going to bother to cite EMs, since it is not a technique that is well suited to detrmining cell health. I recognize this tactic: insist on evidence using a technique that is not well suited to answering the question, then when people provide evidence of the kind demanded (as has been done multiple times in this thread), nitpick it because it is does not clearly answer the question (meanwhile ignoring abundant evidence using methods that are far better suited to answering the same question).

  253. #255 trrll
    July 8, 2007

    Science is not democratic. It’s an elitist discipline if any, and doesn’t have to obey any democratic consensus or consider anybody’s feeling. Scientific institutions and the scientists that work in them, however, are a very different matter. They should not censor questioning, even the most radical questioning in an oligarchical manner.

    Sorry to burst your bubble, but scientists and scientific institutions have work to do that they regard as more important than repeatedly answering the same fallacious criticisms from zealots who want to re-argue a scientific question that virtually the entire scientific regards as having been settled over a decade ago. HIV denialists actually get far more attention from scientists than, say, people who write letters to physics departments insisting that they can prove that special relativity is wrong, or who write to math departments insisting that they have a construction for squaring the circle. A few scientists devote their time, without compensation, to re-arguing this long-settled debate simply because this is one area where denialism is not merely annoying working scientists, but actually killing people.

  254. #256 SmellyTerror
    July 8, 2007

    I love this thread! Pure comedy gold.

    What makes it great is that the denialists get so utterly, completely trashed, but still manage to keep their offensive, gleefully mocking tone. It’s like the Monty Python black knight, sans limbs, still full of offensive overconfidence. “Come back you yellow bastard, I’ll bite your legs off!”

    I honestly think they know, deep down, that they’re wrong. No-one could possibly fail to grasp simple concepts, over and over. No-one would resort to claiming that their concerns are never addressed, when the responses are right there on the same page, unless they were in deep, DEEP denial.

    They are supernaturally dense. It’s just not possible to be that stupid. They must be doing it on purpose.

    Guys, give up. You lost. Badly. You’re just humiliating yourselves now.

  255. #257 Pope
    July 8, 2007

    Wow Trrll,

    Good one. Touche! Did you write it yourself, or did you quote from the script? Do you pat yourself on the shoulder every night before you go to bed? Do you get those steamy eyes and that familiar choking feeling in your throat that only really, really decent people get from knowing that they’ve devoted their valuable time to save lives, and (GASP!) without compensation too? Do angels play violin in your wet dreams?

    We don’t have to ask any of those questions of the next moron, who I’m sure makes Tara proud of her blog. He cribbed his comment from Roy Hinkley “right there on the same page“.

    In the face of such overwhelming proof of intelligence and originality, and most of all sheer righteousness, how could I possibly hold this bridge any longer?

  256. #258 SmellyTerror
    July 8, 2007

    See? Perfect example. Pope launches an attack on Trrll’s answer without even saying what his objection is! Could he have missed that Trrll beat the textual crap out of him in the previous posts? Does he fondly believe that his vague insults (do they actually mean anything?) actually constitute a rebuttal? He’s “accusing” Trrll of… what? Being employed? And apparently thinking this is some kind of devastatingly witty argument!

    Surely not. Surely no even-slightly-rational person could genuinely think he’s actually winning this exchange.

    …and cribbing from Roy Hinkley? WTF? Uh, I said the answer is on the same page as your protestations that there was no answer because – stay with me here – it is on the same page. How would you prefer I phrase it? I don’t see that it’s such a witty or original phrase that anyone would need to crib it from anyone else. It’s a simple statement of fact in the plainest english I can think of.

    Might as well accuse people of plagiarism for using the word “the”.

  257. #259 Pope
    July 8, 2007

    Gee, for somebody who accuses others of being dense, you must belong to an entirely new category. Just one hint, and this is really the last I can bothered with you. Feel free to take that as a “textual victory” (there at least was a novel expression)

    If you will actually look at the Gallo paper I think you will see it very nicely answers all of your questions so far (…) To put it bluntly:
    “Look you stupid bastard, you’ve got no arms left.”
    http://en.wikipedia.org/wiki/Black_Knight_(Monty_Python)

    Posted by: Roy Hinkley | July 7, 2007 06:33 PM

    No-one would resort to claiming that their concerns are never addressed, when the responses are right there on the same page (…)What makes it great is that the denialists get so utterly, completely trashed, but still manage to keep their offensive, gleefully mocking tone. It’s like the Monty Python black knight, sans limbs, still full of offensive overconfidence. “Come back you yellow bastard, I’ll bite your legs off!” (Moron)

    Now go stink somewhere else.

  258. #260 SmellyTerror
    July 8, 2007

    Wait a second, so you’re focussing on the fact that we both made the same joke (yup, I missed Roy’s – I was foolishly reading the science), and not even bothering to defend yourself against the substance.

    Wow. Score one for the Pope! Actually, I think you’ll find that the black knight is a pretty popular symbol for idiot perseverance in the face of ignominious defeat. That at least two posters have applied it to you guys here is supposed to be good for you… how?

    “Hey, everyone thinks I’m an idiot. I win!”

    You manage to remember all the throw-away remarks, but somehow miss the answers you repeatedly ask for, and get. Staggering. How on earth do you expect this to convince anyone of your side of the argument?

    …and did you just call me stinky? What are you, twelve?

  259. #261 Alan Kellogg
    July 8, 2007

    Hypothesis: Bad science is strident, good science is calm. Now, in this thread, who has been strident and who has been calm?

    BTW, some people [waves] don’t need to respond to every little snit somebody has over something they’ve said.

  260. #262 Chris Noble
    July 8, 2007

    They should not censor questioning, even the most radical questioning in an oligarchical manner.

    Nobody is censoring you. Most people ignore you and other Denialists because despite your pretence you are not interested in the answers to your questions. You are not interested in learning anything. Most scientists are only too ready to help people understand their field of study.

    Anybody can go to a library and pick up an introductory book about virology if they really want to learn. But that isn’t what Denialists do. They start with the premise that HIV doesn’t exist or doesn’t cause AIDS and then they attempt to find “anomalies” in the “orthodox” science. Or even better they go to Denialist websites where other Denialists have already collected these “anomalies”. Then they appoint themselves to be the arbiters of science and under the pretence of asking questions start to attack the integrity and intelligence of scientists that work in the field.

    Take the Perth Group as an example. They had their oxidative theory of cancer before AIDS was observed. When AIDS was recognised all of a sudden their oxidative theory now postdicted AIDS. At this stage they had not even heard of retroviruses. After HIV was discovered and demonstrated to cause AIDS they all of a sudden became experts in the isolation of retroviruses despite never having had any practical experience. It is possible to teach yourself a lot of the science if you are honestly interested. But they aren’t interested in understanding the science. Their only objective is to find self-serving justifications for ignoring the science.

  261. #263 Jon H
    July 8, 2007

    noreen Martin writes: “In Africa, places with low selenium have high AIDS cases.”

    Those places have ALWAYS had low selenium. So why hasn’t AIDS been endemic there for centuries?

  262. #264 Jon H
    July 8, 2007

    I get the impression that the real problem with HIV denialists is that people with immune system problems just don’t like being lumped in with Teh Gheys.

  263. #265 Robster, FCD
    July 8, 2007

    Pope, you don’t have radical questions. You have old, already answered questions, and long discarded hypotheses. You don’t have criticisms. You have nitpicking of data and a misunderstanding of the process of science.

    The hypotheses and claims of the denialists aren’t considered worthwhile by scientists because these concepts were passed over in favor of better and more substantial research.

    If you have something to contribute, it needs to be an alternative hypothesis that is more solid than HIV as the causal factor of AIDS. You don’t have one.

    If there is to be a debate, it should be based on time for evidence. We can let the denialists go first. How much time will it take them to stand up, say, “We don’t have anything.” and sit down?

  264. #266 Andrew Maniotis
    July 9, 2007

    Dear AIDS apologists or denialists,

    Have you taken the AIDS test that medical students must pass after they receive their mandatory HIV test before beginning medical school?

    Find the best answer:

    1. Reverse transcriptase (RT) is a specific marker for “HIV” because:

    A) It is a normal protein found in the uninfected cells of bacteria, yeasts, insects and mammals.

    B) RT is important for telomere replication at the tips of normal chromosomes.

    C) RT is now seen in market magazines concerning biotechnology stocks regarding a variety of normal, non-pathological contexts.

    D) Because worms develop AIDS.

    E) All of the above.

    E) A, B, C, but not D or E.

    2. Read the following information and provide the best title:

    In symptomatic patients with HIV infection, early treatment with zidouvdine delays progression to AIDS, but did not improve survival, and was associated with MORE side effects. There were 43 deaths, 23 in the early-therapy group, and 20 in the late-therapy group. The medium time from the diagnosis of AIDS to death was 16 months in the early therapy group, and 19 months in the late-therapy group.
    The racial and ethnic groups appeared to respond differently to the timing of zidpovudine therapy. Fewer minority (African American and Hispanic) patients died in the late therapy group (two deaths) than in the early-therapy group (nine deaths), but the difference was not significant. Among non-Hispanic white patients, early therapy significantly delayed the onset of AIDS but had no effect upon survival. Minority patients were much more likely than white patients to be intravenous drug users (40% vs. 10%).
    After two years of follow-up, we found no difference in survival between the two treatment groups.

    A) AZT is a “life-saving” drug?

    B) AZT kills more healthy patients (early group) than sicker (late treatment) patients.

    C) You should hit white patients hard and early but only treat black and hispanic patients late, cause they’re “different biologically.”

    D) AZT increased survival.

    E)AZT disproportionately harmed Blacks and Hispanics, and provided no benefit to the quelling of advancing immune suppression in Caucasians.

    F) B&E

    3. HIV test kits are nearly 100% accurate because:

    A) At present there is no recognized standard for establishing the presence of absence of antibodies to HIV-1 and HIV-2 in human blood.

    B) Abbott’s 1997 Laboratory’s ELISA test kit package insert says:”ELISA testing alone cannot be used to diagnose AIDS.” (Abbott 1997).

    C) Epitope’s 1997 (the maker for one of the Western Blot kits) package insert says: “Do not use this kit as the sole basis for HIV infection.” (Epitope 1997).

    D) Roche’s 1996 “Amplicor” test kit’s insert states:
    “The amplicor HIV-1 monitor test is not intended to be used as a screening test for HIV, nor as a diagnostic test to confirm the presence of HIV infection.” (Roche 1996).

    E) These disclaimers are typo’s on the “HIV” test kits and should be ignored.

    F) Because Seville Marketing of British Columbia, Canada, on two Web sites had advertised the “Discreet” home HIV test kits as producing 99.4% accurate results based on three independent studies, yet three minutes after performing the test according to the package instructions, 15.4% of the results were inaccurate; after eight minutes, 29.6% of the results were inaccurate; and 59.3% of the tests produced inaccurate results after 15 minutes, and the FTC will seek a permanent ban on sales and advertising of the kits in the United States and a permanent order to seize any kits that are imported.

    G.Because NucliSens(R) HIV-1 QT package insert says:
    “The NucliSens(R) HIV-1 QT assay is not intended to be used as a screening test for HIV-1 nor is it to be used as a diagnostic test to confirm the presence of HIV-1 infection.”

    H) Because COBAS AmpliScreen HIV-1 Test, version 1.5 says:
    “This test is not intended for use as an aid in diagnosis.”

    I) Because the clinical implications of antibodies to HIV-1 in an asymptomatic person are not known.

    J) Because OraSure(R) HIV-1 Western Blot Kit says is not intended for use with blood, serum/plasma or urine specimens, or for screening or reinstating potential blood donors.

    K) Because Defer et al. in a paper entitled, “Multicentre quality control of polymerase chain reaction [viral load] for detection of HIV DNA” (AIDS 6: 659-663, 1992), claimed that: False-positive and false-negative results were observed in all laboratories (concordance with serology ranged from 40 to 100%).

    L) Because Busch et al., in a paper entitled, “Poor sensitivity, specificity, and reproducibility of detection of HIV-1 DNA in serum by polymerase chain reaction” claimed that: PCR-DNA tests on 151 ELISA-negative people found that 18.5% (28 people) had positive PCRs. Furthurmore, only 25.5% of people diagnosed HIV-positive had positive PCR’s.

    M) Because viral load does not correlate with T-cell numbers, and progression of disease can only be predicted in 4%-6% of any HIV-positives studied (out of 2,800).

    N) Because out of 37,000,000 samples, 12 PCR-positive or 2 (ELISA positive) were found.

    O) None of the above.

    P) All of the above.

    4. “HIV” is the virus that causes AIDS, but it causes anemia because:

    A) Because as a retrovirus, it really doesn’t need to intercalate its genome into target cell nuclei.

    B) Because although it only may infect 1 in 10,000 T cells, it also infects, like Ss sickle-cell anemia, 50/100 RBC’s to cause anemia.

    C) Because RBC’s are actually made by muscle cells, and it is well known that HIV causes muscle wasting, which decreases the production of RBC’s.

    D) Because patients selectively biased and targeted by AIDS doctors as high risk patients are put on AZT, which depresses all cell division.

    E) Because AIDS is neither a disease of too few or too many lymphocytes, but a disease that affects neurons, glia, endothelial cells, liver cells (which is why liver failure is now the leading cause of death in Cleveland).

    5. Nevirapine decreases MTCT of HIV:

    A) Because single dose of nevirapine is the cornerstone of the regimen recommended by the World Health Organization (WHO).

    B) Because Max Essex thinks feline leukemia virus is the AIDS virus.

    C) Because nevirapine resistance is detected (with the use of standard genotyping techniques) in 20 to 69% of women and 33 to 87% of infants after exposure to a single, peripartum dose of nevirapine.

    D) Because no women in the placebo group and 41.7% in the nevirapine group had virologic failure.

    E) All of the above.

    F) None of the above.

    6. There are no good animal models of AIDS:

    A) Because it is well known that some viruses are very species specific, and will not jump species.

    B) Because HIV came from monkeys and not hominoid primates such as chimps because black people have their children play with dead monkey carcasses because they can’t afford toys for them, and somehow this virus got into the gay community from black children in Africa eating (or “playing with”) monkeys.

    C) Because hungry blacks living in Africa eat monkeys and HIV can infect through kissing, and eating food.

    D) Because SIV is a better model for HIV infection than HIV.

    E) Because chimps that live in retirement homes actually have very low stress levels, and stress created by an “HIV diagnosis” can be very immune suppressive (to humans), and because chimps are dumb and unless they are taught to sign, they don’t know they have an HIV infection, and thus stress plays no role as a co-factor and they can’t develop AIDS (unless they understand they are infected, as one transfused monkey did).

    F) Because the structural proteins of HIV, the virus that causes AIDS, have been found in dogs, sheep, and goats (bacteria, worms, and other animals if you believe that RT is specific to HIV and is found in all these critters as Varmus and Temin believed), it is difficult to study immune suppression in collies and worms, or bacteria.

    7. A registry has been established to monitor fetal outcomes born to women exposed to efavirenz and other life saving ARVS, and HAART:

    A) Because neural tube defects have been noted among women taking Efavirenz (Sustiva).

    B)Because drug-induced liver toxicity with highly elevated liver enzymes (greater than 20 times the upper limit of normal) has been observed in 39% of healthy volunteers receiving rifampin 600 mg once daily in combination with ritonavir 100 mg/saquinavir 1000 mg twice daily (ritonavir boosted saquinavir).

    C) Because females and patients with higher CD4 cell counts are at increased risk of liver toxicity (because they are healthier when they begin “the life-saving drugs” than are people with lower counts.

    D) Because females have a three-fold higher risk of symptomatic nevirapine liver toxicity than males, and females with CD4 cell counts above 250 cells/mL have a 12-fold higher risk of symptomatic liver toxicity than females with CD4 cell counts below 250 (11% vs. 0.9%).

    E) Because males with CD4 cell counts above 400 cells/mL have a five-fold higher risk of symptomatic liver toxicity than males with CD4 cell counts below 400 (6.3% vs. 1.2%).

    8. Dr. Nobel said to a nameless AIDS apologist named Raven that “I’ll save Maniotis the effort because all of those studies you cited are meaningless because the allopathic authors have to claim success or else they wouldn’t get their pharma funding: (refering to “In Alberta, HAART dropped the AIDS mortality by 80% in HIV+ that many patients died of other causes”):

    A) Because Dr. Nobel doesn’t like Raven.

    B) Because “all of those studies” (Raven) cited “are meaningless because the allopathic authors have to claim success or else they wouldn’t get their pharmainc funding.”

    C) Because Tara Smith, an epidemiologist, says that “HIV” is like all diseases and that mutations happen in the CCR5 receptor that protect some folks from getting ill, but that pregnant women should be put on nevirapine, AZT, 3Tc, and saquinavir just in case they aren’t mutant women.

    D) Because the Concorde study showed NO mortality benefits of AZT, and was a much longer, and larger study than the Fischl FDA approval study in which the 19 patients who were transfused to keep them alive all died anyway after about a year, arms of the trial were switched, the trial was unblinded, and the Freedom of Information Act documents that describe the study had sentences which were “blacked out” so we have no way of knowing what really happened in that study.

    E) Because The 2006 Lancet study of 22,000 patients over the past 10 years on meds, entitled, “HIV Treatment Response and Prognosis in Europe and North America In The First Decade of HAART: A Collaborative Analysis” concluded with: “Virological Response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality.” (see page 453)

    9. The DAIDS 1997 official “HIV” culturing manual, under quality control, Section VI, page 45, advocates, “Do not use PHA stimulated PBMC older than 3 days post stimulation” when testing them for the absence of HIV from your healthy donor source:”

    A) Because it is part of a test using (some of those kits listed above in question 3) of sequential samplings of undetermined infected or uninfected cell supernatants for at least 21 days wherein two consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml, of which the second value is at least four times greater than the first value or “out of range” (O.D.>2).

    B) Because it is a test using sequential samplings of undetermined infected or uninfected cells for at least 21 days wherein two consecutive HIV p24 antigen VQA CORRECTED values that are “out of range (Optical density.> 2).

    C) Because it is a test using sequential samplings of undetermined infected or uninfected cells for at least 21 days wherein three consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml, where neither consecutive value is > four times the previous sample, but the third value is at least four times greater than the first.

    D) Because someone is considered “HIV” positive if they exhibit 30 but not 29 picagrams/ml of p24 protein on the second test.

    E) Because someone is not considered “HIV” positive if they exhibit 40 pg/ml on the first test, but 4 picagrams/ml p24 on the second test.

    F) Because a woman named Christine Maggiore is really “HIV” positive although she never has tested positive on two consecutive tests and has never been ill.

    G) Because “control cells” or cells derived from “a healthy donor source are cells that consistently test less than 30 pg/ml.

    10. “Original antigenic sin” is a term “HIV” vaccinologists use to describe:

    A) When a vaccinated individual is exposed to a noncross- reactive strain of HIV that induces the production of antibodies specific for the vaccine strain that are unable to neutralize the newly encountered strain (in other words when a vaccine doesn’t work).

    B)The fixing of an immune response in a non-adaptive pattern.

    C) When vaccinated individuals may be no worse off than unvaccinated individuals because unvaccinated individuals also have a lag in generation of antibody to HIV because their immune response has not been “primed” by vaccination.

    D) The conclusions of The Office of Technology
    Assessment Book (1995 Congress of the United States: Office of Technology assessment. Adverse Reactions to HIV Vaccines: Medical, Ethical, and Legal Issues. Roger C. Herdman, Director) presented to the 1995 Congress of the United States in 1994 by the AIDS Research Advisory Committee (ARAC) of the National Institute of Allergy and Infectious Dieases (NIAID) that recommended that Phase III clinical trials with enveloped vaccines should not proceed in the United States because of scientific, political, and ethical issues, and the significant level of scientific uncertainty about the wisdom of immediate trials.

    E) Vaccines may cause a false-positive HIV screening testing test…resulting in discrimination against vaccine recipients in, for example, military service, health insurance, life insurance, employment, and travel.

    F) Participation in an HIV vaccine trial, itself, may result in stigmatization, as others may assume that all vaccine trial participants are members of groups, such as injection drug users and men who have sex with men, who are at increased risk for HIV infection.

    G) Vaccinees, relying on the protection afforded by an experimental vaccine, may engage in behaviors that increase their risk for HIV infection.

    H) There is the potential for the viruses to be inadequately attenuated, for an adequately attenuated viral vaccine to cause disease in immunocompromised individuals (Read AIDS patients), and for an adequately attenuated virus to revert to virulence. There is also concern that a live attenuated vaccine could induce tumors.

  265. #267 DT
    July 9, 2007

    Andrew, I got bored with your manufactured list of misquotes and lies half way through the first question.
    If you have any genuine hypothesis to advance about the cause of AIDS, please let us see it. Otherwise stop spamming the thread with your inconsequential and scientifically irrelevant thoughts. You might fool a couple of the intellectually-challenged denialists into thinking you are being oh so humorous and clever, but every one else sees you for what you really are.

  266. #268 Adele
    July 9, 2007

    Repeat DT’s comment for me. Thank you.

    How many times did we go over the “endogenous RT” already?

    If HIV RT activity doesn’t exist and all anyone measures is endogenous RT
    OR
    If endogenous RT overwhelms HIV RT measurements
    OR
    If endogenous RT just interferes with HIV RT measuring
    THEN
    Every time I do an RT assay I would confirm Andrew’s theory that scientists all dumb and confuse HIV RT with endogenous RT. I’v been doing them for I think about ten years now off and on thank god because they’re damn boring and I never saw what I should see if Andrew’s right.

    I had this above but again, here’s a good experiment and its results. And I’m doing primary cells so people don’t object to cancer cells and artificial activation, but it doesn’t matter.
    1)Primary cells with replicating virus 175000 cpm
    2)Primary cells with virus with several inactivating mutations 500 cpm
    3)with killed virus 400 cpm
    4)Primary cells all by their selves 150 cpm
    5)Nothing not even cells just some saline 95 cpm

    WE wash off the virus after a few hours so any virus we measure later is coming from inside the cells. After some days we take some liquid off the cells and put it in a centrifuge to take out any dead cells and floating things. So all we’ve got now is liquid with tiny stuff in it like virus. We centrifuge it fast to pellet the virus. Detergent to break open virus. All the little proteins spill out yes RT too. Then we give the RT some stuff it can work on and measure how much work it does with radioactivity, counts.

    Now look back up at those results.
    The machine always detects something. It’s called noise. Theres 95 counts in the saline by itself. Not much more in the cells by themselves. This tiny difference could be random or maybe some real endogenous RT activity. The killed virus and the mutant virus are again slightly higher something might have got through one or two cells were susceptible to the mutant maybe or something or one or two virions not killed. But guess what? The “normal” virus gives us three logs higher than any of this. 175 000 versus 500 the second highest.

    If endogenous RT is what everyone is reading when they think HIV RT, I should get 175 000 counts in everything with cells in it.

    Is there another explanation? Maybe the virus on the cells does something toxic to them and they make more endogenous RT enzymes. OK, but my controls like killed virus don’t make RT. Or maybe the virus has to get in the cells and do something. Ok, but my mutant virus with just a few point mutations that’s kind of the exact thing as the real virus except its defective post integration, that one doesn’t make RT either.

    I can’t think of a good explanation for that except HIV has a RT I’m measuring

    Especially since, this cell enzyme Andrew talks about isn’t made in our cells much. it’s silenced. Yes, epigenetically. It gets made in cancer cells mainly.

    So why would it be outside primary cells anyway in quantities high enough to confuse it with virus RT?

    Andrew should have answered these questions before instead of joking around but he hasn’t yet.

  267. #269 Adele
    July 9, 2007

    In the Gardasil debate this denialist idea came up its shared with fundamentalists and now Andrew says it too,
    Vaccinees, relying on the protection afforded by an experimental vaccine, may engage in behaviors that increase their risk for HIV infection

    So I guess we should also,

    Take railings off balconies and stairs because they encourage people to engage in risky behavior at great heights

    Outlaw the use of seatbelts antilockbrakes airbags and bumpers because they encourage bad driving

    Take locks off doors because they give people a false sense of security from crime

    Destroy ambulances because they make people think medical help is close and they take more risks

    Stop making doctors get degrees because people trust them too much. They’ll take care of themselves more if there’s no “experts” to talk to.

    Right, Andrew?

    I’ve met parents who say, I’m not giving my child this Hepatitis vaccine because we dont want her doing drugs or having sex outside of marriage. So sad but this idea is all around. No prevention. Just the wrath of God as cure.

  268. #270 Andrew Maniotis
    July 9, 2007

    No Adele,
    Don’t outlaw balconies or ambulances just yet. And its not about the rath of God. So good for you to respond specifically to my points on my test. You probably would get and F in my class.

    The Vaccine Adverse Events Reporting System (VAERS) shows that the hepatitis B vaccine damages far more individuals than there are persons who exhibit the hepatitis B syndrome. Evidence obtained from the American Association of Physicians and Surgeons (AAPS) and other physicians, vaccine-monitoring agencies such as the National Vaccine Information Center (NVIC), the CDC and World Health Organization, the Illinois Vaccine Awareness Coalition, the hepatitis B vaccine manufacturers Merck and GallaxoSmithKline, and evidence from the peer reviewed scientific literature, all show that the risk of groups such as infants and children acquiring liver hepatitis associated with hepatitis B virus (HBV) is nearly 0%. In all comprehensive statistical surveys available, the actual incidence of the hepatitis B syndrome in the US has remained constant at about 2 to 4 cases/ 100,000 individuals despite widespread mandated and aggressive vaccination programs in all but 4 states [1].
    The data also show that the hepatitis B syndrome, when it does occur in non-vaccinated individuals, spontaneously resolves in almost 100% of those who became seropositive for the HBV molecular markers (HBsAg, anti-HBsAg, HbeAg, anti-HbeAg, or HBV-DNA). The liver syndrome is quite rare (0.00024%-hovering near zero percent for both adults and children), while over 10% of hepatitis B vaccine recipients experience adverse reactions. According to the Merck package inserts, 10.4% experience adverse reactions, and 1% are serious enough for emergency room admission.
    Some of the severe adverse effects include autism, Stevens-Johnson Syndrome, arthritis (both transient and permanent), Guillain-Barré Syndrome, myelitis including transverse myelitis, seizure, febrile seizure, peripheral neuropathy including Bell’s palsy, diabetes mellitus, pancreatitis, encephalitis, multiple sclerosis, thrombocytopenia, systemic lupus erythematosus, lupus-like syndrome, vasculitis, optic neuritis, radiculopathy. Lesser vaccine effects include vomiting, abdominal pains, vertigo, dizziness, pruritus, angioedema, urticaria, lymphadenopathy, insomnia, dysuria, hypotension, increased risk of shingles, migraine, severe muscle pain and weakness, hypesthesia, alopecia, petechiae, increased sedimentation rate, tinnitus, conjunc vitis, visual disturbances, syncope, tachycardia, keratitis, irritability [2].
    The practical and economic impact of the effects of this mandated recombinant hepatitis B vaccine policy is devastating infants, families, and the nation, because the nature and frequency of the vaccine damage is typically so debilitating. The damage experienced during the French mandatory hepatitis B program prompted France to discontinue its hepatitis B program several years ago, and a class action lawsuit compensated some 15,000 families that had been devastated from hepatitis B vaccine injury [3].
    The efficacy of the vaccine has also been challenged. According to some long-term studies in populations said to exhibit “endemic” frequencies of markers indicating endemic hepatitis B “infection” such as Gambia and Egypt, antigenicity (the presence of the HbsAg antibody among the vaccinated) does not persist beyond about 5 years [4], yet expression of the hepatitis B syndrome confers immunity and antigenicity for life [5] in nearly 100% of those who are unvaccinated and experience the full-blown syndrome that spontaneously resolves without significant morbidity in almost all cases [6]. A study conducted with Egyptian children, reported a similar lack of long-term antigenicity as determined by antibody levels. The study population comprised six equal groups (30 children in each group, 15 boys and 15 girls) at different post-vaccination intervals following the completion of the third dose of HB vaccine: 1 month (group 1), 1 year (group 2), 2 years (group 3), 3 years (group 4), 4 years (group 5), and 5 years (group 6). “63.3% of the children in group 1 had a good immune response (anti-HBs > 100 mIU/mL), in groups 2 and 3 this had dropped to 43.3%, to 23.3% in group 4, 6.7% in group 5 and in group 6 (5 years post-vaccination) none of the children had a good immune response (0.0%)” [7].
    The “cryptic argument,” that every person on the planet must be vaccinated because the hepatitis B “virus” can hide in cells in “chronic carriers” for decades without causing clinically detectable disease, and then mysteriously, decades later, “cause” hepatocellular carcinoma, ignores the fact that seropositivity for the hepatitis B antigens may not have anything to do with serum hepatitis. In the vast majority of seropositive individuals without liver disease, the presence of the HBV markers may represent non-specific markers of immunological stress, or merely represent a normal genetic polymorphism, as was originally thought by Baruch Blumberg (who discovered the Au antigen, HbsAg, in the blood of a black Australian aboriginal, and was awarded the Nobel Prize that he shared with NIH’s former Neurobiology Program director, D. Carlton Gajducek–the discoverer of the so-called “slow virus” prion diseases). For these discoveries, the doctors were jointly given The Nobel Prize in Physiology or Medicine in 1976 “for their discoveries concerning new mechanisms for the origin and dissemination of infectious diseases,” because the infectious agents and mechanisms of disease causation were believed not to conform to the standards of accepted pathogen isolation, the idea of distinctive genetic (nucleic acid) identity, the timing of infection to demonstrable cell pathology or morbidity, or to the classic proofs of pathogenicity worked out by Koch. For instance, D. Carlton Gajducek championed the idea that “infectious proteins” devoid of nucleic acids were at the basis of slow, debilitating neurodegenerative disorders (e.g., kuru, CJD, Mad Cow, scrapie in sheep)–syndromes that are characterized by extremely long latency periods after initial “infection,” and destruction of the brain tissue years or decades after “infection.” Although the concept of slow viruses, and pathogens devoid of nucleic acids were vigorously challenged and rejected by many in the scientific establishment during the 1980′s because the idea challenged the established biochemical chain of events worked out for all other infectious agents, and because these syndromes appeared to be both infectious and run in families, Stanley Pruisner believed Gajducek’s hypotheses to be plausible, and found that the hypothesized disease-causing PRP protein was present in both diseased and healthy hamsters (for which another Nobel Prize was awarded).
    Blumberg termed the rare “hepatitis B” antigen, Au, for Australian antigen, because the Au antigen was first found in the blood of a healthy black, Australian aboriginal man, but he also detected it in the blood samples of Micronesians, Vietnamese, Taiwanese, Native Americans, and patients with Down syndrome, leukemia and transfusion patients. Blumberg acknowledged, however, that the vast majority of people, who test positive for HbsAg or HbeAg, never become sick, develop hepatitis, or cancer of any kind.
    For instance, as the first to identify the hepatitis B antigen in their survey of genetic polymorphisms in blood samples, Blumberg and Alter reported that leukemia patients (not liver cancer patients), patients with Down syndrome, hemophiliacs, and blood transfusion recipients tested positive more than the general population for the hepatitis B antigen, yet rarely developed liver hepatitis [8], suggesting there is no specificity or pathogenicity with respect to Au marker and the appearance of the rare hepatitis B syndrome (because these syndromes are manifested due to vastly different etiologies).
    Therefore, despite the presence of (Au) HBsAg antigen in a blood sample of a rare patient with full-blown hepatitis or liver cancer, the antigen did (does) not predict who would (will) develop clinically detectable hepatitis, and is not a specific marker for the development of liver cancer. Consequently, the genetic polymorphic “causes,” or physiological stress “causes” of hepatitis as a form of autoimmune dysfunction or stress have been largely ignored, and instead, an infectious viral cause for hepatitis was advanced, as it was for pellagra, SMON, and a variety of other syndromes.
    Blumberg and his colleagues reasoned that a virus might cause hepatitis because something smaller than bacteria that was associated with inducing transfusion hepatitis could pass through filter pores too small for bacteria to pass. Yet not only viruses, but foreign and antigenic proteins also can pass through these filters, and it has been well established in the medical literature since that era that foreign proteins can profoundly disturb the immune system, specific organs, and organ systems.
    Although some agencies such as the World Health Organization and others claim that about 40-60 percent of liver cancer is attributable to HBV, how do we explain the fact that about 1/3 of Down patients also express the Au antigen, and 1 in 10 leukemia patients express the antigens, according to Blumberg, yet Down syndrome isn’t due to a virus – its due to chromosomal non-disjunction.
    Regardless of what “causes” the rare hepatitis B syndrome or the appearance of the hepatitis B “markers” (which most physicians admit is likely due to an autoimmune disease process set into motion by a viral infection), and despite the ill-defined molecular markers that appear in 1/3 of Down syndrome children, and in 1 in 10 leukemia patients according to Blumberg [8], abundant evidence accumulated by the VAERS and the CDC shows that the hepatitis B vaccine is strongly associated with an unacceptable frequency of debilitating life-long illnesses.
    Despite widespread mandated hepatitis B vaccines for more than a decade, and claims that it can prevent heptatocellular carcinoma, no evidence whatsoever exists linking hepatitis B causally with hepatocellular carcinoma, as no animal models have ever exhibited this carcinoma after experimental infections, and no liver cell culture of normal human or animal liver cells has ever been induced to change into cancerous cells after adding the “hepatitis B agent” to them.
    As titles of papers about Hepatitis B published in journals as prestigious as Science sometimes suggest [9], it is reasonable to ask why neither chimps show liver pathogenicity, cellular damage, or develop anything resembling hepatitis in modern studies when they are experimentally infected with “hepatitis B,” nor do humans show cytotoxic damage either [10]. In this respect, one might reasonably wonder why “hepatitis B” and “hepatitis C,” are not considered primarily acquired autoimmune diseases, rather than infectious viral diseases, since cellular pathology in most cases is not present?
    It also should be added that the antigenicity (the presence of the “hepatitis B” antibodies among the vaccinated) does not persist beyond about 5 years, yet hepatitis infections of all kinds confer immunity and antigenicity for life in those who are unvaccinated and experience a full-blown hepatitis B syndrome that spontaneously resolves in almost all cases. Moreover, despite widespread mandated hepatitis B vaccination in 47 states, liver cancer rates have increased in the US from 4 cases/100,000, in 1992, to 5.5 cases/100,000, since at the end of 1999, and leukemia rates have slightly decreased according to the NCI and CDC’s official records.
    One should rightly ask if a decade even qualifies as long enough to make such claims about a vaccine that prevents liver cancer, or which is associated with 10% of leukemia cases decades later. First of all, epidemiological studies cannot be used to claim a causal connection between the expression of a protein in a person’s blood, and the development, or non-development of a cancer, decades after infection. In addition, a Japanese study” claims that heavy drinking rather than transfusions or cigarette smoking accounted for at least 41% of hepatocellular carcinoma patients harbouring antibodies against hepatitis B and C antigens in this country, 50 years after atomic bombs (not a risk factor for cancer?) were dropped by the U.S. on two of its civilian populations, such as Hiroshima, 175 miles away [11].
    In this regard, the hepatitis B antigens may be only non-specific markers for some cancers or other grave medical conditions, as Blumberg first believed. The claim that seropositivity for HBV markers is linked to liver cancer decades later is unsupported by evidence, and, it is like claiming that a freckle on an infant signals that melanoma will develop decades later.
    As scientists and physicians, or as concerned citizens, we should no longer allow this dangerous state-mandated vaccine program to proceed, while it continues to cause hundreds of vaccine damaged persons for every one person the vaccine supposedly protects.
    By so doing, we are irresponsibly risking the health of a generation of infants and children, without providing parents with information about the adverse vaccine reactions, because of propaganda that suggests that by vaccinating them, we will insure that they will not contract hepatitis B or liver cancer if they grow up to become needle-using drug addicts, persons with multiple sex partners, prisoners, mental health patients, or health care workers exposed to human blood.
    This kind of fear mongering and propaganda not only ignores evidence showing that these possibilities are without foundation, but functions to stifle legitimate questions about the biology of the hepatitis B syndrome, or legitimate questions concerning the benefits and consequences of vaccination that should have been addressed before this (or any) vaccine was mandated. The Advisory Committee on Immunization Practices (ACIP) should have asked the following legitimate questions:

    1. Why is such alarm regarding hepatitis B sweeping across the planet now as a sexually transmitted syndrome, when jaundice (and assumed hepatitis) has been recorded in the medical literature since the time of the Ancient Greeks?

    2. Because it is claimed that hepatitis B can only be spread through venereal contact or through exposure to infected fluids, are humans more promiscuous now than they were during the Eleusinian orgies and Roman bacchanals chronicled by the ancient poets?

    3. Because the hepatitis B molecular markers are non-specific, what evidence is there to substantiate that 350,000,000 people in the world are “carriers” of HBV, and that 1,000,000 people in the US are carriers?

    4. In this regard, why are the projected figures for hepatitis B syndrome given, when data recording the actual incidence of hepatitis B have been available for 20 or more years?

    5. If the hepatitis B antigens are specific for the hepatitis B syndrome, and if these antigens don’t simply represent markers for certain physiological stress responses such as cancer or long term alcohol or drug use, or if the presence of the hepatitis B antigens don’t merely represent the different incidence and expression of certain Human genetic polymorphisms (differences in the kinds of molecules found in the blood of different peoples, as was originally thought by Blumberg), then why did Bluberg and his collaborators find the hepatitis B antigens present in a vast majority of healthy people who never develop hepatitis, or in patients experiencing other non-liver related illnesses or genetic disorders? In this same context, why did Blumberg clearly indicate that when Millman came to his laboratory in June of 1967, “and calculated the amount of Au in the serum of carriers and estimated that in some it amounted to about 1% of the serum proteins, that his immediate response was that if this was all virus it would be incompatible with the life of the carrier” (p7124, ref. 8)?

    6. Do leukemia and hepatocellular carcinoma share something in common other than a high likelihood of generating molecular mimicry, or other types of mimicry, or is the antigen merely expressed in both diseases in persons whose immunology is altered by cancer, alcoholism, autoimmune stress, or altered for some other reason?

    7. If a hepatitis B (or C) virus could by themselves cause liver cancer decades after infection, then why does the microscopic percentage of those who exhibit the hepatitis B antigens and who develop chronic clinically detectable liver disease, require carcinogenic co-factors “such as fungal aflatoxins” (p. 7121 paragraph 4), or a lifetime of alcohol abuse or drug consumption to develop cancer [8]?

    8. Why can’t the hepatitis B virus (and C virus) be isolated according to standard isolation techniques, even after a Roman effort and after decades of trying, and why did Blumberg insist that nucleic acids were not recoverable from these “virus isolation” preparations (page 7124 paragraph 6 ref. 8), but were inferred to be a virus? In this same context, why did Blumberg clearly present the fact that “Millman and London found that partially purified Au particles that presumably also contained whole virus particles, which we had not yet visualized, could be transmitted by inoculation into experimental animals. The fully purified particles from which the whole virus had been removed were not infectious. The implication was that we could separate the non-infectious particles containing only the surface antigen from the pathogenic whole virus particles.” Is this reason to mount a global vaccine campaign, against what may be inherited genetic and biochemical polymorphisms, that Blumberg believed were at the basis of Au-associated morbidity? Why did Blumberg state that”Additional studies, some of which are still in progress, were consistent with a genetic susceptibility to persistent infection with HBV, which is part of a complex interaction of polymorphic systems. Hence the research on genetic polymorphisms related to differences in disease susceptibility was central to the discovery of HBV” (page 7123 paragraph 9, reference 8)?

    9. What substance(s), then, were actually isolated from sick persons, and modified and developed by Merck as antigenic material to make hepatitis B the first “molecularly derived recombinant” vaccine?”

    10. Why don’t supposedly infectious and pathogenic hepatitis B isolates induce liver disease in chimpanzees, mice, or other organisms [9, also see 10]? Why doesn’t it induce either liver cancer or leukemia in animals? Why have there been no instances reported where “the hepatitis B virus” generated a pathological effect in animal models, or in liver cells infected in vitro that even remotely resembles the hepatitis B syndrome’s hallmarks in those tiny fraction of seropositive individuals who exhibit morbidity consistent with the hepatitis B syndrome?

    11. If the recombinant vaccine is molecularly specific against a hepatitis B virus and if the vaccine confers long-term immunity, then why does the vaccine ‘wear off’ after only several years? By contrast, when the real hepatitis B syndrome resolves in the vast majority of persons in nearly 100% of all cases who develop jaundice and demonstrable liver pathology, then why does this mild and transient syndrome provide lifetime immunity, and produce detectable antibody titres of the hepatitis B antibodies for at least 50 years [5]? If these data are correct and acknowledged even by the vaccine manufacturers, then what is the logic behind vaccinating newborns when their immune and digestive systems are developing and fragile, and when their often hypothesized membership into in IV injecting, multiple sex partner, or blood product exposure risk group might occur a decade or more after the antibodies generated by the vaccine can no longer be detected?

    12. Why have some studies shown an increase in the hepatitis B syndrome when infants are vaccinated? (EG. “Children vaccinated in infancy are at increased risk of hepatitis B virus infection in the late teens” [12]?

    13. Why is the hepatitis B vaccine still mandated after a congressional hearing that put its safety in question, and why aren’t are parents given any information at all about the possible adverse effects of the hepatitis B vaccine that are listed on the manufacturer’s package inserts?

    14. Finally, is vaccine policy written according to politics rather than prudence?

    The Illinois Department of Public Health versus the Parent Teachers Association of Illinois

    A small group of physicians and scientists gained the support of the Illinois PTA in a unanimous decision to support a current halt to the current mandated hepatitis B vaccine. Another way of saying this is that every school representative present at the convention, when shown the data we had obtained, had agreed with our concerns, and immediately held a brief session to advance a motion to direct PTA funding to disseminate literature so that parents would be informed.
    This group of perhaps a thousand parents (mostly women), appeared to have only one concern: the total welfare, protection, and education of the school children of Illinois.
    It should be stated emphatically, that the current hepatitis B mandate threatens not only our children’s health, but also serves to threaten our children’s education and admission to all kinds of institutions (day care and school admission), with the bluff that “if you don’t get your kid vaccinated against this STD, that is detected only in subpopulations of injection drug users and perhaps highly promiscuous persons, healthy black Australian aboriginal men, Micronesians, Vietnamese, Taiwanese, Native Americans, patients with Down syndrome, leukemia and transfusion recipients, he or she cannot enter school to learn how to read and write.” This is not overstating it. Children cannot gain admission into day-care, Kindergarten, elementary schools, junior highs, high schools, and now even colleges, without showing evidence of a mandated (federally-recommended), and dangerous vaccine (hepatitis B).
    Pursuing these issues, we presented the current head of the IDPH (Illinois Department of Public Health Director Whitaker and his staff), with the same publicly available data from Medline, the vaccine manufacturer’s package insert warnings, data from the Vaccine Adverse Events reporting System, the CDC, Vaccine-link, and other databases, that we had presented to the Illinois PTA convention. After visits with numerous Senators, and public officials during the past several years, over a year later, in June of 2005, we finally were granted a brief meeting with the IDPH, after they could put us off no longer.
    As a response to our pleas to institute informed consent regarding the dangers of the hepatitis B vaccine’s side effects and safety record as it appears on the Federal governments VAERS database, and after many weeks of deliberation, Dr. Whitaker and his staff emailed us a one paragraph letter stating:

    “Parents are currently given enough informed consent.”

    Well, one may ask Dr. Whitaker, “how do threats that our children won’t be admitted to school unless they are jabbed with the hepatitis B vaccine (a rare syndrome) and whose safety data we have yet to see, constitute, informed consent?”
    Shouldn’t parents at least be given a list of the adverse syndromes induced by the vaccines that are presented on the manufacturer’s package inserts, as shown above on Merck’s insert? Should parents be shown the VAERS data? Should a list of the hundred or so articles on Medline regarding adverse syndromes induced immediately after vaccination, by mostly private physicians? Shouldn’t parents be informed that the data supposedly supporting the safety of the hepatitis B vaccine in neonates doesn’t exist [13].
    Somebody should tell the public, as we have tried to warn for the past several years, that parents have the right to refuse all vaccines or medical treatments on their children’s behalf, with the aid of a publicly-available form on which either religious or philosophical objection to these experimental medical interventions can be declared.
    The school nurse and Public Health Department, or school admittance policies should not be used to threaten you that you cannot enroll your kid, based on the madness surrounding the possibility that your 5-year-old will transmit a sexual, or needle-borne, or blood-product-transmitted “syndrome” that has a 95% or greater spontaneous resolution rate, to someone else’s 5 year old, (when they have sex or shoot heroin in the gym locker-room, or if they share razor blades-are the reasons typically given to support mandatory vaccination) as the pharmaceutical company and Public Health Service logic goes.
    We beg the Public Health Service to regard your own children as potentially at risk for becoming sexually promiscuous and needle-using drug addicts (or health care workers), and use them as experimental subjects of an expensive vaccine possessing a 10.4% rate of adverse events, so they won’t contract a rare disease that poses almost 0 risk, that will resolve without treatment in most cases, that simply produces harmless antibodies as evidence of exposure, or that may represent immunological stress or a simple genetic polymorphism, as Blumberg first proposed. Please leave our infants and children alone.
    Why in the face of all this damning evidence against the vaccine, does the hepatitis B vaccine mandate still stand with no end in sight? It is because new legislation has insured that there is no incentive, compensation laws, or mechanisms in place anymore to guard against dangerous universally mandated experiments.

    The future is here: Medical Terrorism into law

    From the “Biodefense and Pandemic and Vaccine and Drug Development Act of 2005–a bill to amend the Public Health Service Act to enhance biodefense and pandemic preparedness activities, and for other purposes [14] SEC. 319F-3:

    “(a) Authority- As provided in subsection (b), and subject to subsection (b)(1)(C), a manufacturer, distributor [sic; distributor], or administrator of a security countermeasure, or a qualified pandemic and epidemic product, described in subsection (b)(1)(A) or a health care provider shall be immune from suit or liability caused by or arising out of the design, development, clinical testing and investigation, manufacture, labeling, distribution, sale, purchase, donation, dispensing, prescribing, administration, or use of a security countermeasure, or a qualified pandemic and epidemic product, described in subsection (b)(1)(A).”

    Further, subsection (b)(1)(A)(i) reads:

    “(i) IN GENERAL- No cause of action shall exist against a person described in subsection (a) for claims for loss of property, personal injury, or death arising out of, reasonably relating to, or resulting from the design, development, clinical testing and investigation, manufacture, labeling, distribution, sale, purchase, donation, dispensing, prescribing, administration, or use of a security countermeasure or qualified pandemic or epidemic product distributed, sold, purchased, donated, dispensed, prescribed, administered, or used in anticipation of and preparation for, in defense against, or in response to, or recovery from an actual or potential public health emergency that is a designated security countermeasure or a qualified pandemic or epidemic product by the Secretary in a declaration described in paragraph (2).”

    What’s being described here is almost carte-blanche freedom to use untested vaccines, drugs, medical products, or “security countermeasures”. And there is nothing you, or we, can do about it because it is in the interest of “National Security.”

    References

    [1] 2003CDC MMWR January 24, / 52(RR01):34-6.
    [2] Merck and GallaxoSmithKline package inserts.
    [3] Marshall E, Science; 07/31/98, 281(5377):630.
    [4] The Gambian study: Whittle et al., Observational study of vaccine efficacy 14 years after trial of hepatitis B vaccination in Gambian children. BMJ, 2002 Sept. 14; Vol 325.
    [5] Black FL, Jacobson DL. Hepatitis A antibody in an isolated Amerindian tribe fifty years after exposure. J Med Virol , 1986 May;19(1):19-21.
    [6] 2003 CDC MMWR report.
    [7] el-Sawy IH, Mohamed ON. Long-term immunogenicity and efficacy of a recombinant hepatitis B vaccine in Egyptian children. Eastern Medi terranean Health Journal Vol. 5, Issue 5, p. 922-932, 1999).
    [8] Blumberg BS. Hepatitis B virus, the vaccine, and the control of primary cancer of the liver. PNAS, 1997; 94:7121-5.
    [9] Guidotti et al. Viral clearance without destruction of infected cells during acute HBV infection. Science. 1999 Apr 30; 284:825-9.
    [10] Ordog et al., Perinatal and intrafamily transmission of hepatitis B virus in three generations of a low-prevalence population J Med Virol., 2003 Jun;70 (2):194-204.
    [11] Pyong et al. Case-control study of hepatocellular carcinoma among Koreans living in Osaka, Japan. Jpn J Cancer Res. 1994 Jul;85(7):674-9.
    [12] Hilton Whittle, Shabbar Jaffar, Michael Wansbrough, Maimuna Mendy, Uga Dumpis, Andrew Collison, Andrew Hall. Observational study of vaccine efficacy 14 years after trial of hepatitis B vaccination in Gambian children. BMJ vol 325, 14 September, 2002.
    [13] Lewis E, Shinefield HR, Woodruff BA, Black SB, Destefano F, Chen RT, Ensor R; Vaccine Safety Datalink Workgroup. Safety of neonatal hepatitis B vaccine administration. Pediatr Infect Dis J. Nov;20(11):1049-54, 2001; Also, Testimony of Dr. Marc Geier at IOM hearing, Aug. 2004.
    [14] http://thomas.loc.gov/ Search Bill Title or Number – S.1873RS click ‘enter bill number.’

  269. #271 Robster, FCD
    July 9, 2007

    Andrew, why don’t you just link to your rants instead of serving copypasta. Or are you afraid that we will notice that your letter is reproduced on the crackpot AAPS site (god complex group that wants no oversight of medical practices)?

  270. #272 Adele
    July 9, 2007

    Notice everyone that the question was, how does Andrew explain lack of RT activity in samples that lack actively replicating virus in the experiment I described.

    Andrew had no response a few weeks ago, no response today. He just repeats himself like he hasn’t been debunked.

    Instead of an explanation for RT he copies reams on Hepatitis vaccine.

    So where’s the explanation? Andrew is obviously more interested in his own self promotion than developing an idea further.

  271. #273 Adele
    July 9, 2007

    After I hit post for my comment about outlawing seatbelts and stuff I realized there are actually alot of people who agree with all of that! Probably alot of them are also HIV denialists. And some AAPS members like Robster says.

    Doesn’t matter how hard you try to parody someone like that they’re always a step ahead of you in making a fool of themself.

  272. #274 DT
    July 9, 2007

    So Andrew has spammed us with a cut and paste about Hepatitis B. I know he isn’t too bright, but surely he must know this is a thread about HIV?

    Anyhow, he would have us believe hepatitis B is a harmless irrelevancy from antiquity, where no one gets ill, and where vaccinees get more problems than do those catching Hepatitis B. In fact, it appears from his claims that he thinks Hepatitis B does not exist at all. What next, TB denial, germ theory denial??

    Welcome to the surreal world of denial, folks.

    A few facts:
    Hepatitis B:
    Acute phase: manifestations range from subclinical (70%) to icteric hepatitis (30% – generalised weakness, nausea and vomiting, jaundice, anorexia for up to 3 months) and, in some cases, and fulminant hepatitis in 0.1-0.5% of cases (liver failure and death).
    Chronic phase: (This may occur in those who have failed to clear hepatitis during their initial illness, usually around 5-10% of all cases). Manifestations are chronic hepatitis, cirrhosis, hepatocellular carcinoma (and death).
    Extrahepatic manifestations also can occur with both acute and chronic infection, usually in about 10-20% of cases. These include a serum sickness-like syndrome manifested as fever, skin rashes, arthralgia and arthritis. Serious complications may occur in the form of polyarteritis nodosa and renal glomerular disease and nephrotic syndrome.

    (if I were Maniotis, at this point I would scare-monger even more by cut and pasting dozens of pages of horrible sounding consequences from all these conditions, but I’ll keep things brief)

    In those who acquire Hep B perinatally, there is initial immune tolerance and few apparent problems. All of these kids become carriers, but at around 30 years of age immune tolerance is lost. Seroconversion can result in all the above conditions, and death from hepatic failure may result. Only 20% of people will spontaneously clear the virus when infected perinatally.

    There are 2 billion individuals with serological evidence of hepatitis B infection worldwide. Of these, 400 million are chronic carriers and 500,000 to 1.2 million will die annually from cirrhosis and hepatocellular carcinoma.
    (See Epidemiology and natural history of hepatitis B. McMahon BJ. Semin Liver Dis. 2005;25 Suppl 1:3-8).

    Vaccination:
    Using the definition of >10 IU/L anti-HBs as a positive response, the overall seroconversion rate is about 95 percent in healthy adults.

    The most common adverse reaction is soreness over the site of injection (10-20%). 1-3 % report mild low grade fever, malaise, headache, joint pain and myalgia. These adverse reactions are usually mild and resolve completely.

    The only real possible concern about the vaccine which was thought to be visible above “background noise” was multiple sclerosis. Some reports of a possible association prompted the French Government to suspend routine school-based vaccination for hepatitis B in October 1998. However, at least six subsequent studies have failed to show a statistically significant temporal or causal association between hepatitis B vaccination and multiple sclerosis.

    Studies on vaccine reactions:
    These are best determined within the context of follow up studies on cohorts of vaccinees, rather than the VAERS reporting system which often registers uninterpretable noise.

    Frequency of adverse reactions to hepatitis B vaccine in 43,618 persons. McMahon BJ; Helminiak C; Wainwright RB; Bulkow L; Trimble BA; Wainwright K. Am J Med 1992 Mar;92(3):254-6.

    PURPOSE: To determine the incidence of adverse reactions to hepatitis B plasma-derived vaccine. PATIENTS: Alaska natives (43,618) who received 101,360 doses of hepatitis B vaccine. METHODS: All adverse reactions, excluding transient fever, myalgia, or soreness lasting less than 3 days, were reported. An intradermal skin test was developed to test purported adverse reactions. Records of the entire population were reviewed for Guillain-Barre syndrome (GBS). SETTING: A statewide hepatitis B control program for Alaska natives. RESULTS: Possible adverse reactions occurred in 39 persons. The most frequent adverse reactions were myalgia/arthralgia lasting longer than 3 days (14), followed by skin rashes (eight) and dizziness (seven). Skin tests were performed on 13 persons and were positive in five. Six of the persons with negative skin tests and eight persons who did not undergo skin testing received additional doses of vaccine without any adverse reactions. No increased incidence of GBS was found in the vaccinees. CONCLUSION: Hepatitis B vaccine is safe and most adverse reactions are coincidental.

    Nevertheless, even the VAERS system gives Hep B vaccine the green light:
    Recombinant hepatitis B vaccination of neonates and infants: emerging safety data from the Vaccine Adverse Event Reporting System. Niu MT; Davis DM; Ellenberg S. Pediatr Infect Dis J 1996 Sep;15(9):771-6.

    METHODS: US reports associated with HB vaccination and received between January 1, 1991, and May 31, 1995, by the national Vaccine Adverse Events Reporting System (VAERS) were reviewed as a case series. RESULTS: During 1991 through 1994, 12,520 (32%) VAERS reports were received for events temporally associated with administration of HB vaccine, of which 14% were received for neonates and infants. More reports described serious outcomes for neonates (under 0.1 year old) than for other age groups (40% vs. 6 to 15%). HB alone was administered to 58 (97%) neonates; review of these reports did not reveal unexpected serious events. Among infants (0.1 to 0.9 years old) 192 (9%) received HB vaccine alone and 1469 (66%) received HB in combination with diphtheria-tetanus-pertussis (DTP) vaccine. Similar serious adverse events reported in neonates and infants included fever, agitation and apnea. Events reported for infants receiving HB/DTP and DTP alone were similar and differed from reports filed for infants receiving HB vaccine alone, suggesting that these events may be associated with use of DTP vaccine. CONCLUSIONS: This review shows no unexpected adverse events in neonates and infants given HB vaccine despite use of at least 12 million doses of vaccine given in these age groups. Although VAERS lacks the ability to distinguish coincidental events from true vaccine reactions, this database represents the largest case series of events temporally associated with HB vaccination of neonates and infants.

    MY CONCLUSION:
    Bring on the vaccine, please!!

  273. #275 DT
    July 9, 2007

    Re: the Maniotis Hep B letter on the crackpot AAPS site:

    I can’t help noticing that Maniotis has thrown away the concept of quoting from authority, at least.
    The AAPS Hepatitis Paper is authored by Maniotis, his wife(?) in her role within a Parent Teachers Association, a surgeon from Chicago, a Chinese ophthalmic pathologist and finally a physical chemist (whtever one of those is).

    All of them are obviously global specialists in the relevant fields of epidemiology, immunology, infectious disease and microbiology, and eminently placed to conclusively determine and pronounce on the existence of Hepatitis B, its sequelae and the ability to prevent it through vaccination.

  274. #276 Andrew Maniotis
    July 11, 2007

    Quick question folks.

    How do you sleep at night given Gallo’s Parenzee trial testimony when he says that “if nobody here in the court room is “HIV” positive, there will be no molecules of “HIV” in their blood!

    Together with former head of the NIH Varmus saying that RT is found in worms, mammals, bacteria, and other critters?

    Together with Temin stating that RT is found in many normal contexts?

    Together with Dura et al., saying that they can find it in the thymus of “HIV-negative children.”

    Together with marketing magazines as I have already quoted saying that it is in a number of normal contexts.

    Together with the cancer literature I am familiar with saying that it is in the expression patterns of a variety of tumor cells (tumor cells come from normal pre-existing non-tumor cells as far as I have been able to determine. Where did they pick up their RT, from HIV?

    Where did “HIV” supposedly acquire it’s RT? From outer space? Or from normal (or diseased) cells? It is supposedly a virus after all-with all of its genome, and proteins, and lipids ultimately derived from cells.

    Gelderblom says RT is part of the pol gene along with IN and PR. Where did “HIV” acquire its RT from if not from normal cells (or diseased cells with messed up expression patterns)?

    Just wondering.

    Andy

  275. #277 DT
    July 11, 2007

    Still in wonderland, I see.
    Well I too am wondering….. Why can’t you stick to the point? Why must you post disconnected, rambling irrelevancies that have nothing to do with the thread topic nor previous posts in the discussion? When are you going to tell us your hypothesis as to what causes AIDS?

  276. #278 Adele
    July 11, 2007

    Wonderland, that’s a good one. Nothing Andrew says touches my questions about RT from above.

    In case Andrew had problems reading, the question was, how does Andrew explain lack of RT activity in samples that lack actively replicating virus in the experiment I described. Andrew had no response a few weeks ago, no response today. He just repeats himself like he hasn’t been debunked.

    And no response today.
    Instead he wrote

    How do you sleep at night given Gallo’s Parenzee trial testimony when he says that “if nobody here in the court room is “HIV” positive, there will be no molecules of “HIV” in their blood!

    Same way I sleep at night knowing if there were never any lizards in my bedroom there aren’t any lizard molecules in my bedroom.

    Together with former head of the NIH Varmus saying that RT is found in worms, mammals, bacteria, and other critters?

    Who disputed this? Glycoproteins are also found everywhere. A sheep has glycoproteins, doesn’t mean HIV can’t have glycoproteins too. Doesn’t mean a sheep glycoprotein is the same as a HIV glycoprotein.

    Together with Temin stating that RT is found in many normal contexts?

    Define normal? Like I said before RTs in your body are tightly regulated. You usualy just see them made in cancer cells. Other places they’re silenced. Maybe Andrew needs to learn more about epigenetics.

    Together with Dura et al., saying that they can find it in the thymus of “HIV-negative children.”

    This is new. Dura et al find HIV RT in the thymus of HIV negative kids? Did they do an RT assay? Did they use antibodies? Did they sequence the protein to confirm it? Or was it just a crap experiment with a cross-reacting antibody they didn’t control right? I don’t know since Andrew didn’t even tell us what journal this was or when it was

    Together with marketing magazines as I have already quoted saying that it is in a number of normal contexts.

    “marketing magazines”?! Did Andrew find anything in comic books? Like maybe the Silver Surfer is made of 60% HIV RT?

    Together with the cancer literature I am familiar with saying that it is in the expression patterns of a variety of tumor cells (tumor cells come from normal pre-existing non-tumor cells as far as I have been able to determine. Where did they pick up their RT, from HIV?

    This was covered before. In normal cells TERT the reverse transcriptases for telomere maintenance are silenced epigenetically. Cancer cells get their programming messed up and the RT gets turned on. You can get RT activity you can also measure levels of RT RNA. Guess what? It’s not even close to HIV RT RNA.

    Where did “HIV” supposedly acquire it’s RT? From outer space? Or from normal (or diseased) cells? It is supposedly a virus after all-with all of its genome, and proteins, and lipids ultimately derived from cells.

    I don’t know what to say. I hope Andrew isn’t serious about this. If he is maybe he could talk to some of his colleagues who teach virology. HIV RT translates from HIV RNA transcribed from HIV DNA.

    Gelderblom says RT is part of the pol gene along with IN and PR. Where did “HIV” acquire its RT from if not from normal cells (or diseased cells with messed up expression patterns)?

    Gelderblom? Hans R. Gelderblom? Is he the only one who says RT is part of the pol gene? This is from the textbooks decades old. Andrew is being silly. Infected cells make HIV RT when HIV is there to direct the process via DNA and RNA. Uninfected cells don’t make HIV RT. Unless they’re cancer they don’t usually make any RT and if they do no one should confuse it with HIV RT.

    HIV RT is not in uninfected cells.

  277. #279 Dr. Duke
    July 11, 2007

    Andrew may be only a pathologist, and not a biochemist, but he has surely taken enough biochemisty classes to know that he is being dishonest and misleading about reverse transcriptases.

    His arguments are similar to saying that hair is a property of mammals, so finding hair-like stuctures on plant leaves or other organisms makes us question whether mammals exist. Or claiming that maybe the “milk” in milkweed plants can’t be distinguished from mammalian breast milk.

    Reverse transcription activity is not absolutely specific to HIV, and nobody ever claimed it was. All retroviruses have reverse transcriptase, and there are also other types of viral and non-viral reverse transcriptases. Arguing that someone has claimed that reverse transcriptase is absolutely unique to HIV-1 is a classic straw man argument, and Andrew knows very well he is attempting to mislead people with it.

    The reverse transcriptases produced by lentiviruses have a preference for Mg++ over Mn++ for optimal activity, whereas the reverse transcriptases of most endogenous retroviruses and other retroviruses mostly prefer Mn++. However, this is only one of hundreds of different methods of distinguishing one RT from another.

  278. #280 Dr. Duke
    July 11, 2007

    Andrew the pathological liar wrote:
    “7. If a hepatitis B (or C) virus could by themselves cause liver cancer decades after infection, then why does the microscopic percentage of those who exhibit the hepatitis B antigens and who develop chronic clinically detectable liver disease, require carcinogenic co-factors “such as fungal aflatoxins” (p. 7121 paragraph 4), or a lifetime of alcohol abuse or drug consumption to develop cancer [8]?”

    Where [8] was
    Blumberg BS. Hepatitis B virus, the vaccine, and the control of primary cancer of the liver. PNAS, 1997; 94:7121-5.

    So I downloaded this paper and read all of page 7121, and found that paragraph 4 does not state that toxins and/or alcohol abuse are “required” to cause liver cancer:

    “Some patients infected with HBV, HCV, HDV, and probably
    HGV may develop chronic infection. This may follow an
    acute attack; the virus does not resolve, but remains active or
    sub-active in the body for many years. More and more of the
    liver cells are destroyed, scarring occurs, and liver function
    decreases. Chronic liver disease can be life shortening. For at
    least two of the viruses, HBV and HCV, primary hepatocellular
    carcinoma (HCC) may develop, usually many years after
    the initial infection. The probability of HCC increases if the
    chronic carriers also are exposed to other agents, such as the
    carcinogen aflatoxin, which is produced by Aspergillus fungus
    that contaminates poorly stored foodstuffs. There is also
    epidemiological and other evidence that high body iron stores,
    which can be a consequence of excessive iron intake, also can
    increase the probability of HCC.

    Inhalation of certain types of asbestos fiber particles increases the risk of lung cancer. Likewise, chronic exposure to cigarette smoke increases the risk of lung cancer. Inhaling both asbestos and smoking cigarettes has a synergistic effect, increasing the risk of cancer far beyond the additive total of the increase in risk from both.

    Marsella LT, Marmo C, Saracino V, Del Vecchio R.
    The association of asbestos and cigarette smoke in lung cancer. Note 2
    Clin Ter. 2006 Jan-Feb;157(1):53-9.
    PMID: 16669552

    Kurihara N, Wada O.
    Silicosis and smoking strongly increase lung cancer risk in silica-exposed workers.
    Ind Health. 2004 Jul;42(3):303-14.
    PMID: 15295901

    Liddell FD.
    Joint action of smoking and asbestos exposure on lung cancer.
    Occup Environ Med. 2002 Jul;59(7):494-5
    PMID: 12107302

    Contrary to what Andrew would like to confuse people into believing, this does not mean that asbestos exposure is harmless, or that cigarette smoke is “required” in order for asbestos to cause cancer.

  279. #281 The Watcher
    July 11, 2007

    Dr. Duke is a lentivirolgist, probably infecting the New York City area

    Lentivologist derived from Lentivirus (lenti-, Latin for “slow”) is a genus of slow virologists of the Retrovirologist family, characterized by a long incubation period before awaking to or acknowledging the obvious. Lentivirologists can deliver a significant amount of genetic misinformation into the mind of the host, so they are one of the most efficient methods of misinformation. HIVologists, SIVologists, and FIVologists are all examples of lentivirologists.

  280. #282 franklin
    July 12, 2007

    Andrew,
    Here’s your quick question:

    Quick question folks.
    How do you sleep at night given Gallo’s Parenzee trial testimony when he says that “if nobody here in the court room is “HIV” positive, there will be no molecules of “HIV” in their blood!
    Together with former head of the NIH Varmus saying that RT is found in worms, mammals, bacteria, and other critters?
    Together with Temin stating that RT is found in many normal contexts?

    There is absolutely no conflict between these statements. None whatsoever.

    Hyenas have hemoglobin in their blood, but if there are no hyenas in the zoo then there will be no “hyena molecules” in the blood of any of the zoo animals. This is true even though lions have hemoglobin, tigers have hemoglobin, and bears have hemoglobin (Oh My!). They all have hemoglobin, but none of them have hyena hemoglobin.

    Worms make actin, but they don’t make hyena actin.

    Reverse transcriptases are found in all retroviruses and in other cellular contexts, but the only people with HIV reverse transcriptase in their blood are HIV-infected people.

    Andrew, how do you sleep at night knowing your arguments are so lame?

  281. #283 Chris Noble
    July 12, 2007

    Andrew, how do you sleep at night knowing your arguments are so lame?

    I don’t think he sleeps at night. The black helicopters circling around his house keep him awake.

  282. #284 franklin
    July 12, 2007

    Hey Pope,
    I see you dredged up Dr. Maniotis’s false statements about the DAIDS manual:

    However, I followed Dr. PS Duke’s (aka Harvey Bialy I suspect) exciting link and came upon this good old denialist classic, courtesy of our friend Dr. Maniotis:
    The 1997 DIADS Official “HIV” Culturing Manual also exhibits evidence of AIDS denialism. Under quality control,” Section VI, page 45, the DAIDS manual
warned “HIV” cell culturists: “Do not use PHA stimulated PBMC older than 3 days post stimulation” when
testing them for the absence of “HIV” from your healthy donor source In non-technical language, DAIDS claimed that the way to make sure control cultures (healthy donor source) were indeed not infected with “HIV,” was to quit
watching the control cultures after 3 days. Perhaps DAIDS simply followed Montagnier’s and Gallo’s AIDS denialism, and accepted that it was PHA, and not “HIV” that could, after 3 days, induce the same effect on T-cells not incubated with “HIV” (A), as it did with infected cultures (2-9)? Nevertheless it is denialism, because they warn culturists to terminate control cultures after 3 days, and thus control cultures are NOT terminated at the same times as the “HIV” infected cultures.

    I apologize for repeating myself, but I’m not sure if you saw Dr. Maniotis’s most recent explanation of his DAIDS blunder in the Smallpox thread:

    The DAIDS 1997 official “HIV” culturing manual, under quality control, Section VI, page 45, advocates, “Do not use PHA stimulated PBMC older than 3 days post stimulation” when testing them for the absence of HIV from your healthy donor source,”
    was taken out of context of the argument I was making because in
    “The Reporting Results Section which follows (section VII) a rationale follows that obviously employs both healthy (or non-”infected” cells-although I don’t think anybody tests intentionally non-”infected cells”) in a manner that is irrational to my way of thinking, unless I really don’t understand what is going on.

    If you read the relevant protocols that Maniotis cites from the DAIDS Manual, then you will see that his current explanation, namely, that he “really don’t understand what is going on” is exactly right.
    As already explained by Dale, the assay requires non-infected cells. It is the ability of the patient specimen to induce a productive infection of the normal cells that forms the basis of the assay. The stipulation that the normal cells should not be older than 3 days post-stimulation does not apply to only the control cultures (as falsely claimed by Maniotis), rather it is a quality control mechanism applied to all of the assays (control or patient specimen) to make sure that the normal cells are still able to support a productive infection and thereby avoid false negative results that might be obtained using older cells. This is very clearly explained in the DAIDS Manual, as well as in the papers cited in the bibliography included in the DAIDS Manual. The fact that the use of non-infected cells is “irrational to (Maniotis’s) way of thinking” simply illustrates that he has no clue as to how the assay works and proves that (as Maniotis puts it) he “really don’t understand what is going on.”

  283. #285 Adele
    July 12, 2007

    Chris wrote
    The black helicopters circling around his house keep him awake.

    Don’t forget the firetrucks outside Andy’s house spraying toxic pesticides and mercury through his open windows until his spaghetti tastes like confetti.

  284. #286 Andrew Maniotis
    July 12, 2007

    RE:

    The DAIDS 1997 official “HIV” culturing manual, under quality control, Section VI, page 45, advocates, “Do not use PHA stimulated PBMC older than 3 days post stimulation when testing them for the absence of HIV from your healthy donor source,”

    Why doesn’t somebody answer my simple question. Let me rephrase it using small words:

    The Reporting Results Section which follows (section VII) a rationale follows that apparently employs both healthy (or non-infected cells) and infected cells-although I don’t think anybody tests intentionally non-”infected cells”) in a manner that is rational or what we would considered CONTROLLED. For example:

    Cultures whose supernatant meet one of the following criteria are considered culture positive IF:

    “Two consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml (read: from a healthy donor source), of which the second value is at least four times greater than the first value or “out of range” (O.D.>2) or

    “Two consecutive HIV p24 antigen VQA CORRECTED values (read: from a healthy donor source) that are “out of range (Optical density.> 2); or

    “Three consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml (read: from a healthy donor source), where neither consecutive value is > four times the previous sample, but the third value is at least four times greater than the first,”

    Would you consider a sample negative (read: from a healthy donor source) if the 3 consecutive HIV p24 antigen VQA corrected values read (first test) 25 pg/ml, and (second test) 15 pg/ml, (third test) 5 pg/ml?

    Would you use these cells as uninfected controls?

    Asked another way, are these control cells considered non-infected if they read 25 on the first reading, and 15 on the second and 5 on the third?

    Try a second sample using the first criterion stated above:

    “Two consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml, of which the second value is at least four times greater than the first value or out of range” (O.D.>2)

    First sample =6pg/ml: second sample)=23pg/ml

    Yes? No? Maybe better get other “healthy cells” than go with a 6 and a 23? Or are these two readings enough to say, “Aw-what the heck-they aren’t over 30pg/ml and the second series ain’t quite 4 times greater that the first value of 6, so I will just tell the doc that they are negative, and will tell the patient nothing about it.

    Cheers,

    Andy

  285. #287 franklin
    July 12, 2007

    Andrew,

    Is that your question?

    I thought your original question had something to do with cheerleaders.

    I think a PhD from Berkeley should be able to figure that one out all by himself.

  286. #288 Adele
    July 12, 2007

    Andrew is still dodging. He demands answers but he won’t give any.

    I will answer his question about p24 readings and there’s a good answer.

    BUT only after he gives us a honest response to why I don’t find RT activity in any of my controls. I described my experiment above. I asked simple questions. Andrew Maniotis hasn’t been able to answer.

  287. #289 Andrew Maniotis
    July 12, 2007

    Adele,

    The answer to your question is simple-but it is a tautology.

    If I put some toxic antibody on my cultures, and do a total RNA reading, I get virus-like particle prodcution, and, cell death, all kinds of strange effects. If I put serum from a lupus patient, for instance, on tumor cell cultures, I get viral like production, and increases in nucleic acid “shedding” in the supernatant. Nothing specific.

    In your experiment, there is no proof you are adding something called “HIV” because, according to those of us that are critical of the HIV=AIDS hypothesis, it hasn’t been demonstrated with the certainty that de Harven, for instance showed with MMTV, and I posted the comparative pictures in a previous blog-without any of you even bothering to try to give a response. So yes, you get an increased reading because you are adding something the cells don’t like that you have not characterized.

    You are adding something indeed to the experimental group that gives you those readings in the thousands compared to the controls-you just haven’t proven to us that you are adding something called “HIV” and haven’t shown that if it is indeed a virus you are adding, that it is infectious and induces any of the 47 AIDS-defining illness.

    I and many others, in addition, criticise your use of RT to measure what you think is “HIV,” but alas, again there is a tautology, and judging by the lame comments above,

    “Hyenas have hemoglobin in their blood, but if there are no hyenas in the zoo then there will be no “hyena molecules” in the blood of any of the zoo animals. This is true even though lions have hemoglobin, tigers have hemoglobin, and bears have hemoglobin (Oh My!). They all have hemoglobin, but none of them have hyena hemoglobin.

    Worms make actin, but they don’t make hyena actin.”

    why should I even bother, but here goes. How do you know that the RT you are measuring isn’t endogenous RT that isn’t stimulated once you sprinkle your toxic “antibody” you call “HIV” on your experimental cells (after all you said it is epigenetically silenced in most normal cells-so it is there somewhere).

    “The reverse transcriptases produced by lentiviruses have a preference for Mg++ over Mn++ for optimal activity, whereas the reverse transcriptases of most endogenous retroviruses and other retroviruses mostly prefer Mn++. However, this is only one of hundreds of different methods of distinguishing one RT from another.”

    This is pure crap because you haven’t isolated “HIV” at anywhere close to sufficient purity to claim you have a distinct RT from the “epigenetically silenced” RT that is endogenous.

    Let me try to use some letters to explain it to you.

    A=”HIV” B=Cells. “HIV” particles contain actin, ezrin, and a list of other molecules that Bess et al., found, which again nobody wanted to comment on when I posted that material. Supposedly, “HIV” contains a specific RT, let’s call it HIVrt.

    Back to the letters.

    A+Art +B +Brt=the crud you call a purified “HIV” prep that Bess and others have said in the titles of their papers actually contain more crap than “HIV.”

    You need to separate A+Art from B=Brt in order to claim “HIV” RT is special. You nor anybody else has not done this to anywhere close to the purity needed to make the outragious claims made by all of your religious catechisms.

    Now will you answer my question. Yes, No, Maybe?

  288. #290 franklin
    July 12, 2007

    Andrew,

    HIV reverse transcriptase has been molecularly cloned and can be easily distinguished from any reverse transcriptase encoded in the human genome. Just as hyena hemoglobin can be easily distinguished from the hemoglobin of other mammals.

    Your starting to sound like a case of social promotion at UC Berkeley.

  289. #291 Richard Jefferys
    July 12, 2007

    Perhaps Maniotis shares Etienne de Harven’s views on molecular biology:

    http://www.virusmyth.net/aids/data/edhrecol.htm

    In the article, de Harven (currently president of the “Rethinking AIDS” group) rails against the rise of molecular biology, scorns the “virus hunters” and rues Nixon’s War on Cancer Act. Yet de Harven was happy to feed at the trough of the US Government-sponsored Special Virus Cancer Program from at least 1963 through 1978. I emailed him once to ask about his experience with the SVCP and why he doesn’t mention it on his CV; he never replied.

  290. #292 Richard Jefferys
    July 12, 2007

    Might as well also mention that T cell responses against HIV’s reverse transcriptase are readily detectable in HIV-infected individuals (just Google “rt-specific ctl”). I wonder if Andrew Maniotis has ever talked to a cellular immunologist about their “outragious claims” regarding HIV infection and AIDS.

  291. #293 Kevin
    July 12, 2007

    This is pure crap because you haven’t isolated “HIV” at anywhere close to sufficient purity to claim you have a distinct RT from the “epigenetically silenced” RT that is endogenous.

    Well-said, Dr. Maniotis.

  292. #294 Dr. Duke
    July 12, 2007

    Andrew wrote:

    “This is pure crap because you haven’t isolated “HIV” at anywhere close to sufficient purity to claim you have a distinct RT from the “epigenetically silenced” RT that is endogenous.”

    What part of “infectious molecular clone” do you fail to understand?

    Grisson RD, Chenine AL, Yeh LY, He J, Wood C, Bhat GJ, Xu W, Kankasa C, Ruprecht RM.
    Infectious molecular clone of a recently transmitted pediatric human immunodeficiency virus clade C isolate from Africa: evidence of intraclade recombination.
    J Virol. 2004 Dec;78(24):14066-9.
    PMID: 15564517

    Brehm JH, Koontz D, Meteer JD, Pathak V, Sluis-Cremer N, Mellors JW.
    Selection of Mutations in the Connection and RNase H Domains of Human Immunodeficiency Virus Type 1 Reverse Transcriptase that Increase Resistance to 3′-Azido-3′-Dideoxythymidine.
    J Virol. 2007 May 16;
    PMID: 17507476

    Hu Z, Giguel F, Hatano H, Reid P, Lu J, Kuritzkes DR.
    Fitness comparison of thymidine analog resistance pathways in human immunodeficiency virus type 1.
    J Virol. 2006 Jul;80(14):7020-7.
    PMID: 16809307

    Hammond JL, Parikh UM, Koontz DL, Schlueter-Wirtz S, Chu CK, Bazmi HZ, Schinazi RF, Mellors JW.
    In vitro selection and analysis of human immunodeficiency virus type 1 resistant to derivatives of beta-2′,3′-didehydro-2′,3′-dideoxy-5-fluorocytidine.
    Antimicrob Agents Chemother. 2005 Sep;49(9):3930-2.
    PMID: 16127074

    Abram ME, Parniak MA.
    Virion instability of human immunodeficiency virus type 1 reverse transcriptase (RT) mutated in the protease cleavage site between RT p51 and the RT RNase H domain.
    J Virol. 2005 Sep;79(18):11952-61.
    PMID: 16140771

  293. #295 Dale
    July 12, 2007

    How do you know that the RT you are measuring isn’t endogenous RT that isn’t stimulated once you sprinkle your toxic “antibody” you call “HIV” on your experimental cells (after all you said it is epigenetically silenced in most normal cells-so it is there somewhere).

    If the RT you were measuring were endogenous RT, epigenetically silenced or not, you would still be able to find its sequence in a non infected cell genome ie. in the DNA of your cells both before and after the addition of HIV.

  294. #296 Roy Hinkley
    July 12, 2007

    Andrew Maniotis asked:

    How do you know that the RT you are measuring isn’t endogenous RT…

    Why Andrew, you simply use your secret decoder ring.

    We must have been remiss in issuing yours.

    Here it is:
    http://psyche.uthct.edu/shaun/SBlack/geneticd.html

    May it serve you well.

  295. #297 Adele
    July 13, 2007

    I didn’t expect Andrew to respond since there’s no good answer to my questions except HIV on cells infects and later produces RT when it’s a functional virus. But he did respond and that’s interesting because the main thing you take away is, he didn’t understand the question or my experiment.

    you get an increased reading because you are adding something the cells don’t like that you have not characterized.

    First Andrew should remember I also put heat-inactivated virus on the cells. I also put a mutant virus that doesn’t complete its whole replication. These virus have the same stuff as regular virus. If the cell doesn’t like the regular virus it shouldn’t like the mutant virus because their exactly the same thing except for a couple base changes in the RNA inside them. Like maybe five changes or ten changes or maybe less out of 10,000 The heat inactivated is exactly the same except it’s been denatured. at least partly.

    Second if the replicating virus is the only thing the cell doesn’t “like” it’s weird you get the exact same result if you transfect proviral DNA into the cell instead of using virus. Replicationg virus, you get ginormous RT, same proviral DNA except with two or three mutations, you get no RT. So if Andrew’s right the cell can go, “Hey there’s a G at 4533 instead of a A so let’s not respond to this virus, or DNA.” That’s absurd. If Andrew’s got evidence it’s not he needs to show it or shut up with his nutty conspiracy theories.

    Third if Andrew ever learned more about HIV research he would know you always characterize the virus you make. You sequence it to make sure it’s not contaminated with other strains. You do antigen tests on it to see how much of it there is. You can do infectivity for how infective the prep is, that’s kind of the same thing as before. If you have alot of techs and money you could do an EM too but why? Etienne doesn’t like it but molbio does the same verification alot easier. Some people even do mass spec and stuff to look at viral and host proteins in the virion. Characterizing your virus is a standard thing.

    By the way I know some people who do protein stuff with viruses. I don’t think they’ve ever seen endogenous RT in the virion. Hmm.

    So Andrew didn’t answer my question to satisfy anyone who knows something about this. But he did answer it in his own way and I promised, so. Here’s my answer to his idiotic quesiton about p24 and being positive if a reading’s near the cuttoff.

    A p24 antigen test shouldn’t be used as your only diagnosis test. Also a cuttoff isn’t so set as you want to think. If it’s close you do it again and you do other tests like PCR to make sure its not false.

    There’s a thing in statistics. Margin of error. These antigen tests measure colors. Is there anything that’s completely colorless. So you get a value for every test you do and it’s never zero. In your margin of error there can be values of protein concentration. It doesn’t mean there’s actually protein there. That’s why they come up with some kind of cuttoff because in their testing they did with the ELISA with recombinant protein and also validated samples probably hundreds or thousands of them they know a certain percentage of positive samples will always be above that usually WAY above it. And they know negative samples will always be below it.

    Yes rarely you’ll get a antigen result near the cuttoff depending where you are in the infection. Usually there’s no question though. If there is there’s a hundred other tests to do to confirm it.

    Andrew is completely full of it, making up hypothetical stuff he doesn’t even know about to hang on.

  296. #298 Andrew Maniotis
    July 13, 2007

    So I guess you would run with the cells being 29pg/ml or some similar permutation as being “normal healthy controls.” You guys really don’t know how to do a controlled experiment. A simple yes is really all you needed to say. Or yes, we use cells that are showing 28pg/ml for our healthy normal controls, while cells over 30 are considered infected.

    RE: the heat inactivated virus.

    You are correct. I did forget about the heat inactivated virus not ringing up the counts in the experiment you described. Normally this would be a good control for real viruses like Herpesvirus. But what you detect here must be an endogenous noxious protein that is heat stable?

    You can’t say otherwise-sequencing or not-mobio or not. It doesn’t matter cause there ain’t no gold standard which is the virus itself. You don’t know if the sequence you are consistently getting is the same sequence due to the same stimulus generating the same pathological effect.

    RE:
    “If it’s close you do it again and you do other tests like PCR to make sure its not false.”

    I’m sure the DIADS folks and those reference labs that follow their manual do this over and over until they find “a healthy donor source” that would consistently ring up <30pg/ml or some relative equivalent on a different test. How often does it happen, I ask, where you get a 21 and then a 29pg/ml reading? 2 or 12 times out of 37 million times for “low risk folks?” Only a false positive rate of 10/12, regardless of the retest and the 8 “seroconversions” to the PCR test’s rate of detection?

    Wonderful certainty here to risk a person’s life by then convincing them they are going to die.

  297. #299 Adele
    July 13, 2007

    Andrew still missed my controls. Perhaps all those pesticides sprayed through his windows gave him ADHD?

    To recount replicating virus gives ginormous RT. Virus with a post-entry block because of a few bases changed out of 10,000 gives no RT. Heat inactivated virus gives no RT. And Andrew says,

    But what you detect here must be an endogenous noxious protein that is heat stable?

    I guess he means NOT heat stable. Because then his imaginary noxious protein in the virus would cause production of endogenous RT but in heat inactivated virus it wouldn’t.

    Unfortuantely Andrew forgot that other control, the one with a virus that’s got a couple of mutations keeping it from replicating right after it gets into the cell. So our imaginary noxious protein is there and its not heat denatured. But it doesn’t produce that RT effect here!

    That’s not all. We get the same results if we use proviral DNA transfected in. DNA of regular virus, you get RT. DNA of the mutant, again its exactly the same DNA except for like .01 percent changes, doesn’t give you RT. There’s no protein here. Absolutely not that “noxious” human protein Andrew imagines. Just DNA. And the same results.

    Re the p24 thing, I won’t dignify Andrew’s grasping stupidity with a response. I’ll just remind everyone, this is not about patients, it’s about cell culture. No patient should ever be diagnosed based on p24 of 29.4 vs 29.6 and as far as I know no one is. That happens in Andrews fever not reality. And Andrew is the only one trying and convincing people they are going to die, no one says this stuff except the deniosaurs.

    you know everyone is always talking about Monty Python and the knight with no arms and legs. I would say that’s Duesberg. Maniotis is like that but without a body or brain even, a dis embodied mouth that just keeps on going No Gold Standard No Gold Standard. Well Many-lie-tis doesn’t know a gold standard from a hole in the ground.

    Also like William jennings Bryan could have said to him “You shall not crucify mankind upon a cross of gold.”

  298. #300 Robster, FCD
    July 13, 2007

    Excellent takedown, Adele. The controls are solid, especially the proviral DNA.

  299. #301 Andrew Maniotis
    July 13, 2007

    Adele,
    There is no evidence that you aren’t seeing the effects of what you think is “HIV” is harming or infecting the cells in any way: Can’t show it in chimps, in non-activated T-cells (red blood cells, neurons, muscle cells, or whatever cell type you want to be the target of “HIV’s” malicious nature this month), etc. But its fun to publish long papers about culture artifacts like “HIV” or HERV’s, and even more fun to tell the public health agencies that these are emerging threats that need billions thrown at them to increase “HIV” infection with microbicides as Moore and others have accomplished, increase the leading cause of death as liver failure in HAART-treated patients, administer experimental vaccines that damage the immune system, etc.

    You are sure proud and sure of yourself and your science through! Sure hope you are right! By contrast, I hope someday you will realize your errors, and apologize to whom ever will listen to you.

    Gene
    Volume 390, Issues 1-2, 1 April 2007, Pages 175-179
    ASILOMAR 2006

    Copyright © 2006 Elsevier B.V. All rights reserved.

    The potential of retroviral vectors to cotransfer human endogenous retroviruses (HERVs) from human packaging cell lines

    Udo Zeilfeldera, Oliver Franka, Sandra Sparaciob, Ulrike Schönc, d, Valerie Bosche, Wolfgang Seifartha and Christine Leib-Möscha, c, Corresponding Author Contact Information, E-mail The Corresponding Author
    aMedical Clinic III, Faculty of Clinical Medicine Mannheim, University of Heidelberg, 68305 Mannheim, Germany
    bDepartment of Molecular Virology, University of Heidelberg, 69120 Heidelberg, Germany
    cGSF-National Research Center for Environment and Health, Institute of Molecular Virology, 85764 Neuherberg, Germany
    dAlopex GmbH, 95326 Kulmbach, Germany
    eForschungsschwerpunkt Infektion und Krebs, F020, Deutsches Krebsforschungszentrum, 69120 Heidelberg, Germany
    Received 30 June 2006; revised 10 August 2006; accepted 10 August 2006. Received by M. Batzer. Available online 3 September 2006.

    Abstract

    Using a versatile and highly sensitive retroviral microarray, we have investigated particle preparations from three different human packaging cell lines harboring retroviral vector systems based on human immunodeficiency virus (HIV) and murine leukemia virus (MLV). 293Rev/Gag/Poli cells inducibly express high titers of HIV-derived particles for packaging of HIV vectors. The Phoenix-GP and the Anjou 65 cell lines constitutively express MLV vector particles. We compared the transcription profiles of human endogenous retroviruses (HERVs) in all cell lines with the HERV sequences present in the particles. In addition, the influence of the transfected vector plasmid on the copackaging of HERVs was investigated. All particle preparations showed a defined pattern of endogenous retroviral sequences that differed from the cellular HERV expression pattern. HERV transcripts were observed in the particle preparations independent of whether a vector construct was coexpressed or not.

    Furthermore, our results suggest that particle preparations are frequently contaminated by cellular vesicles (exosomes) containing cellular RNAs including HERV transcripts.

    Keywords: Human endogenous retroviruses; HERV; Retroviral vector; Packaging cell line; Copackaging; DNA chip; Microarray; Gene therapy

    Abbreviations: CMV, cytomegalovirus; DEPC, diethylpyrocarbonate; ELISA, enzyme-linked immunosorbent assay; ERV, endogenous retrovirus; GFP, green fluorescent protein; HERV, human endogenous retrovirus; HIV, human immunodeficiency virus; IRES, internal ribosome entry sequence; MLV, murine leukemia virus; MOP, mixed oligonucleotide primers; MMTV, mouse mammary tumor virus; PCR, polymerase chain reaction; PGK, phosphoglycerate kinase; RCR, replication-competent retrovirus; RT, reverse transcriptase; RRE, Rev responsive element; RSV, Rous sarcoma virus; SV40, simian virus 40; VSV-G, vesicular stomatitis virus glycoprotein.

    Corresponding Author Contact Information
    Corresponding author. GSF-Research Center for Environment and Health, Institute of Molecular Virology, Ingolstädter Landstr. 1, D-85764 Neuherberg, Germany. Tel.: +49 89 3187 3270; fax: +49 3187 3329.

    RE:Re the p24 thing, I won’t dignify Andrew’s grasping stupidity with a response. I’ll just remind everyone, this is not about patients, it’s about cell culture. No patient should ever be diagnosed based on p24 of 29.4 vs 29.6 and as far as I know no one is.

    Thanks for answering my question. Its just a shame that people’s lives are based upon your junk science that ejected cause and effect along with controlled experiments.

    Sheesh!

    Andy

  300. #302 Adele
    July 13, 2007

    I told Andrew about my controls. He had something to say about ONE of them. His explanation was a stretch, heat denatured protein, and he got it wrong anyway, he said heat stable protein, but it was a possibility. The others all three of them he can’t respond to because they prove he’s completely wrong. So he makes jokes and insults and pastes alot from irrelevant papers.

    The junk science is Andrew’s. Science that doesn’t have hypotheses or experiments at all. Much less controlled experiments like mine. Actually I wouldn’t call his stuff science.

    Andrew says,
    “There is no evidence that you aren’t seeing the effects of what you think is “HIV” is harming or infecting the cells in any way: Can’t show it in chimps, in non-activated T-cells (red blood cells, neurons, muscle cells, or whatever cell type you want to be the target of “HIV’s” malicious nature this month), etc.”

    I’ve seen HIV infecting two primary cell types this week alone. No stimulation required. Is Andrew such a Kool-Aid drinker he can’t read the literature?

    When Andrew wants to talk about my other controls that will be fun. But he won’t. He’ll post some more stuff on HERVs or how pesticides get sprayed on his pasta or whatever.

  301. #303 Adele
    July 13, 2007

    Andrew and Eugene Semon should get together if they haven’t already. They’re both ignorant about microvesicles and HERVs and they both deny HIV exists. Or maybe Gene Semon is just another Andrew sock. Who knows? Who cares?

  302. #304 Roy Hinkley
    July 13, 2007

    Adele,

    I think you’re being too hard on Dr. Maniotis:

    The junk science is Andrew’s. Science that doesn’t have hypotheses or experiments at all. Much less controlled experiments like mine. Actually I wouldn’t call his stuff science.

    Why, I saw a control being used in Dr. Maniotis’ work just the other day. HIV integrase was tested to see if it had the same chromosome reconstituting ability as Topoisomerase.

    It did not. Obviously, very powerful conclusions can be drawn from a well controlled experiment like this. The most obvious, of course, is that HIV does not exist.

  303. #305 cooler
    July 13, 2007

    Dont listen to adele. I highly question her claims that she has a masters in biology and works in a lab, what kind of lab lets you sit on the internet all day and make posts?

  304. #306 Robster, FCD
    July 13, 2007

    Roy,

    Care to explain what you mean by “chromosome reconstituting ability” means? Just because two proteins have similar activities does not mean that one exists. If this passes for Maniotis style science, Adele is being too polite, if anything.

  305. #307 Roy Hinkley
    July 13, 2007

    Robster,

    Briefly, and I’m sure incompletely, chromatin was stripped, or partially stripped from condensed chromosomes. Topoisomerase II was added and the chromosomes recovered a condensed structure. When HIV integrase was added (it’s apparently from the same family as Topoisomerase II) the chromosomes were not reconstituted. Experiments were conducted in the absence of ATP to show that it was not due to the enzymatic activity of topo II.

    The conclusion that HIV does not exist is not drawn in the paper, for obvious reasons ie: the HIV hierarchy censoring results that show HIV does not exist. But Maniotis does cite this series of experiments elsewhere as calling the existence of HIV into question. See his manifesto the ABC’s of AIDS denial.

    Here’s the abstract for the paper:
    http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=9548561&dopt=Abstract

    You should of course read my comments about the nonexistence of HIV and censorship by the hierarchy as dripping with sarcasm.

  306. #308 franklin
    July 13, 2007

    Andrew,

    You still haven’t been able to figure out the the qualitative macroculture assay from the DAIDS manual?

    Maybe you should try doing an experiment and setting the assay up in your lab. At least then you could speak from experience.

  307. #309 Andrew Maniotis
    July 14, 2007

    Adele,

    I’d love to employ the mutants that you say you have, to do real first class molecular virology like you do in your “lab,” except I don’t know how you keep the little fragile “HIV” buggers that can’t even be photographed in a sucrose density gradient from mutating, especially under the highly un-natural conditions of culturing, stimulation, in cancer cells, etc., from month to month or from experiment to experiment?

    If your mutants are stable, as you imply, you have achieved nothing less that thwarting the enormous power of “HIV” to mutate from second to second in order to evade the “life saving medications” in its quest to kill all those people despite “compliance.”

    But if:

    “Well over 875,000 women and infants have received a single dose of nevirapine. A single dose of nevirapine is the cornerstone of the regimen recommended by the World Health Organization (WHO) to prevent mother-to-child transmission among women without access to antiretroviral treatment and among those not meeting treatment criteria. However, nevirapine resistance is detected (with the use of standard genotyping techniques) in 20 to 69% of women and 33 to 87% of infants after exposure to a single, peripartum dose of nevirapine. Among 60 women starting antiretroviral treatment within 6 months after receiving placebo or a single dose of nevirapine, no women in the placebo group and 41.7% in the nevirapine group had virologic failure (P<0.001). Women who had received a single dose of nevirapine had significantly higher rates of virologic failure on subsequent nevirapine-based antiretroviral treatment than did women who had received placebo. This apparently deleterious effect of a single dose of nevirapine was concentrated in women who initiated antiretroviral treatment within 6 months after receiving a single dose of nevirapine. We did not find that a previous single dose of nevirapine compromised the efficacy of subsequent nevirapine-based antiretroviral treatment in women who started antiretroviral treatment 6 months or more after delivery. Among the 30 HIV-infected infants, a single dose of nevirapine (one each to mother and infant) as compared with placebo was associated with significantly higher rates of virologic failure and smaller CD4+percentage increases in response to subsequent nevirapine-based antiretroviral treatment”[Lockman S. et al., Response to Antiretroviral Therapy after a Single, Peripartum Dose of Nevirapine. The New England Journal of Medicine 356 january 11, 2007],

    then how can your claim even be credible? Do you remember Harrington’s Chinese Menu Approach piece I posted earlier, or “The Power of Prayer” over “HIV’s” ability to mutate? I guess “HIV” doesn’t mutate in culture or in your “lab” but only does so under the selective pressure of “life-saving” drugs like nevirapine that was withdrawn from the US for its toxicity, but then given to 875,000 African mother-infant pairs to “see what would happen.”

    Also, Adele, how on earth did you get your cells infected without stimulating them?

    “I’ve seen HIV infecting two primary cell types this week alone. No stimulation required. Is Andrew such a Kool-Aid drinker he can’t read the literature?”

    But how can this be?
    You ought to immediately write Montagnier and Gallo to tell them their efforts with PHA, IL2, polybrene, cancer cell “amplification of HIV” etc., were all for nothing-and while you are at it, write the DAIDS folks and tell em that all that PHA stimulation they do to declare folks with 30 pg/ml or more (or 2×7 plus 4 times 2-16 on 2 consecutive tests where the last test is at least 4 1/2 times the first test) are dead men walking, while they tell the folks with < 29.06 pg/ml that its ok to donate blood and have wild sex, that they are full of it, and need to revise their manual ASAP! You might, in addition, show how you can now infect
    non-stimulated chimps (chimps that don’t have high risk behaviors), red blood cells to cause “HIV” associated “anemia,” infect neurons and glia to cause AIDS dementia, muscle cells to cause AIDS wasting, or whatever other cell type you want to be the target of “HIV’s” malicious nature this month), etc.”

    RE: Hinkley (are you related to the one who did the shooting a few years back)?

    “Why, I saw a control being used in Dr. Maniotis’ work just the other day. HIV integrase was tested to see if it had the same chromosome reconstituting ability as Topoisomerase.”

    “The conclusion that HIV does not exist is not drawn in the paper, for obvious reasons ie: the HIV hierarchy censoring results that show HIV does not exist. But Maniotis does cite this series of experiments elsewhere as calling the existence of HIV into question.”

    The “HIV” integrase we used, and the name of the vendor we obtained it from (who has fortunately since gone out of business)- is in the figure legend of our paper. We used it because on gene-base searches, “HIV-integrase” came up as a molecule that bound to the minor groove of DNA, in a manner identical to topoisomerase IIa. Therefore, to determine if topo’s dramatic activity had something to do with minor-grove binding of DNA as “HIV”s integrase activity was claimed to, we tested topo and “HIV-integrase” (and various other molecules with established activity) side by side. Of course, “HIV-integrase” had no observable activity, and so we had to conclude it as a negative result, and had to conclude that topo’s profound effects and activity were independent of its minor-grove-binding nature (and from other experiments concluded that its activity was primarily charge-driven and lysine dependent).

    But one might think that something with the power to alter chromatin and DNA to the extent that a provirus could be integrated such as “HIV-integrase” would have some measurable activity in these sensitive assays, but it did not.

    We didn’t make a big deal about it at the time, because as a negative result, it suggested a number of things:

    A. The “HIV integrase”we obtained could have been damaged in transit or not active because it was denatured.

    B. HIV integrase requires ATP (but we also tried it in the presence of ATP and it didn’t work).

    C. The activity of “HIV” integrase is sooooooooo subtle, that its activity escaped our detection.

    C. HIV doesn’t exist as an exogenous retrovirus, so how on earth could its integrase?

    Now my lab is testing the effects of cigars versus pipe-smoke on acquiring “HIV” infections:

    Thu Sep 21, 8:12 AM ET

    LONDON (Reuters) – “Smoking, already linked to several illnesses, may also increase the risk of infection with HIV, the virus that causes AIDS.

    In a review of studies that looked at the association between smoking and HIV, British doctors said five of the six studies they analysed showed smokers had a higher chance of becoming infected.

    Nine of 10 other studies in the review that tracked the progression from HIV to AIDS found no link with smoking.

    “The studies identified in this systematic review indicate that while smoking might be independently associated with acquiring HIV infection, it does not appear to be related to progression to AIDS,” said Dr Andrew Furber, of the South East Sheffield Primary Care Trust.

    Furber and his colleagues, who reported the findings in the journal Sexually Transmitted Infections, said tobacco smoke may increase susceptibility to HIV infection by modifying a variety of immune system responses.

    Research has shown that smoking is a leading cause of preventable death. It increases the risk of heart attack and stroke, respiratory problems, lung and other types of cancer.

    The researchers suggest in the study that public health measures that encourage smokers to quit could also improve the effectiveness of HIV/AIDS prevention programmes.

    About 40 million people worldwide are living with HIV/AIDS. Nearly 5 million were newly infected in 2005 and more than 3 million adults and children died of AIDS in the same year.”

    Maybe second hand smoke is responsible for at least part of the AIDS pandemic in children as well? Its a fascinating if not clever virus, to say the least!

  308. #310 Andrew Maniotis
    July 14, 2007

    Dear Franklin, Adele, Dr. Duke, Hinkley (Hinkley, is this you? http://www.gilligansisle.com/prof.html)

    Why don’t you all ever try to even respond to my questions? As Franklin I believe said about cheer-leaders…following some questions I stated, it would be most helpful for you to address the following issue of Bess et al:

    RE:

    Not one molecule of “HIV’s” proteins would be present in a whole stadium full of sports fans, given none of them were HIV postive.’

    Well gee Mr. Gallo, Mr. Fauci, Mr. Wainberg, I got 29 “units” of p24 in my blood, so I guess its safe that I can go after the cheerleaders or donate blood tomorrow! I ain’t got 30 pg/ml on two consecutive tests, so I OK! For shame! I’d rather take my chance with phrenology as a test for intelligence, or burning witches to see if they die (as you did to Christine’s family). But I’d bet that, naïve to the absolute junk science of the “HIV/AIDS” religion, and if somehow convinced to take an “HIV” test (or now under mandatory testing conditions at my “routine checkup” without any informed consent as is currently in place by the Nazi administration), that I’d finally fulfill Jesse Helm’s dream-to be afraid of any cheerleaders, and to regard for sure selectively biased populations such as gays (and African Americans) as being the object of “God’s revenge.” How are you supposed to feel if you blew a 29 on an AIDS breathalizer p24 test?

    The DIADS culturing manual, in light of the warnings of Larent-Crawford are even more disturbing, and suggest, if you really think about it, that not only are there no animal models of “HIV,” but there are no in consistent vitro models either, despite the DIADS attempt to codify a single set of protocols for normal stimulated lymphocyte culturing coupled to a diagnostic that doesn’t make any sense.

    Most heartbreaking of all, perhaps, is the fact that the equation of p24, or the spate of other “hidden epitope antibody tests or phony nucleic acid testing described in the last half of the DIADS handbook, all suffer from the same problems that Bess et al., (1997) so eloquently described (Microvesicles are a source of contaminating cellular proteins found in PURIFIED HIV-1 preparations”). In other words, on top of there being no consistent cell culturing model for “HIV’s” so-called pathogenic effect (principally but not only due to the problems with mitogen interference that causes, according to Laurent-Crawford et al., unbalanced signals and apoptosis or syncytial formation or persistant non-pathogenic viral production depending on whether lymphocytes are “immature or “mature” there is still, no evidence whatsoever, that p24 has anything to do with an exogenous virus called “HIV.” I’d like to give a few examples:

    1. If you go to figure 3 in this paper, one cannot tell a piece of cellular debris from any other piece of debris or crap. And this is where p24 was isolated from under the best PURIFICATION conditions that “HIV” science could muster? If you want to see what a virus prep for purification should look like, see http://www.virusmyth.net/aids/news/edhlettercont.htm

    And note that in this EM photograph, there isn’t any crap that can co-purify and be mistaken for a unique, exogenous, viral protein, or at least it is highly unlikely given the purity of the prep. The author points to the two pieces of shit in the prep that aren’t viral in nature in a background of hundreds that are identical.

    2. The Bess et al., authors specifically state that: “Identification and analysis of the virus are complicated by the presence of cellular membrane vesicles which COPURIFY with the virus.”

    3. “We recently reported a proteolytic procedure (Ott et al., 1995b) that effectively removes greater than 95% of proteins associated with these membrane vesicles. This procedure has allowed us to demonstrate that the cytoskeletal proteins, actin, ezrin, moesin, and cofilin are located IN THE INTERIOR of virions.”

    Funny-I never saw this in any testbooks…along with pol, env, p24, p32, etc., that actin, ezrin, moesin, and cofilin were part of “HIV’s” deadly arsenal it carries into cells from other infected cells.

    Question: If actin, exrin, and cytoskeletal proteins are located INSIDE the virions, how can one tell if p24, which is a faint band on most cellular gels that come from non-infected cells in most labs, isn’t also a cellular protein? The gel shown in figure 1 (the non-infected lane) has weaker bands at all of these weight designations that supposedly the infected supernatants were run (B,C). In fact the p24 band is extremely PRESENT in lane A, which is the uninfected lane. This gel is the basis for giving someone cancer chemo on their cornflakes for life as Moore pointed out? For shame!

    4. “PHA activated human PBLs were also shown to produce microvesicles that incorporated cellular proteins (Fig. 6).”

    5. “In addition to proteins, microvesicles were also shown to contain both RNA and DNA. Approximately 10ug of RNA and 4 ug of DNA were found per mg of protein. The major RNA species in microvesicles were ribosomal 28S and 18S subuitis and some low molecular species, PERHAPS tRNA.”

    Could these nucleic acids form little dark “cones” one might ask? Hard to tell you say. Look at figure 3 and tell me in those several dark cone-containing pieces of cellular crap, do you see your father, the sea, Mana from heaven, the “HIV” genome, your future?

    6. “We have been unsuccessful at separating microvesicles from HIV- by centrifugation techniques (data not shown).” What! It’s shown in figure 3!

    7. GP120 may do the trick (if it isn’t a cellular protein which it is).

    8. “Clearly, future experiments utilizing purified viruses must be carefully controlled to account for the effects of cellular antigens present on microvessels” (like p24 and all the other so-called proteins and nucleic acids thought to be specific to “HIV”). Clearly indeed!#@###$@

    9. “Numerous other cellular proteins have been identified in PURIFIED preparations of HIV-1. It is not known if these are physically associated with HIV particles and, if so, whether or not they have a role in the virus replication cycle. IDENTIFICATION OF WHICH CELLULAR PROTEINS ARE ASSOCIATED WITH THE VIRUS IS A PREREQISITE TO STUDYING THE POTENTIAL FUNCION OF CELLULAR PROTEINS IN THE VIRUS REPLICATION CYCLE.”

    SHOULD READ:
    IDENTIFICATION OF WHICH CELLULAR PROTEINS ARE ASSOCIATED WITH THE VIRUS IS A PREREQISITE TO MAKING A GODDAMN TEST KIT, WHETHER OR NOT IT IS PROTEIN OR NUCLEIC ACID BASED, AND THEN USING IT TO RISK THE LIVES OF MILLIONS OF PEOPLE WHO WILL BE FORCED TO TAKE DANGEROUS CHEMOTHERAPIES BASED ON A p24 or nucleic acid-based test that has been developed from the likes of this junk science.

  309. #311 Andrew Maniotis
    July 14, 2007

    When the FDA recalls defective “HIV” tests or statistic software, how long does it take the medical community to respond to the typical recall? For instance, are testing labs immediately provided with the lot numbers of defective testing merchandise in a timely manner, and are patients who received these tests quickly notified about the recall of the test they were subjected to? A few recent cases may here be illustrative:

    Recall of HIV p24 Antigen Test Kit
    Globus Media REcall HIV test
    ORTHO Antibody to HBsAg ELISA Test FDA recall Ortho HBsAG System
    Recall of Antibody to Human Immunodeficiency Virus Type 1 p24 Antigen Test Kits
    Recall lancets for HIV kit
    FDA Recall of NucliSens HIV test kit
    FDA Recall of HCV EIA 2.0 Test Kit
    Market Withdrawal of HIV-1 – HCV Assay, FDA recall Procleix
    FDA Recall HIV-1 – HIV-2 Plus O EIA Testing Software
    Recall of HIV Types 1 &2 (Synthetic Peptide)
    FDA Recall of Amplicor HIV test kit

    Why hasn’t humoral, cellular, or mucosal immunity been evoked in “HIV” vaccine trials? [1995 Congress of the United States: Office of Technology assessment. Adverse Reactions to HIV Vaccines: Medical, Ethical, and Legal Issues. (Roger C. Herdman, Director]? Something wrong with the molecular nature of the components vaccinated into these experimental human being vaccine recipients?

    J Int Assoc Physicians AIDS Care. 1998 Mar;4(3):45-6.
    Does the HIV-1deltakURNe vaccine strain hold the key to curbing HIV infection? An interview with Ronald Desrosiers, PhD.

    Desrosiers R.
    AIDS: Dr. Ronald Desrosiers of the New England Primate Research Center at the Harvard Medical School provides his opinions on the HIV-1deltakURNe vaccine strain. Dr. Desrosiers explains what this strain represents and how it was chosen for live-attenuated HIV vaccine human safety trials. Further, Desrosiers discusses the balance in using highly attenuated vaccines and protection effectiveness, whether it is possible for the vaccine strain to revert to a disease-causing form, the possibility of transmission of a vaccine virus to unvaccinated individuals, and the issue of cancer development through insertional mutagenesis.

    Continuing from Reactions to HIV Vaccines: Medical, Ethical, and Legal Issues:

    “Safety Concerns Associated with Attenuated Virus
    There are four primary safety concerns about attenuated viral vaccines that have been recognized” (11,22,104).

    1. Level of attenuation. Inadequate attenuation (reduction of virulence) of virus may result in a vaccine that induces the disease4 that it was designed to prevent; over-attenuated virus may fail to induce protective immune responses. However, even an appropriately attenuated virus may show virulent behavior when not constrained by a competent immune system , such as in vaccine recipients with immue systems compromised by cancers, immunosuppressant drugs, and other non-AIDS causes. The highly infectious nature of SIV administered orally to monkeys at birth, before the monkey’s immune system has developed, has rasied new questions about safety of vaccines in immunocompromised individuals (79).
    2. Stability of attenuation. The vaccine strain could undergo genetic reversion to a more virulent form during the lengthy course of replication in the vaccine. Tis risk is of particular concern with vaccines using attenuated strains of HIV, as the human immunodeficiency virus is cyharacterized by rapid and frequentg genetic mutations.
    3. Possibility of secondary spread. Spread of attenuated virus to contacts of vaccines (secondary spread) may provide the virus with further opportunity to revert to virulence (e.g. vaccine-induced poliomyelitis in contacts of vaccinees.) However, if it can be assured that the level of attenuation of the virus remains stable, secondary spread of the virus may be beneficial, because the attenuated virus could induce protective immunity in contacts. Sufficient spread of the attenuated virus would result in the induction of herd immunity (as had occurred with poliovirus vaccine.” (But if the virus is constantly mutating in people, or able to be induced to mutate with a single dose of Nevirapine, then how could any be stable? See 2007, January).
    4. Possibility of induction of tumors. Other members of the retrovirus family regularly produce tumors (e.g., mouse tumors and a form of human leukemia). Theoretically, the prolonged residence of a live attenuated HIV vaccine strain in vaccinees could allow the retrovirus to rpoduce tumors. Recent evidence for a direct role for HIV infection in the etiology of some T-cell lymphomas suggest a need to proceed cautiously while continuing to investigate the long-term potential of these vaccinees to produce tumors (92, 104)…(From page 52, 2nd pararaph-)…The protective mechanism of attenuated SIV vaccine is unclear. It is not correlated with antibody or cytotoxic T lymphocytes responses, and mucosal immunity is not involed.”

  310. #312 Richard Jefferys
    July 14, 2007

    What are you dribbling on about now, Andrew? No live attenuated HIV vaccine has ever been tested in humans, some doctors from the International Association of Physicians in AIDS Care wanted to volunteer for a study but it never happened because of safety concerns.

    And why are you obsessively citing a 12 year old report on vaccine trials? There are three ongoing efficacy trials, two involving attenuated adenovirus vector-based constructs that evoke HIV-specific CD4 and CD8 T cell responses in the majority of recipients.

    I’ve also been wanting to ask you about that child with cancer you mentioned in one of your posts on Barnesworld; you had some idea for treating him that you couldn’t try? What was that?

  311. #313 franklin
    July 14, 2007

    Andrew,

    You’re neglecting to include your disclaimer on your posts. You already admitted that your mistaken views about HIV assays might simply refelect the fact that you “really don’t understand what is going on.” All your subsequent posts about the assays are based on your inability to interpret the results of the assay–asking for help in determining what the assay results mean.

    There seems to be no controversy–we all seem to agree that everything can be explained by remembering that you “really don’t understand what is going on.” Your helplessness in figuring out the meaning of the assay results just continues to reinforce this interpretation.

    But please remember to append your disclaimer to your future posts to make sure new readers will understand your position:

    “I really don’t understand what’s going on.”
    –Andrew Maniotis, July 6, 2007

  312. #314 Dale
    July 14, 2007

    Andy writes SHOULD READ:
    IDENTIFICATION OF WHICH CELLULAR PROTEINS ARE ASSOCIATED WITH THE VIRUS IS A PREREQISITE TO MAKING A GODDAMN TEST KIT, WHETHER
    Never mind, franklin’s right “I really don’t understand what’s going on.”
    –Andrew Maniotis, July 6, 2007
    pretty much explains your confusion.

  313. #315 Andrew Maniotis
    July 15, 2007

    Jeffreys,
    RE:

    “And why are you obsessively citing a 12 year old report on vaccine trials? There are three ongoing efficacy trials, two involving attenuated adenovirus vector-based constructs that evoke HIV-specific CD4 and CD8 T cell responses in the majority of recipients.”

    Because at that time 1995 there was claimed to have been (at least) 30 vaccine trials in the Congressional document I cited (closer to 80 if you look at the tables of this document-so there has been sufficient time to analyze these-and to discover there was no activation of T-cells claimed, no humoral immunity documented, no mucosal immunity that was apparent, and no cellular immunity demonstrated, largely because the stimulating antigens are not non-self-from an exogenous “HIV.” And you’ll tell me that “HIV” isn’t immunogenic. Try telling that to the millions of “HIV-positives” that are thought to be infected.

    RE:
    “I’ve also been wanting to ask you about that child with cancer you mentioned in one of your posts on Barnesworld; you had some idea for treating him that you couldn’t try? What was that?”

    Can you be more specific about that Barnesworld post? I don’t remember writing anything about a child with cancer.

    Franklin, Dale, (Adele), Duke, and others,

    I guess you can’t answer my questions. Somehow, I’m not surprised. As for your stonewalling, dodging the issues, making up diseases, etc., all I can say is that we clearly can see that you are revisiting the tactics of the Spanish Grand Inquisitors, or patriotic commission run by Senator Joe McCarthy, with Ronald Regan at his side, attempting to cleanse America of normal scientific discourse. “Have you now, or ever been, someone who dared ask a question regarding the reality and pathogenesis of “HIV,” and its role in causing the previously known 47 diseases or syndromes now collectively called “AIDS?” And Sir, do you know anyone, especially scientists or physicians, who have asked such a question? Could we please have their names now?”

  314. #316 Dale
    July 15, 2007

    “Have you now, or ever been, someone who dared ask a question regarding the reality and pathogenesis of “HIV,” and its role in causing the previously known 47 diseases or syndromes now collectively called “AIDS?” And Sir, do you know anyone, especially scientists or physicians, who have asked such a question? Could we please have their names now?”

    Well as I understand it, Harvey Bialy and Peter Duesberg have asked such questions. Sadly, like yourself, they apparently don’t seem to understand the answers.

  315. #317 franklin
    July 15, 2007

    Andrew,

    You said: “Franklin, Dale, (Adele), Duke, and others, I guess you can’t answer my questions.”

    As far as I can tell your question relates to the proper interpretation of specific results on a DAIDS Virological Assay. I already explained that given your education at UC Berkeley, you should be able to figure out the answer all by yourself. Try reading the supporting bibliography in the DAIDS Manual, and if that doesn’t work–set the assay up yourself.

    You like to pretend that your education gives you credibility that apparently you lack. You state that the use of unifected cells in this assay is “irrational to (your) way of thinking,” yet the use of unifected cells is ESSENTIAL to the assay.

    By the way, you still haven’t explained how you came to “quote” Stramer et al. (2004) as saying they had studied “non-risk donors”. Nor have you explained the meaning of the term you made up–”non-risk donors”–and falsely attributed to Stramer.

    So far, I’ve only been able to confirm the truth of one statement you have made:

    “I really don’t understand what’s going on.”
    –Andrew Maniotis, July 6, 2007

  316. #318 Richard Jefferys
    July 15, 2007

    Andrew Maniotis wrote:

    Because at that time 1995 there was claimed to have been (at least) 30 vaccine trials in the Congressional document I cited (closer to 80 if you look at the tables of this document-so there has been sufficient time to analyze these-and to discover there was no activation of T-cells claimed, no humoral immunity documented, no mucosal immunity that was apparent, and no cellular immunity demonstrated, largely because the stimulating antigens are not non-self-from an exogenous “HIV.” And you’ll tell me that “HIV” isn’t immunogenic. Try telling that to the millions of “HIV-positives” that are thought to be infected.

    No, I won’t tell you HIV isn’t immunogenic because it’s plenty immunogenic. The antigens used in these vaccines are from exogenous HIV, unless you’re seriously attempting to suggest that the HIV genes inserted in a vector such as ALVAC have a match in the human genome.

    For immunogenicity data from HIV vaccine trials, you should look in PubMed. Even the gp120 subunit HIV vaccines activated CD4 T cells and generated CD4 T cell and B cell memory and gp120-specific antibodies. ALVAC induces HIV-specific memory CD8 T cell responses in ~20% of recipients, ALVAC was also in studies by 1995. Mucosal HIV-specific memory CD8 T cell responses have also been documented in some ALVAC recipients. Since 1995, newer vaccine vectors have been designed that are much better at inducing HIV-specific memory CD4 and CD8 T cells, they do so in the majority of recipients (the problem with reliably inducing CD8 T cells did not relate to HIV’s immunogenicity, it related to efficiently accessing the class I antigen processing pathway with non-replicating vectors). The two vaccines that are currently in efficacy trials are Merck’s Ad5 vector which encodes the Gag, Pol and Nef proteins from HIV-1 and the Vaccine Research Center’s DNA prime/Ad5 boost which encodes Gag, Pol, Nef and three Env proteins from clades A, B & C.

    Can you be more specific about that Barnesworld post? I don’t remember writing anything about a child with cancer.

    David Steele deleted it very quickly so I guess it’s lost to posterity.

  317. #319 Adele
    July 16, 2007

    Maniotis wrote,

    I guess you can’t answer my questions. Somehow, I’m not surprised. As for your stonewalling, dodging the issues, making up diseases, etc.

    Andrew “answers” questions by questioning if things exist. Like my stocks of virus at minus 80 degrees that I sequenced after I made them are supposed to mutate all by themselves in the freezer before I use them. Or maybe revert to wild type in a single round of replication. That’s how he “answers” my RT results. And by the way they’re not like big results they’re just standard things you use to test new cells you get in or validate stuff.

    When he’s so far out there how do you answer someone like that.

  318. #320 Shawn Hannity
    July 16, 2007

    “Like my stocks of virus at minus 80 degrees that I sequenced after I made them are supposed to mutate all by themselves in the freezer before I use them. Or maybe revert to wild type in a single round of replication. That’s how he “answers” my RT results. And by the way they’re not like big results they’re just standard things you use to test new cells you get in or validate stuff.”

    Adele, are you some sort of budding young scientist? Do these comments have something to do with life on Mars? What in heaven’s name are they supposed to mean?

  319. #321 Fritz the Cat
    July 16, 2007

    Gosh Richard, do all of your precious victims really need their CD4 cells activated?

  320. #322 Phineas T
    July 16, 2007

    And here we have a serious contributor named “Franklin” who doesn’t know what a “non-risk donor” means.

    Of course, it logically follows that risk assessment must be something that Dr Maniotis has made up.

  321. #323 Manual Virus
    July 16, 2007

    “…they apparently don’t seem to understand the answers.”

    Dale, a more appropriate statement defining “HIV” researchers could not be made.

  322. #324 Meme Machine
    July 16, 2007

    Oh Adele, such little faith you have that you have to impute such existential positions to Maniotis and Semon.

    Of course deadly HIV exists.

  323. #325 Adele
    July 16, 2007

    More numbers for everyone.

    Cooler said

    Dont listen to adele. I highly question her claims that she has a masters in biology and works in a lab, what kind of lab lets you sit on the internet all day and make posts?

    Between when cooler wrote that and this comment
    Me, 330 words
    Andrew Maniotis, 3,326 words

    I think you find similar result with other times. So does Cooler question Maniotis is a professor? Don’t professors have alot more time issues than techs?

  324. #326 Jimi Hendrix
    July 16, 2007

    Too bad the Moore Bergman propaganda film

    http://health.scribemedia.org/2007/06/22/fighting-aids-denialism/

    didn’t show the 3 fold variable size differences reported by the Wellcome Trust Centre for Human Genetics at Oxford University team showed, when they claimed that (BBC News Tuesday, 24 January 2006, 14:04 -”3D structure of HIV is ‘revealed’”):

    “Scientists have created a map showing the 3D structure of the virus which causes Aids.

    The variable size and shape of HIV has made it hard to map, the team said in the journal Structure.

    So the UK-German team took hundreds of images of viruses, that are 60 times smaller than red blood cells, and used a computer program to combine them.

    Oxford University’s Professor Stephen Fuller said the 3D map would assist in understanding how the virus grows.

    Unusual features

    He told the BBC: “You say can you show me the structure of the HIV virus and the question is which one.

    [YES THIS IS A GOOD QUESTION BY THE OXFORD SCIENTIST-WHICH ONE INDEED??????]

    “HIV is very variable. It varied in diameter by a factor of three.” [MAYBE SOME "HIV" VIRIONS ARE HAPLOID, DIPLOID, AND TRIPLOID?????] HA HA HA HA HA-THAT’S A JOKE].

    The way the research team, from the Wellcome Trust Centre for Human Genetics at Oxford University, dealt with this was by taking multiple images at different tilts.

    [THE APPARATUS WAS TILTED, NOT THE RESEARCHERS]!

    Working with colleagues in Heidelberg and Munich, they took about 100 images of 70 individual HIV viruses and then looked at similarities.

    Despite the variability, the team found some consistent features.

    T-Cells

    This included the finding that the core of virus – which is cone-shaped – spans the width of the viral membrane.”

    But there are spikes on the outside which bind to human immune cells, called T cells, and allow the virus to invade them.

    [NOT JUST ANY T-CELLS-CD4+ T-CELLS. DAVID HO AND OTHERS HAVE SHOWN IN SCIENCE, FOR INSTANCE, THAT CD4+ T-CELLS ARE THE ONLY RESIDENT POPULATION IN THE GUT'S LYMPH PATCHES SHOWN OF COURSE TO BE "WIPED CLEAN" (BECAUSE OF "HIV'S INCREDIBLY NARROW CD4+ CELL TROPISM) VERY SOON AFTER INFECTION, WHILE AT THE SAME TIME, THE VIRUS IS LYING DORMANT AS A PROVIRUS IN 1: 10,000 T-CELLS ELSEWHERE SOMEWHERE ELSE. WE NOW KNOW THAT AIDS CAN BE A DISEASE OF BOTH TOO FEW absolute AND TOO MANY absolute LYMPHOCYTES, AS IN THE CASE OF ELIZA JANE. BUT WE ALSO KNOW THAT HIV IS VERY SPECIFICALLY TARGETING ONLY THE CD4'S, DESPITE WHAT DENIALISTS SAY REGARDING NO CORRELATION BETWEEN VIRAL LOAD AND T-CELL NUMBERS].

    The significance of this is that whereas most viruses have internal structures which define the size, in the HIV virus it is the membrane which defines the size.”

    [FUNNY HOW TMV AND OTHER VIRUSES THAT HAVE BEEN SHOWN CAPABLE OF SELF-ASSEMEBLY FROM ISOLATED AND SEPARATED CONSTITUTENTS IN VITRO ALL HAVE THE SAME SIZE AND SHAPE BECAUSE THE CONSTITUENT MOLECULES HAVE STRUCTURAL CONSTAINSTS THAT DEFINE THE CURVATURE, GYRE, SIZE, AND OVERALL SHAPE OF A VIRUS, AS THEY DO A MICROTUBULE-I KNEW THERE HAD TO BE SOMETING SPECIAL REGARDING THIS FEATURE WITH HIV! SEEMS LIKE IT BREAKS ALL THE RULES. EVOKES ANTIBODIES BUT A VACCINE CAN'T BE GENERATED AGAINST ITS CONSTITUENT COMPONENTS, KILLS WHILE AT LEVELS OF 1:1000-10,000 T-CELLS WHILE WIPING THE GUT "CLEAN" IN A FEW MONTHS, ETC].

    YET WITH CELLS, SUBCELLULAR ASSEMBLAGES, ETC, ISN’T IT TRUE THAT MEMBRANES DON’T DEFINE OR DICTATE STRUCURE OR MORPHOLOGY-BUT IT IS THE PROTEIN SCAFFOLDS AND NUCLEIC ACIDS AND OTHER MOIETIES (LIKE POLYAMINES) THAT DON’T BEHAVE ACCORDING TO A FLUID MOZAIC CONSTRAINT MODEL, WHICH IS WHY YOU CAN LIGHTLY TREAT CELLS OR VIRUSES WITH NON-IONIC DETERGENTS AND PRESERVE MORPHOLOGICAL STRUCTURE PRECISESLY? MAYBE “HIV” EVOLVED DIRECTLY FROM THE FIRST MICELLES FORMED OF HYDROCARBON MOLECULES IN THE PRIMORDIAL OOZE. IF THIS IS THE CASE, WHY DID IT SUDDENLY SHOW UP IN 1981(1959? 1971 IN ST. LOUIS?]. MAYBE IT IS A PROPHECY LIKE THOSE OF NOSTRADOMUS (SP) TO DELIVER GOD’S REVENGE FOR THOSE WHO FORNICATE!!! SOMEBODY NAMED NOAH SHOULD START BUILDING AN ARC]!

    This could inform the development of more effective therapeutic approaches Professor Stephen Fuller Wellcome Trust Centre for Human Genetics.

    This puts constraints on the way it can assemble, the team said.

    RIGHT! RIGHT! RIGHT-OH-OLD CHAP!

    Professor Fuller said: “Identifying how the virus grows will allow us to address the formation of this important pathogen and how it accommodates its variability.”

    “This could inform the development of more effective therapeutic approaches,” he added.”

    [IT CERTAINLY COULD]!

    “But Professor Fuller, who continues to work on HIV, acknowledges that a new HIV vaccine or treatment resulting from his research was a long way off.”

    [WAY WAY OFF!!! T'WOULD SEEM THEY NEED TO FIRST ISOLATE IT AND SHOW, AS A CONTROLLED INDEPENDENT VARIABLE, THAT IT HAS A CONSISTENT MORPHOLOGY, HAS SOME PATHOGENIC EFFECTS ON CELLS IN CULTURE, OR EVEN IN AN ANIMAL MODEL].”

    But he says the research could provide an insight into the way to prevent the virus from assembling.

    [ANTIBODIES AND ENDOGENOUS GAMMAGLOBULINS FOUND IN HEALTHY INDIVUALS NUTRALIZE "IT," ACCORDING TO SOME AIDS DENIALISTS I COULD QUOTE.]

    Treatments?

    Like any virus, HIV is not a cell but rather strands of genetic code wrapped in protein.

    [RIGHT! "HIV" ISN'T A CELL AT ALL, BUT CONTAINS ACTIN AND OTHER CYTOSKELETAL PROTEINS ACCORDING TO BESS ET AL.].

    The virus invades living cells and take them over by usurping the cell’s genetic code with its own.”

    [USURP IS PROBABLY AN UNFORTUNATE WORD CHOICE-RETROVIRUSES INTEGRATE THEIR GENOMES AND, LIKE GAJDUSEK'S PRIONS, REMAIN SILENT FOR YEARS WHILE THEY DISTROY THE GUT LYMPH NODES AT THE SAME MOMENT].

    Roger Pebody, treatment specialist at HIV/Aids charity Terrence Higgins Trust, said: “Revealing the 3D structure of HIV may not sound very exciting but it’s actually really useful [PROFITABLE], giving us more information about the virus and how it grows.

    [HE OUGHT TO WRITE TO ADELE, SHE SAYS SHE CAN GROW "HIV" IN NON-PHA-STIMULATED PRIMARY T-CELL CULTURES (ADELE-ARE ALL THESE CD4+ OR ARE THESE MIXED LYMPHOCYTE/MONOCYTE/MACROPHAGE POPULATIONS?) WITHOUT STIMULATING THE HELL OUT OF THEM AND OXIDIZING THE CELLS TO CREATE TOXIC EFFECTS WITH PHA DEPENNDING ON "THE MATURITY" OF THE CELLS OF COURSE-ACCORDING TO LAURENT-CRAWFORD ET AL.,]! HOURAY ADELE!

    “The more we understand about HIV, the more likely we are to be able to develop effective treatments and hopefully one day a cure.”

    [SOMEBODY OUGHT TO WRITE THE BBC AND TELL THEM ABOUT THE LIFE-SAVING MEDS, SO THEY WON’T EDGE INTO AIDS DENIALISM AND SAY THINGS LIKE:”develop effective treatments and hopefully one day a cure.”

    Also, somebody ought to tell Dr. Moore and Bergman to show “HIV” particles on their 20 minute propaganda piece that are also 3 different sizes instead of particles all the same size. At least the AIDS establishment ought to clean up their data a bit. They also might want to provide a picture on this propaganda movie that shows at least 1 particle with a “wedge-shaped core.”

    Someone might also want to tell that cunning legal mind, Bergman, in addition, that treating pregnant women with therapies that might be “effective” and “hopefully one day will cure” might not work so well when the retrovirus has intercalated its genome in a cell passed from mother to infant during labor, no matter how many grams of AZT or nevirapine she wants to give them, or regardless of whether or not 47% of the women will develop mutant viruses after one dose of nevirapine (Lockman et al.,). What might happen instead, is that these drugs may suppress normal immune functioning, cause diarrhea, vomiting, bone marrow suppression, liver failure, or perhaps just suppress the normal immune system functioning, including those cells that may be responsible for generating high RT readings, or p24 levels that exceed 30 pg/ml, or other so-called specific retroviral signatures. Maybe Bergman should advocate full-body radiation to kill any “HIV-harboring T-cells, plus of course, AZT, Nevirapine, 3Tc, ddI, sequinavir, mycoplasma removal agent, and perhaps for good measure, prophalactic bactrim for at least 28 days, and a good dose of amoxicillin to ward off any potential microbial “flair-up” these AIDS-infested women may harbor during pregancy? Certainly, if the mothers don’t comply, Bergman ought to have suggested putting g-tubes into them to force them to take these “life-saving meds” so their babies won’t grow up to infect low-risk people by accident!

    Try to overlook the remarks of Moore and Bergman regarding denialists all being heterosexual racists and homophobes motivated by deep resentments toward these minority groups. Its not true. Lee Evens is no racist, nor is President Mbeki, and they have their opinions, as does Sam Mlongo, and others.

    Peace
    Jimi

  325. #327 Bill Collector
    July 16, 2007

    It is certainly entertaining, at the very least, to review the insults and piling on directed at Andrew Maniotis that carefully avoid his substantive points. Included are such wonderful irrelevancies as hundreds of ways to distinguish reverse transcriptases, of course plural in the case of “HIV-1″, since we no longer can ignore Brian Foley’s admonitions on the “singular” fallacy. How about distinguishing the kinetics of nucleotide incorporation, say comparing synthetic versus wild-type templates? Could that possibly help us in the search for what’s real and what’s artifact? Could it even be true – gasp – that RT in terms of reaction-rate governance, has more of a “preference” for the synthetic template (that’s a polymer chain of lots and lots of rA’s bound to priming oligo dT’s) than either of the two famous divalent cations?

    But some of us – still capable of wonder – might dig in on what exactly are these reverse transcriptase exosomes – so called microvesicles. Could they have a biological function that have something to do with the cellular proteins that are found in the “purified” fraction? BTW, can any of the resident experts here tell us how many cellular proteins have been documented as parts of RT microvesicles/exosomes? And why, if such a process has been going on since the origin of DNA – you can say one of life’s seeds – it should suddenly turn on us? But HIV has different sequences, they plead. And over and over they assert, HIV proteins are unique. So any fool can see this must be proof of pathogenicity. Proof? Or always assumed? At least always in every paper that’s tossed at the unwary. And yet, when one scrutinizes for the differences that make a difference – we get nothing but more assumptions and pointless pointing … look at those T cells or look what we can do in this culture …

    The “DNA-directs” old textbook fallacy: consider the original period when the hypothesis was formed. Introns had just been discovered. Very little was known about transcriptional regulation in eukaryotic cells. It was assumed to be the same as prokaryotes, which turns out to be a highly inaccurate picture. The basic presentation was “wily HIV insidiously inserts itself into the genome and DIRECTS it’s own replication from this position”. It’s now understood that this supposition or habit of thinking that governed in the early 80′s mind is no longer appropriate given “epigenetics”, novel discoveries in transcriptional regulation, etc.

    There are indeed whole sets of questions that never get answered by the fine crew here. So logically, one can default, at least at this point, to a preliminary risk assessment that after hundreds of millions of years of being imbedded in vertebrates, it is highly unlikely that a set of retroviruses came flying out of primate genomes to cause the worst plague in history.

    So why not now, in the light of so much new data since Gallo’s heyday: this retrospective analysis on retroviruses? (A retro on retros.) Doesn’t real progress mean questioning the pharmaceutical companies as they happily invent new diseases to expand markets? Why should any retrospective risk assessment that adds to our understanding of a potential threat to public health be declared out of the bounds of scientific discourse?

    Is it the economy that forces us to accept such verdicts of institutionalized science? Are antioxidants and medical marijuana a threat to Big Pharma? Will revisionism increase the peril to our economic health? How many jobs would be lost and what kind of ripple effect through the biotech industry would occur if a moratorium was declared on the HIV research?

    Anyway, there’s a guy waving at me from a black helicopter …

  326. #328 Adele
    July 16, 2007

    Maniosemon or Eugeniotis writes
    HE OUGHT TO WRITE TO ADELE, SHE SAYS SHE CAN GROW “HIV” IN NON-PHA-STIMULATED PRIMARY T-CELL CULTURES (ADELE-ARE ALL THESE CD4+ OR ARE THESE MIXED LYMPHOCYTE/MONOCYTE/MACROPHAGE POPULATIONS?)

    I didn’t say T-cells. HIV infects other cells too. Maybe you can look them up on google and write jokes about them for your split personalities.

  327. #329 franklin
    July 16, 2007

    Some apologist for Maniotis wrote:

    And here we have a serious contributor named “Franklin” who doesn’t know what a “non-risk donor” means.
    Of course, it logically follows that risk assessment must be something that Dr Maniotis has made up.

    I see no evidence that Professor Maniotis understands the field of risk assessment, much less that he invented it. I suspect that he made up only the phrase “non-risk donor”, since a Medline search returns zero (0) documents containing that phrase–not even the paper he was purportedly “quoting”.

    On the other hand, Professor Maniotis purports to be a serious scientist, but his claims about HIV/AIDS have repeatedly been shown to be due to invented quotes, quotes taken out of context, or complete misunderstandings of simple clinical or virological methods.

    Most of the distortions we have pointed out in his writings have gone undetected for months by the HIV denialist sites on which he usually writes, even though all that is required to detect his lies is to read the papers he cites. It seems that none of the regular contributors to the HIV denialist sites is “serious,” since none of them shows any evidence of actually having read the papers cited by Maniotis.

  328. #330 franklin
    July 16, 2007

    Another Maniotis apologist wtote:

    It is certainly entertaining, at the very least, to review the insults and piling on directed at Andrew Maniotis that carefully avoid his substantive points.

    Professor Maniotis has made no substantive points. He has only provided distorted or flat-out-false statements about the work of other scientists, as amply documented in his posts.

    That the denialists continue to defend the integrity-challenged claims of Maniotis simply illustrates their desperate need to deny reality.

  329. #331 Roy Hinkley
    July 16, 2007

    Bill said:

    The basic presentation was “wily HIV insidiously inserts itself into the genome and DIRECTS it’s own replication from this position”. It’s now understood that this supposition or habit of thinking that governed in the early 80′s mind is no longer appropriate given “epigenetics”, novel discoveries in transcriptional regulation, etc.”

    Got that everyone?

    Epigenetics exists, therefore HIV does not.

    Profound…

    ly….

    stupid.

  330. #332 Adele
    July 16, 2007

    Franklin,

    Ok, but “denialists”? I think we’ve just seen an encore performance of Eugene Semon.

    One day.

    Ten thousand names.

    Zero knowledge of epigenetics OR HIV.

    The Eugenedrew Semoniotis show.

    Coming soon to a blog near you.

  331. #333 Andrew Maniotis
    July 22, 2007

    Adele said:

    I didn’t say T-cells. HIV infects other cells too. Maybe you can look them up on google and write jokes about them for your split personalities.

    Posted by: Adele | July 16, 2007 03:23 PM

    Gee Wizz Adele. Do these mysterious non-T cells you use have CCR5 receptors? I know Gallo said something as to the effect that “HIV” can infect endothelial cells, and some macrophages perhaps, but the target has always been the CCR5-bearing T-cells (either young or old-doesn’t matter although these lymphocytes behave differently according to Laurent-Crawford et al., with respect to their susceptibility to “HIV” infection and how they exhibit pathogenicity-see the Discussion of that paper-in other words read the whole paper one of these days).

    How bout muscle cells. Doesn’t “HIV” cause slim disease or wasting? Is it multiplying in their mitochondria? Perhaps “HIV” is replicating in Z-bands to cause wasting. What about neurons or glia-do they also have CCR5 receptors attached to their dendrites or filopodia, and why aren’t they “wiped clean soon (moments) after infection” as are the gut’s lymphoid tissue as Ho, Desroisiers and other hacks claimed in their “It’s the gut stupid Science article” that proposed to revise the incubation period for “HIV” infection.

    Shouldn’t you tell those affected with “AIDS” that their muscle cells are all actively dividing to promote retrovirus production because retroviruses must integrate their genomes and propagate in ACTIVATED DIVIDING CELLS?

    How about anemia? Don’t you need to get that “HIV” genome into those enucleated red blood cells or was this an effect of AZT?

    How about McDonald et al.s funny claims about dendritic cells, and how “HIV” “hides” in cytoplasmic vesicles until the dendritic cell ‘presents” the little bad “HIV” virions to an uninfected cell (without the retrovirus infecting its nucleus-just sort of hangs out for awhile until the dendritic cell decides to infect another T-cell)?

    Adele, I can’t tell you what your confidence certainty means to me…to all of us. I’m sure whatever cell you can infect without PHA activation (other than cancer cells of course, which are a little different than primary T-cells), you ought to be given an award…something like the Failure of Fear Award for Irreproducible Results perhaps. Keep on lying…

    BTW-are your healthy control cells with or without these CCR5 receptors that you claim aren’t T-cells producing levels of p24 consistently below 30pg/ml, because if they ain’t, you know you should not consider them from a healthy donor source, and throw them in the trash along with everything else you have done.

    Cheers,

    Andy

  332. #334 DT
    July 22, 2007

    “Do these mysterious non-T cells you use have CCR5 receptors?”

    Aside from T cells, the CCRs that permit HIV entry are found on other cells such as monocyte-macrophage lines. This, FYI, includes microglial cells and dendritic cells.

    It is becoming a little tedious constantly correcting the Maniotis view of reality. At least there is some hope that he can learn from previous errors- I note the message has sunk home with him that RBCs are not nucleated.

  333. #335 Andrew Maniotis
    July 22, 2007

    DT,

    I learned some time ago that Human RBC’s aren’t nucleated. My question to you and the others has been to explain how “HIV” infection causes anemia in half of patients, to the extent they are given transfusions (of course ignore the fact that they are on AZT or HAART, whose package inserts state that anemia is present in about half the patients as does the clinical trial literature?

    Instead of ignoring my points, simply admit that you don’t have a clue and save everybody from having to endure your lies/distortions.

    For example, if dendritic cells (which are nucleated), disseminate “HIV” infection, why do the little “HIV” virions “wait” in their cytoplasmic vesicles until the dendritic cell delivers them like the angel of death to unsuspecting T cells elsewhere? Why doesn’t “HIV” undergo the same pathway of infection in a dendritic cell thought to be the hallmark of “retroviruses,” and first go to the nuclei of the dendritic cells. McDonald et al actually show the little red “vpr-”labeled particles jumping in and out of a nucleus 3 times. Amazing little virus!!!!

    Amazing mythology of science being erected by the AIDS establishment.

    For shame.

  334. #336 DT
    July 22, 2007

    Andrew, I find it very ironic you accuse me of lies and distortions, when all I have done is correct your own. You have already demonstrated your capacity for playing fast and loose with the truth several times on this blog (and have even acknowledged it, I recall).

    You implied only T-cells had the requisite receptors for HIV entry – I merely disabused you of this idea. In return I get accused of telling lies?

    If you want an example of distortions/lies, let’s look at your latest post shall we (we could select almost any at radom):

    I learned some time ago that Human RBC’s aren’t nucleated. My question to you and the others has been to explain how “HIV” infection causes anemia in half of patients, to the extent they are given transfusions (of course ignore the fact that they are on AZT or HAART, whose package inserts state that anemia is present in about half the patients as does the clinical trial literature

    This claim is revealing. You now admit you “learned some time ago” that RBCs are not nucleated (I believe I recall that previously you had tried linked AZT’s toxicity to its action within the cell nucleus). Your knowledge of pathology presumably does not extend to the make up of (nucleated) erythroid precursor cells within the bone marrow, which is where AZT’s toxicity takes effect.

    I am also intrigued you say AZT causes anemia in “half of patients to the extent they are given transfusions”. You say the package inserts and trial literature attest to this.

    Well, I recall that transfusion-dependent anemia occurs in between 5-10% of patients on AZT. The only trial literature I can find that comes anywhere close to “half” is the Fischl data where anemia occurred in 39% of those with advanced disease (AIDS) who were also on high dose AZT. Of course, anemia is a common finding in AIDS patients, even without any contribution from AZT. I hope you do not suggest all anemia in AIDS cases is solely the result of AZT?
    https://content.nejm.org/cgi/content/abstract/323/15/1009

    http://www.aidsmap.com/en/news/8D480CE7-8E2B-4F01-9487-913431A85B86.asp
    This presents data from a meta-analysis of 54 long term clinical trials involving 12640 patients with HIV showed that 1.5% to 1.8% of those on AZT in current treatment doses (500-600mg/d) had anemia -In contrast the rates of anemia in those NOT on the drug were 0.6% to 1.1%. No mention of your “50%” anywhere, and that’s from 54 clinical studies. Are you reading the “clinical trial literature” from another parallel universe or something? (Don’t answer that [It was rhetorical] – I know you are reading from the “Virusmyth” version of reality). The incidence of severe grade 3/4 anemia (the sort that requires transfusions) was only 1% in those on AZT as opposed to 0.3% to 0.6% of those not on the drug.

    (You know, the more I find out about this drug, the more I am amazed at how lethal it is!) The only caveat on this study is the fact that the meta-analysis was done by Glaxo Smith Kline. I know this will be enough for you to scream “Conspiracy!”, but it is not original company “data on file” being reported (which I would be suspicious of), but a collation of 54 clinical trials that have already been published in the literature.

    So in summary, there is nothing to suggest what you claim. Perhaps you are deliberately lying about the data, or perhaps you have access to some that confirms your claim of 50% transfusion dependent anemia rates. If so I am sure we all would all like to see it.

  335. #337 Drug Lobby
    July 23, 2007

    DT, how can a natural nucleoside, i.e. thymidine, modified by an azido group to prevent further nucleotide incorporation into the polymer chain possibly be specific to a reaction never shown to be happening in the first place in AIDS patients: the 70S RNA template-directed incorporation of nucleotides into a “preintegration complex” by reverse transcriptase in the cytoplasm, presumably after cellular entry via the endosome pathway? In other words the presumed efficacy is nonexistent.

    But the toxicity considering the obvious non-specificity, is there any way that incorporation of available nucleoside analogues such as AZT in necessary DNA synthesis cannot occur? Do the analogue chain terminators make a detour somehow to avoid substantial impairment of DNA synthesis?

    Well … yes, there are reactions with non-DNA molecules. According to Heinrich Kremer, MD: “The reactive azido molecule group is used in the experimental mitochondrion research in order to block the cytochrome oxidase enzyme in the mitochondria respiration chain. The intact mitochondria (former bacterial cell symbionts that appear in all human cells except red blood corpuscles) work with molecular oxygen (02) to produce 90% of the adenosine triphosphate (ATP) energy carrier molecules necessary for human life. The blockade of the respiratory enzyme cytochrome oxidase by AZT prevents conversion of electrons into O2. The immediate result is reduced ATP production and an increased synthesis of toxic oxygen radicals. The cells suffer from loss of energy.” ETC at http://www.virusmyth.net/aids/data/hkmbeki1.htm

  336. #338 Wewant Chris
    July 23, 2007

    Is that all you have Mr. Hinkley, a caricature of my position and an insult?

    That’s your substantive response?

  337. #339 Phineas
    July 23, 2007

    And then there’s the absolutely fascinating Franklin who believes a claim has been made that Maniotis invented risk assessment.
    And the entertainment – Bill O’Reilly style – continues: “Professor Maniotis has made no substantive points. He has only provided distorted or flat-out-false statements about the work of other scientists, as amply documented in his posts.”
    Really, Franklin, it must be so nice to have a blog-home like this where you can just make it up as you go along, right?
    We need to take note of this example of uncritical acceptance by your “friends”, who are not doing you a service, and the contrast with critical thinking at “denialist” websites.
    And what did the invention of an AIDS virus have to do with cancer risk assessments, especially lymphomas? Any fool can see that Andrew Maniotis has nothing to contribute on this subject.
    So those who are not STUPID know that the intelligent course of action is simply never to end the volley of cheap shots. How scientific.

  338. #340 Adele
    July 23, 2007

    Gene or whoever you are,
    Please don’t abuse Tara’s patience. Another thread just got closed down because of Semon style sockpuppet abuse. I don’t want that do you? Please pick a name and stick to it like the rest of us do.
    Thanks.

  339. #341 Adele
    July 23, 2007

    Gene asked how can a natural nucleoside modified by an azido group possibly be specific to a reaction And then he says In other words the presumed efficacy is nonexistent

    Like asking “how can a couple of pins be specific for a lock? In other words its impossible to pick a lock.” Newsflash to IDers it doesn’t have to be designed for something to fit by chance. They found AZT when they screened a few hundred chemicals.

    “the 70S RNA template-directed incorporation of nucleotides into a “preintegration complex” by reverse transcriptase in the cytoplasm, presumably after cellular entry via the endosome pathway”

    This is funny!

    OK, the RT incorporates nucleotides into DNA not the preintegration complex. The DNA’s not the preintegration complex its just inside it. With the RT.

    Ok and you can’t get the virus core into the cytoplasm by endosome. If its in a endosome its not in the cytoplasm. You need envelope fusion from outside cell or from in an endosome whatever.

    Does this man need a virology textbook because I have an extra one I can send him.

  340. #342 Epidemiology-LISA
    July 23, 2007

    Is Adele, the lovable one-gal lab crew, the one for you?

    She makes, sequences and grows her own stocks of non-T cell, non-stimulated non-cancerous cell line HIV all by herself. She keeps them at an undisclosed location, which isn’t in Australia, at minus 80 degrees until use. She enjoys watching children get injected with thimerosol, but disapproves of Kevin inflicting PCP on himself by overdosing on doctor’s advice. In her spare time she feeds the monkeys until they all come down with AIDS brought on by injections administered by Adele, the one-gal lab crew, herself with her non-T cell, non-stimulated non-cancerous cell line HIV, grown at home in an undisclosed location which isn’t in Australia.

    NB. The last bit of information was repeated to prevent any speculation in Murchian origins for either Adele or her HIV.

  341. #343 Adele
    July 24, 2007

    Epidemigene Simonelisa that’s really very funny. Isn’t it “murchasonian” though not “murchian”? Another question can you get through a comment without saying Murchason ERVs epigenetics or Bill OReilly?

    Again please stick to one name. WEll you killed the thread already so who cares?

  342. #344 Drug Lobby
    July 24, 2007

    Dear dear Adele, how can you be so confused over the point on AZT specificity? You see that post as an argument for Intelligent Design? You compare polymerization chemical reactions to locks and keys?

    Of course the azido group on the thymidine is a human design with the purpose of terminating the DNA chain, stopping the reverse transcription process cold, so to speak, that is destined in theory to become the “preintegration complex”.

    If you can explain to me why the AZT won’t terminate any DNA polymerization reaction it encounters, I’m all ears.

  343. #345 Adele
    July 24, 2007

    Simple misunderstanding about AZT gene and I might even explain it if you stop using sockpuppets.

  344. #346 Andrew Maniotis
    July 24, 2007

    For DT:

    Glad to see you are familiar with the fraudulent 1987 trial of Fischl et al. Did you read John Lauretson’s book and see how the FDA data on the trial is blacked out when he obtained it from the freedom of information act and posted it in the end of his book? There is no way of knowing exactly how many patients received transfusions during this trial (but it was at least about half as you agreed)because it is clear that some of the patients were swapped between the AZT group and control group at the last minute, to further scew the results from the miserable and unblinded 4 month long results they already had (before the decided to keep the fudged Boston arm of the study). When I think of AZT, I think of this study, as you did.

    Therefore, there is progress here, so I am going to drop my defensive tone and resume in this blog a sincere attitude I started with, if that’s ok with you all.

    My stance has been all along, but perhaps not obvious because of the criticisms I have made, that I realize doctors and pharmaceutical companies aren’t trying to hurt but to help. I work at a medical school. I know that. The denialists, by and large, are trying to improve things through criticism, and my posts have been no exception. I have honestly learned from this blog, as I have over the years-e.g. I used to think AZT was 100% fatal until I began meeting people who were taking the stuff for 10 years or even 12 years and were not dead although they had a plethora of side effects (often debilitating) that could all be found on the package insert. That these patients taking AZT should even be alive 10 years after AZT violates biochemistry, and all I thought I knew about the biochemistry of DNA-chain termination in living cells and especially cancer cells (but humans aren’t living cells they are organisms and group connected organisms at that, as are all primates at some point during their life cycle. These and other realizations prompted me to rethink my entire cancer therapeutics program (yes, reading the AIDS literature is relevant to cancer research) and rethink how we approach toxic cancer chemo with FuDR and other DNA disruptive agents, and I begin to understand the principles I posted before on this blog that were only to be ridiculed by those of you who KNOW what cancer and AIDS really is all about. Instead of a reductionist explanation, I began seeing that there are two great medical traditions in Western Medicine that are governed by “a law of similars” strategy (vaccination-where a like substance is presented to the organism at a low dose or in attenuated form with the hope of repeating Pasteur’s Poully-Fort demonstration with anthrax, that something in the organism will recognize an imbalance created by the like substance or attenuated antigen, and be able to restore the balance, naturally (eg. Coley’s toxins, modern cancer immunotherapies, vaccines, etc.). By contrast the “law of contraries strategy” that exists in Western Medicine a la Virchow, Erhlich, and Koch, and the German dye industry (and which dominates the reductionist approach), where a molecule binds to a side chain (like a dye binds to a fabric fiber) specifically and “kills” the thing ( I gave examples before you can see-penicillin is the prime example).

    AZT’s toxicity profile does not make sense according to a “principle of contraries” or reductionism because of the mitochondrial toxicity and the ability it must not have to distinguish host cell DNA from any other (which is why it probably acts as an antibiotic in many AIDS patients and why it reduces “viral load” signals because it suppresses all kinds of bone marrow, immune cells, B cells, etc., that generate these spurious signals (EG p24, non-specific RNA signals, HERV’s, etc.).

    By virtue of the law of similars, AZT makes sense. As an immunotoxin, it does what the homeopathic law of similars describes precisely: it boosts immune cell production shortly after the first doses (at low doses) for some time, but at high doses it kills the cells outright. So here I formally propose to you that AZT is a homeopathic remedy that stimulates T-cells precisely because it is so immunotoxic because these cells require DNA synthesis so much-so in effect it is like giving a perpetual vaccine every morning on your cornflakes, as Dr. Moore is fond of saying.

    Then I remember reading, I god help me get the goddamn quotes right (you ought to check because I have made all corrections in a book I am writing that you all have suggested-as well as distortions of information that have crept in over the years):

    McKinney et al., in an article entitled, “A multicenter trial of oral zidovudine in children with advanced human immunodeficiency virus disease” (NEJM. 1991 Apr 11;324(15):1018-25) reported that:

    “Children treated with zidovudine continued to have bacterial and opportunistic infections. The effect of the drug on the frequency of these events could not be assessed because of the lack of control groups…One or more episodes of hematologic toxicity occurred in 54 children (61 percent)anemia (hemoglobin level, <75g per liter) in 23 children (26 percent) and neutropenia (neutrophil count, <0.75X10^9 per liter) in 42 (48 percent).

    Dalakas in “Mitochondrial toxicity of antiviral drugs” (Nat Med. 1995 May;1(5):417-22) claimed that:

    “Clinical manifestations of ANA [Antiviral Nucleoside Analogs, such as AZT] toxicity: It is self-evident that ANAs, like all drugs, have side-effects. However, the prevalent and at times serious ANA mitochondrial toxic side-effects are particularly broad ranging with respect to their tissue target and mechanisms of toxicity: … Haematalogical toxicity [anemia, and other blood disorders] … Myopathy [muscle disorders] … Cardiotoxicity [heart disorders] … Hepatic toxicity [liver disorders] … Peripheral neuropathy [nerve damage]?”

    When Fischl et. al repeated their human experimentation in 1990:

    Fischl et al., in “A randomized controlled trial of a reduced daily dose of Zidovudine in patients with the Acquired Immunodeficiency Syndrome” (NEJM. 1990;323(15):1009-14) reported that:

    “178 subjects (34%) had a hemoglobin concentration below 5 mmol per liter [anemia]…A greater proportion of subjects in the standard-treatment [high dose AZT] group had a first episode of severe anemia earlier in the study, as compared with the proportion in the low-dose group. 134 subjects (26%) received red-cell transfusions (65 in the standard-treatment group and 69 in the low-dose group)…230 subjects (44%) had a [low] neutrophil [infection fighting white blood cells] count…134 (51%) in the standard-treatment group and 96 (37%) in the low-dose group…22 subjects (4%) had a [low] platelet [blood clotting cells] count?”

    Harrison’s Principles of Internal Medicine states: “[AZT], used for treating [HIV], often causes severe megaloblastic anemia caused by impaired DNA synthesis?”

    AZT alone has some of the following warnings on its package insert printed in bold and CAPITALIZED type:

    “WARNING: RETROVIR (ZIDOVUDINE, AZT) MAY BE ASSOCIATED WITH HEMATOLOGIC TOXICITY INCLUDING GRANULOCYTOPENIA AND SEVERE ANEMIA PARTICULARLY IN PATIENTS WITH ADVANCED HIV DISEASE.”

    “PROLONGED USE OF RETROVIR HAS BEEN ASSOCIATED WITH SYMPTOMATIC MYOPATHY SIMILAR TO THAT PRODUCED BY HUMAN IMMUNODEFICIENCY VIRUS. RARE OCCURRENCES OF LACTIC ACIDOSIS IN THE ABSENCE OF HYPOXEMIA, AND SEVERE HEPATOMEGALY WITH STEATOSIS HAVE BEEN REPORTED WITH THE USE OF ANTIRETROVIRAL NUCLEOSIDE ANALOGUES, INCLUDING RETROVIR AND ZALCITABINE, AND ARE POTENTIALLY FATAL.”

    Other side effects of AZT that have been listed on the AZT package insert also include:

    “Persistent headaches lasting longer than 1 month, anemia, dementia, diarrhea, muscle wasting, candidiasis, non-specific oral lesions, severe fatigue, enlarged liver and liver failure, heart failure, diabetes, unmasking of opportunistic infections including CMV retinitis, spontaneous bleeding in hemophiliacs, lymphoma, severe skin rashes, Stevens-Johnson syndrome, and other toxic reactions, back pain, body odor, chest pain, chills, edema of the lip, fever, flu syndrome, hyperalgesia, syncope, vasodilation, bleeding gums, constipation, dysphagia, edema of the tongue, eructation, flatulence, mouth ulcer, rectal hemorrhage, lymphadenopathy, arthralgia, muscle spasm, tremor, twitch, anxiety, confusion, depression, dizziness, emotional lability, loss of mental acuity, nervousness, paresthesia, somnolence, cough, dyspnea, epistaxis, hoarseness, pharyngitis, rhinitis, sinusitis, acne, changes in skin and nail pigmentation, pruritus, rash, sweat, urticaria, amblyopia, hearing loss, photophobia, taste perversion, dysuria, polyuria, urinary frequency, urinary hesitancy.”

    There also have been numerous mutagenesis studies regarding AZT and drugs with similar mechanisms of action that have been published. For example, among infants of mothers given AZT “to prevent the vertical transmission of “HIV”‘, the peer-reviewed literature has reported physical deformities result including:

    “misshapen heads, triangular faces, misplaced ears, extra fingers, albinism, cavities in the chest, webbed fingers, spontaneous abortion, and “congenital” birth defects of the heart, chromosomal damage and various cancers. ”

    Other important warnings on the package insert of AZT carcinogenesis, mutagenesis, and impairment of fertility include:

    “Zidovudine was administered orally at three dosage levels to separate groups of mice and rats (60 females and 60 males in each group). Initial single daily doses were 30, 60, and 120 mg/kg/day in mice and 80, 220, and 600 mg/kg/day in rats. The doses in mice were reduced to 20, 30, and 40 mg/kg/day after day 90 because of treatment-related anemia, whereas in rats only the high dose was reduced to 450 mg/kg/day on day 91 and then to 300 mg/kg/day on day 279.”

    “In mice, seven late-appearing (after 19 months) vaginal neoplasms (5 nonmetastasizing squamous cell carcinomas, one squamous cell papilloma, and one squamous polyp) occurred in animals given the highest dose. One late-appearing squamous cell papilloma occurred in the vagina of a middle dose animal. No vaginal tumors were found at the lowest dose.”

    “In rats, two late-appearing (after 20 months), non-metastasizing vaginal squamous cell carcinomas occurred in animals given the highest dose. No vaginal tumors occurred at the low or middle dose in rats. No other drug-related tumors were observed in either sex of either species.”

    “It is not known how predictive the results of rodent carcinogenicity studies may be for humans. At doses that produced tumors in mice and rats, the estimated drug exposure (as measured by AUC) was approximately 3 times (mouse) and 24 times (rat) the estimated human exposure at the recommended therapeutic dose of 100 mg every 4 hours.”

    ” In the presence of metabolic activation, the drug was weakly mutagenic at concentrations of 1000 µg/ml and higher. In an in vitro mammalian cell transformation assay, zidovudine (AZT) was positive at concentrations of 0.5 µg/ml and higher. In an in vitro cytogenetic study performed in cultured human lymphocytes, zidovudine induced dose-related structural chromosomal abnormalities at concentrations of 3 µg/ml and higher.”

    “In two in vivo micronucleus studies (designed to measure chromosome breakage or mitotic spindle apparatus damage) in male mice, oral doses of zidovudine 100 to 1000 mg/kg/day administered once daily for approximately 4 weeks induced dose-related increases in micronucleated erythrocytes. Similar results were also seen after 4 or 7 days of dosing at 500 mg/kg/day in rats and mice.”

    Human chromosome breakage results are reported on the package insert also:

    “In a study involving 11 AIDS patients, it was reported that the seven patients who were receiving Retrovir (1200 mg/day) as their only medication for 4 weeks to 7 months showed a chromosome breakage frequency of 8.29±2.65 breaks per 100 peripheral lymphocytes. This was significantly (P< 0.05) higher than the incidence of 0.5±0.29 breaks per 100 calls that was observed in the four AIDS patients who had not received Retrovir.”

    A skull and cross bones warning appears on the Sigma Catalogue purchasing information for AZT: Rather than muscular men climbing a mountain, the following warning is advanced:

    Toxic by inhalation, in contact with skin and if swallowed. Target organ: Blood Bone Marrow. If you feel unwell, seek medical advice (show the label where possible). Wear suitable protective clothing.

    So, all in all, AZT is good stuff to give a pregnant woman? No I don’t think so.
    A developing fetus. Perhaps not.
    The devil’s in the dosage. Perhaps. But the data suggests no specificity for AZT and any so-called retroviral reverse transcriptase, but does suggest a homeopathic law of similars is at work (with lower doses of AZT) which stimulates production of the very cells it eventually will kill. The fact that people take it continuously and for years violates every principle we know about cancer chemo, other than a law of similars as I have stated.

    It is really good to be sure, therefore, if someone really has 30pg/ml p24 or 29 pg/ml of p24 before doing drug experiments with drugs like these. Especially with children I would think.

    Ok-now sling your insults.

    Cheers,

    andy

  345. #347 Andrew Maniotis
    July 24, 2007

    Not for the faint of HAART!

    In Botswana, Step to Cut AIDS Proves a Formula for Disaster

    http://www.washingtonpost.com/wp-dyn/content/article/2007/07/22/AR2007072201204_4.html?hpid=topnews

    By Craig Timberg
    Washington Post Foreign Service
    Monday, July 23, 2007; Page A01

    NKANGE, Botswana — Doctors noticed two troubling things about the limp, sunken-eyed children who flooded pediatric wards across Botswana during the rainy season in early 2006: They were dying from diarrhea, a malady that is rarely fatal here. And few of their mothers were breast-feeding, a practice once all but universal.

    After the outbreak was over and at least 532 children had died — 20 times the usual toll for diarrhea — a team of U.S. investigators solved the terrible riddle.

    A decade-long, global push to provide infant formula to mothers with the AIDS virus had backfired in Botswana, leaving children more vulnerable to other, more immediately lethal diseases, the U.S. team found after investigating the outbreak at the request of Botswana’s government.

    The findings joined a growing body of research suggesting that supplying formula to mothers with HIV — an effort led by global health groups such as UNICEF — has cost at least as many lives as it has saved. The nutrition and antibodies that breast milk provide are so crucial to young children that they outweigh the small risk of transmitting HIV, which researchers calculate at about 1 percent per month of breast-feeding.

    “Everyone who has tried formula feeding . . . found that those who formula feed for the first six months really have problems,” Hoosen Coovadia, a University of KwaZulu-Natal pediatrician and author of a recent study on formula feeding, said from Durban, South Africa. “They get diarrhea. They get pneumonia. They get malnutrition. And they die.”

    That’s what happened in Nkange, a tiny village on the sandy northern edge of the Kalahari Desert. In a cluster of several dozen homes here, eight children under 2 died during the four-month-long diarrhea outbreak, according to interviews with families. Only two had ever been breast-fed, and only one was being breast-fed at the time of the outbreak.

    Chandapiwa Mavundu, 28, a mother of three who has HIV, said she never breast-fed her son, Kabelo, because government nurses warned her not to.

    When he died at 8 months, after two months of withering diarrhea and vomiting, she could not muster the strength for the long walk to the graveyard. Instead, Mavundu stayed behind, she said, weeping amid the thatch-roofed huts and the dust and the goats as a hastily assembled parade of relatives carried her son’s shrunken body away in a tiny, cream-colored coffin.

    “That was the only boy child I had,” said Mavundu, who has sad, wide-set eyes and long braids that dangle past her shoulders. “I loved him very much.”

    The medical records kept by Mavundu and other families here echoed the finding of the U.S. investigators: Government clinics often ran out of cans of formula, forcing parents and grandparents to buy cow’s milk or feed their children with diluted porridge or even flour and water.

    Many of the babies had recurrent sicknesses and registered steep drops in their growth patterns during their final months. When the diarrhea struck, it was severe, prolonged and difficult for even doctors to cure. One child survived diarrhea only to die soon after from pneumonia, another disease that breast-feeding helps prevent.

    “Since I was a girl, I can’t remember a time when we lost so many kids,” said Ntselang Swimbo, 66, whose 9-month-old grandson died during the outbreak. “Once a kid got diarrhea, you knew the chance of surviving was almost zero.”

    The vast diamond reserves in this landlocked southern African nation have allowed Botswana’s government to build a safety net unmatched on the continent, offering its 1.8 million citizens cradle-to-grave support for education and health care. And though it has one of the world’s highest rates of HIV, with one in four adults infected, it has some of Africa’s most celebrated programs to combat AIDS, including effective measures to prevent mothers from infecting their children during pregnancy and birth.

    The country was also a pioneer in the international drive to protect babies at risk of becoming infected through breast-feeding. In 1997, the United Nations began urging new mothers with HIV to use formula wherever supplies could be provided safely and reliably. Botswana, with an extensive public water system, good roads and a legacy of competent governance, joined the UNICEF-led effort and agreed to pay for the program as a standard service to new mothers.

    Chandapiwa Mavundu’s 8-month-old son died during a diarrhea outbreak in Botswana last year that a U.S. team has linked to the use of infant formula.

    There were skeptics. Some international public health experts, including Coovadia, cautioned that few Africans had the means to prepare formula in a sanitary manner — a process that requires access to clean water, utensils, formula powder and heat for sterilization.

    And even for those who could make formula safely, some experts warned, breast-feeding’s other health benefits could not easily be replaced. A study by Coovadia and other South African researchers published in the medical journal Lancet in August 1999 found that breast milk alone, when not mixed with other foods, was no more likely to infect children than formula.

    But Botswana’s health officials were determined to begin the programs. In a recent interview, Health Minister Sheila D. Tlou angrily recalled a conference of international policymakers in Montreal a month after the Lancet article appeared. Some favored urging mothers with HIV in rich countries to use formula while telling those in poorer, less-developed ones to breast-feed.

    “We saw red!” Tlou said. She recalled asking other participants in the meeting: “Why are you sentencing all of our children to death? And why are you sentencing all of us to psychological damage in knowing that we were the ones who infected them?”

    The program started slowly because few women were willing to be tested for a virus that at the time was a death sentence. But as Botswana expanded the availability of antiretroviral drugs, which can dramatically extend and improve lives, HIV testing gradually became routine for pregnant women.

    Those with the virus received a series of antiretroviral pills in the final weeks of their pregnancies, and their newborn children received a dose of syrup laced with another powerful anti-AIDS drug in their first hours of life.

    The rate of HIV among babies born to mothers with the virus fell from 40 percent in 2002 to 6 percent. Demand for the free government formula soared.

    Among the beneficiaries was Mavundu. She didn’t have reliably sterile utensils or a stove, as U.N. agencies envisioned in their policy statements. But she did have access to firewood for cooking. And the seemingly clean water that flowed from a communal tap was just an eight-minute walk from her compound, consisting of round, dirt-floor huts and a fenced yard that she shared with her family and its livestock, including packs of voracious chickens.

    Unusually for rural Africa, there was also a government clinic nearby and, she was told, a reliable supply of Nan, a popular formula marketed by the international food group Nestlé, to keep her playful, chubby-cheeked son strong and healthy.

    But it was a promise, Mavundu soon discovered, that the government was unable to keep.

    “Sometimes it was there,” she recalled. “Sometimes it was not there.”

    A Shifting Consensus

    The government later blamed hitches in its contracting system for the formula shortages. But supply was not the only problem uncovered by the investigators from the U.S. Centers for Disease Control and Prevention, which announced its findings at a scientific conference in Los Angeles in February.

    Testing of government water pipes in 26 villages in northeastern Botswana found contamination in every one, apparently caused by flooding during the heavy rainy season. Tests of the stools of sick babies also found dangerous waterborne pathogens such as cryptosporidium and an especially virulent strain of E. coli.

    Investigators determined that it was mainly the babies who were not breast-fed who got sick from the dirty water. Among a group of infants at one hospital, those admitted for diarrhea were 50 times more likely to be fed formula or cow’s milk than those admitted for other ailments. Cow’s milk is more difficult for babies to digest and lacks the antibodies found in breast milk.

    In one village the team visited, 30 percent of the formula-fed babies had died; none of those being breast-fed had.

    The report also reflected the shifting scientific consensus on breast-feeding. In the years since Botswana began its formula-feeding program, studies have increasingly shown that the risk of HIV transmission comes mainly from the combination of breast milk and other foods, such as formula and solids, that damage the lining of a baby’s intestines, inviting infection.

    In one study in Botswana, breast-fed babies contracted HIV at a slightly higher rate than those fed with formula, but formula-fed babies were more likely to die. By the time the children in the study reached 18 months, similar numbers from both groups were alive and free of HIV.

    Putting a mother on an effective combination of antiretroviral drugs, which are widely available in Botswana and some other African nations, also dramatically cuts the risk of transmission through breast-feeding — likely to less than 2 percent, Coovadia said.

    “You can protect kids, and you can give them the benefits of breast-feeding,” he said.

    UNICEF, after distributing 365,000 packs of formula in eight African countries — and providing training and technical assistance to the program in Botswana — began phasing out its infant-feeding programs in 2002.

    UNICEF officials also participated in an October 2006 conference that issued new guidelines reemphasizing the importance of breast-feeding and warning that formula can be dangerous in all but the most developed, reliably sanitary settings.

    “There are very few places where those conditions exist,” Alan Court, director of programs for UNICEF, said in an interview from New York.

    Health officials in Botswana remained unconvinced. Tlou, the health minister, said the outbreak was a one-time occurrence that should not, by itself, dictate a new policy. Officials instead are focusing on making formula feeding safer by encouraging women to boil water and feed their babies using cups, which are easier to clean than bottles.

    She also said the ministry will monitor emerging studies to determine if a change is warranted. “We are amenable to research, especially our own research,” she said.

    The debate, which has consumed global public health officials for years, has not reached the grieving mothers of Nkange village. None expressed any suspicions about water contamination or about the dangers of feeding formula rather than breast milk to babies.

    “It was just an outbreak,” Swimbo said.

    Mavundu, who is pregnant again, has reached the same conclusion. Her new baby is due in October.

    “I think it’s a boy,” she said, smiling, with her hand on her rounded belly.

    Since the loss of Kabelo, Mavundu has also started on a combination of antiretroviral drugs that should control her AIDS symptoms and also make breast-feeding far safer. But no one has told her that.

    When rainy season arrives in the first months of her new baby’s life, she said, “I know that I will give the Nan.”

    *Question:

    Can you be “HIV” positive with a value of 2 consecutive tests exceeding or equaling 30pg/ml p24 protein versus 29pg/ml of p24 protein, and do you need toxic antiretrovirals if you have a consistent value of 30pg/ml value versus a consistent p24 value of 29pg/ml or lower? Why are healthy control cells considered by the DAIDS culturing manual to be 29pg/ml or less on consecutive tests while diseased,’HIV’ infected cells are valued at 30pg/ml or more (*see below).

    Does anyone know if these woman who were dissuaded from breast feeding and who tested positive for “HIV” were tested according to The DAIDS 1997 official “HIV” culturing manual, where it says, under quality control, Section VI, page 45, “Do not use PHA stimulated PBMC older than 3 days post stimulation when testing them for the absence of HIV from your healthy donor source,” and in the Reporting Results Section (section VII), a rationale follows that apparently employs both healthy (or non-infected cells) and infected cells-although I don’t think anybody tests intentionally non-”infected cells”) in a manner that is rational or what we would considered CONTROLLED. For example:

    Cultures whose supernatant meet one of the following criteria are considered culture positive IF:

    “Two consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml (read: from a healthy donor source), of which the second value is at least four times greater than the first value or “out of range” (O.D.>2) or

    “Two consecutive HIV p24 antigen VQA CORRECTED values (read: from a healthy donor source) that are “out of range (Optical density.> 2); or

    “Three consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml (read: from a healthy donor source), where neither consecutive value is > four times the previous sample, but the third value is at least four times greater than the first,”

    Would you consider a sample negative (read: from a healthy donor source) if the 3 consecutive HIV p24 antigen VQA corrected values read (first test) 25 pg/ml, and (second test) 15 pg/ml, (third test) 5 pg/ml?

    Would you use these cells as uninfected controls?

    Asked another way, are these control cells considered non-infected if they read 25 on the first reading, and 15 on the second and 5 on the third?

    Try a second sample using the first criterion stated above:

    “Two consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml, of which the second value is at least four times greater than the first value or out of range” (O.D.>2)

    First sample =6pg/ml: second sample)=23pg/ml

    Yes? No? Maybe better get other “healthy cells” than go with a 6 and a 23? Or are these two readings enough to say, “Aw-what the heck-they aren’t over 30pg/ml and the second series isn’t quite 4 times greater that the first value of 6, so I will just tell the doc that they are negative, and will tell the patient nothing about it?

  346. #348 Adele
    July 24, 2007

    Andrew has a serious problem with the first anti HIV drug. Hmmm, so does every doctor and scientist and even me! It was a good try but not good enough when they found better things.

    Andrew wants us to live in a world where there aren’t any drugs where there aren’t any vaccines were if there’s a chance a kid will get a stomach ache from a medicine that saves her life she shouldn’t have it. She should just die and save the rest of our tax money. Right andrew? Very sad.

    Its funny even though everyone agrees AZT shouldn’t be used by itself anymore with a few exceptions Andrew still has to selectivley quote sloppy cut and paste like this
    “Children treated with zidovudine continued to have bacterial and opportunistic infections. The effect of the drug on the frequency of these events could not be assessed because of the lack of control groups…One or more episodes of hematologic toxicity occurred in 54 children (61 percent)anemia (hemoglobin level,

    why does he cut it off? HEre’s why, the authors say
    Many of these abnormalities resolved spontaneously, but 30 children required transfusions or a modification of the dose of zidovudine. Only three children had to stop receiving the drug because of hematologic toxicity.

    and later
    There was marked improvement in weight gain, cognitive function (mainly in children less than 3 years old), serum and cerebrospinal fluid concentrations of p24 antigen, and the proportion of cerebrospinal fluid cultures negative for HIV. CD4+ lymphocyte counts (mean at base line, 0.263 x 10(9) per liter) improved during the first 12 weeks, although the improvement was not sustained through the 24th week.

    No AZT’s not a great drug on its own mainly because the virus mutates not the side effects, but they aren’t good. Not as bad as Andrew says though and everythings a poison at the right dose.

  347. #349 Dale
    July 24, 2007

    Andy writes Can you be “HIV” positive with a value of 2 consecutive tests exceeding or equaling 30pg/ml p24 protein versus 29pg/ml of p24 protein, and do you need toxic antiretrovirals if you have a consistent value of 30pg/ml value versus a consistent p24 value of 29pg/ml or lower? Why are healthy control cells considered by the DAIDS culturing manual to be 29pg/ml or less on consecutive tests while diseased,’HIV’ infected cells are valued at 30pg/ml or more (*see below).

    No, no, and it’s the sensitivity of the assay. And you haven’t stated it quite correctly anyway. It’s two consecutive measurements >30 with the second being at least 4x the first or three consecutive measurements >30 with the 3rd being at least 4 x the first. To me that reads there’s got to be at least one measurement of 120 or more.

    Does anyone know if these woman who were dissuaded from breast feeding and who tested positive for “HIV” were tested according to The DAIDS 1997 official “HIV” culturing manual, where it says, under quality control, Section VI, page 45, “Do not use PHA stimulated PBMC older than 3 days post stimulation when testing them for the absence of HIV from your healthy donor source,”
    It’s highly unlikely they were tested by HIV culturing as that is both expensive and not as sensitive as antibody testing.

    Would you consider a sample negative (read: from a healthy donor source) if the 3 consecutive HIV p24 antigen VQA corrected values read (first test) 25 pg/ml, and (second test) 15 pg/ml, (third test) 5 pg/ml?

    Would you use these cells as uninfected controls?

    Asked another way, are these control cells considered non-infected if they read 25 on the first reading, and 15 on the second and 5 on the third?

    Yes, yes and yes. See above.

    First sample =6pg/ml: second sample)=23pg/ml

    Yes? No? Maybe better get other “healthy cells” than go with a 6 and a 23? Or are these two readings enough to say, “Aw-what the heck-they aren’t over 30pg/ml and the second series isn’t quite 4 times greater that the first value of 6, so I will just tell the doc that they are negative, and will tell the patient nothing about it?

    From reading the manual I would imagine that third and fourth and possibly 5th readings would be made; readings are continued until the cultures are clearly positive by criteria 1 or 2 or 28 days old. Were there still a question, I assume the cells would be tested by PCR.

  348. #350 Andrew Maniotis
    July 24, 2007

    Libya Announces Transfer of Medics

    Anybody know how “HIV” can be transfered so efficiently to so many all at once through “pills?” I guess when the AIDS establishment decides someone tests positive because of sex it is worthy of a homicide trial, but here they just say, “woops!”

    Statement by Secretary Condoleezza Rice
    Washington, DC
    July 24, 2007

    We applaud today’s decision by the Bulgarian and Libyan governments to
    transfer the five Bulgarian nurses and the Palestinian doctor to Bulgaria,
    which follows the Libyan Higher Judicial Council’s July 17 commutation of
    the medics’ death sentences. The United States had repeatedly urged Libya
    to find a way to allow the medics to return home. This is an important step in Libya’s continuing positive reengagement with the international
    ommunity.

    Along with its European allies, the U.S. has contributed to efforts to ensure this long overdue outcome, including through the establishment of the Benghazi International Fund, a private initiative to provide care and assistance to the over 400 HIV-infected children and their families.

    We remain concerned about these young victims and will continue our support for Their treatment, including through our contribution to the Baylor College of Medicine’s Pediatric AIDS Initiative’s program in Libya and other
    initiatives.

    I wonder if they’ve read that:

    “viral load is only able to predict progression to disease in 4% to 6% of HIV-positives studied, challenging much of the basis for current AIDS science and treatment policy” [Rodriquez B, Sethi AK, Cheruvu VK, et al. Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection. JAMA 296(12):1498-506, 2006;Cohen J. Study says HIV blood levels don’t predict immune decline. Science 313(5795):1868, 2006.

    Woops!

    Cheers,

    Andy

  349. #351 Dale
    July 24, 2007

    Woops is right Andy. Hopefully ‘they’ have read Rodriquez more carefully than you apparently have. Because although it says a lot of things, it doesn’t say that viral load is only able to predict progression to disease in 4% to 6% of HIV positives studied.

  350. #352 Adele
    July 24, 2007

    Yeah Andrew’s quoting himself again not Rodriguez.

    Here’s from the far right AAPS-TWYCSLOS, American Association of Physicians and Surgeons who wish this was a Theocracy Where You Can Shoot “Libs” on Sight:

    “Andrew Maniotis, Ph.D., of the University of Illinois at Chicago notes that “viral load is only able to predict progression to disease in 4% to 6% of HIV-positives studied, challenging much of the basis for current AIDS science and treatment policy” (JAMA 2006;296:1498-1506). Moreover, influenza vaccination is a cause of false positive screening tests and indeterminate Western blot tests (NEJM 2006;354:1422-1423).”

    The first part of the quote’s not even from him, its on a fake HIV information site for a while.

  351. #353 DT
    July 24, 2007

    Andrew “Ok-now sling your insults” Maniotis, I asked for documentation of transfusion-dependent anemia in those recieving AZT, not a list of its side effects. You are on record as saying the incidence of this particular side effect is 50% as shown by product leaflets and published studies.

    I am not here to sling insults, I just want the truth from you. Can we have some citations for your claim?

    All you did was quote:
    1. The original Fischl study, which even though patients had advanced AIDS, which causes anemia, showed only a third on AZT had anemia,
    2. The McKinney study (again looking at advanced AIDS) which had 27% with anemia that needed dose adjustment of AZT OR transfusion (Thanks for the true numbers on this one, Adele!). Presumably the percentage needing transfusion is somewhat less than 27%.
    3. Another Fischl study where 26% of patients on AZT needed transfusion.
    4. Product leaflets for AZT which do not indicate what percentage of patients on AZT get severe anemia.

    I, on the other hand, referred you to a meta-analysis of 54 different published trials where the incidence of anemia requiring transfusion was 1% (versus up to 0.6% in thoses not on AZT), and I did not need to massage the numbers or leave out data to beef up my claim, like you have.

    My question is a simple one, and remains the same: Can you provide a citation for your claim that transfusion dependent anemia occurs in 50% of those on AZT? One paper will do, just one….

  352. #354 cooler
    July 24, 2007

    Azt is a chemotheraputic drug that wasnt even patented because it was so useless and dangerous. The damn guy that invented says its a horrible drug. What is wrong with you people? Give a drug that kills dividing cells to treat a disease thats supossed kill cells as well, that makes a lot of sense, for an infection thats in only a small % of tcells.

    You guys need help. In a hundred years this is going to be looked at as the dark ages of medicine, and you guys will be laughed at in the history books.

  353. #355 Dan
    July 24, 2007

    In a hundred years this is going to be looked at as the dark ages of medicine, and you guys will be laughed at in the history books.

    We won’t have to wait that long.

    Although, it’s not so laughable as it’s incredibly tragic…and pathetic the way these “scientists” hold onto the greatest failure of modern medicine. They really are a sorry lot.

  354. #356 Adele
    July 25, 2007

    DT,

    Don’t hold your breath waiting for the reference. Andrew drops his misquotes, disappears and comes back a week later with something different. Its flu false positive one week and when we show he misquoted its some vaccine and then its AZT the next week.

    Andrew gives a quote up there about viral load. He gives his source. Thing is, the source doesn’t have that quote in it. Andrew lied to us again. I’m done taking anything from Andrew seriously.

    If I was still interested in Andrew I might ask him this question though since he’s down with the anti-immigrant AAPS, “American Association of Phact-challenged Surgeons” Do people in the AAPS think undocumented aliens should be lethally injected as a matter of policy when they come to an ER, or do they just think it should be left up to each “American-Associated Phact-challenged Surgeon”?

  355. #357 Adele
    July 25, 2007

    I want to clarrify this.

    I didn’t say Andrew thought this stuff about immigrants I’m sure he just hangs with the ultra right AAPS neanderfolk because they’re the only people who take him seriously.

  356. #358 Adele
    July 25, 2007

    The diarrhea deaths in Botswana has been on my mind.

    There’s over a thousand peer-reviewed articles on breastfeeding and HIV. Nobody with cred who says HIV doesn’t get transmitted by breastfeeding. And everyone who works on this wants to keep babies and mothers alive. So if there’s controversy its because scientists are trying to find the facts and best approach.

    I’ve read about maybe ten or twelve of thos articles but abstracts from alot more but not all. I don’t expect Kevin and Maniotis and other people to read many of these articles and they obviously haven’t. But they haven’t even read the Lancet article from earlier this year the one they all talk about. And they don’t even read the Washington Post article Maniotis pasted up there.

    In the article
    The rate of HIV among babies born to mothers with the virus fell from 40 percent in 2002 to 6 percent. Demand for the free government formula soared.

    OK, so first formula helped to cut this rate. No expert denies safe formula cuts transmission.

    SEcond thing though the only reason Coovadia and other people are even considering exclusive breastfeeding is antivirals. They get viral load down far enough risk of breastfeeding isn’t nearly as high anymore. So low if you have to choose between bad formula and breastfeeding with good antivirals breast could be best but it’s still being looked at and too early to know.

    Didn’t the denialists read the article? They go on about how bad the drugs are. Then they say breastfeeding is so great. But the only reason its so great is, its possible because of the drugs! No drugs, we’d still be at 40% transmission.

    The other thing about the article they didn’t see. It was a rainstorm not formula feeding spreading diarrhea. The 532 children who died, that rate was 20 times the usual deaths in a year. It was rainy season, some sewage or something got in water pipes, and kids died. Breastfeeding protects the linings better than formula. It wasn’t formula killed people it was E. coli. If you could know in advance it was a bad rainy season maybe breastfeeding is better for that time. But this was a special incident. Its not like formula is blanket bad and breast is blanket good.

    More complicated that Lancet study Kevin and people always talk about without reading it the mothers there who chose formula that’s right CHOSE they weren’t forced were the ones with really low CD4s and they knew it and that’s why they chose formula. So they weren’t as healthy and there babies probably too.

    Another thing, the Lancet authors only looked at 6 months. But other people show transmission risk from breast is highest between 6 and 24 months. And also at 6 months survival it doesn’t account babies who will die of AIDS at 4 or 5. So some situations, breast is best up to six months maybe but by five years it can even out or favor formula.

    Lots of other stuff but obvi very complicated. I’m glad and probably all those women who have to deal with this are glad it’s not men like Andrew and Kevin who get to make the choice for them. People who just say well breast is natural so breast is best and who cares what happens to your baby it makes me feel better.

    While Kevin and Andrew exploit tragic deaths from a rain born local diarrhea problem and twist them into a science bashing tool, hundreds of MDs and other people are working on getting answers that are going to help people. That’s science for you.

  357. #359 DT
    July 25, 2007

    Adele, the Botswana episode demonstrates how difficult it is sometimes in the developing world without access to the things we take for granted. The moms are really between a rock and a hard place – Either breast feed and risk infecting your baby with HIV, or bottle feed and risk infecting your baby with gastroenteritis (and acquire the stigma of being “HIV” because you bottle feed). Either option could be lethal.

    For a first world perspective, one needs to look no further than at Christine M -she had the choice available to her to bottle feed EJ. This would doubtless have been a very safe option in sunny California, and have minimal risk of causing harm by causing E. coli gastroenteritis. The Botswana moms ostensibly face the same choices, but the consequenses of their choices are quite different because of the situation in which they live.

    Re Cooler on AZT and its origin:

    “Azt is a chemotheraputic drug that wasnt even patented because it was so useless and dangerous. The damn guy that invented says its a horrible drug.”

    I presume Cooler means David Belz, the developer of AZT. Belz was said to have claimed that “AZT was shelved for two reasons: My studies showed that it caused cancer at any dose and it was too toxic even for short term use.” (This claim being widespread in denialist circles, and picked up more or less by our fact-challenged “rethinker”, Cooler).

    This is what Belz had to say when asked directly if he had said what he was quoted as saying (and this is true, since it comes direct from David Crowe on Virusmyth):

    “Now let me say that I am aware of the existence of certain quotes attributed to me on the Internet, such as the one you mentioned in your letter. Such quotes are completely untrue!”

    Regarding its chemotherapy potential:

    “I prepared 1 gram of crystalline AZT and sent it to my friend Dr. Alan Sartorelli, Professor of Pharmacology at Yale University, for testing against animal cancers. It proved to be completely inactive in all of the test systems he employed. In my laboratory I found AZT incapable of inhibiting the growth of Jensen sarcoma cells in vitro at very high concentrations. Thus, AZT showed no activity as a potential anticancer drug at that time.”

    Statements from Cooler that AZT was both “useless” as a cancer drug and “dangerous” are nonsense, and represent something of a biochemical paradox. Antimetabolite activity and potential use as a chemo agent will usually parallel cellular toxicity. We know from its developer that AZT was shelved purely because it had no demonstrable anticancer or antimetabolite activity, and not because it was shown to be toxic or because it caused cancer. Belz did not go on to study AZT’s potential to cause cancer, or study its toxicity, as he told David Crowe.

  358. #360 Nestle
    July 25, 2007

    Adele, you’re a liar and a denialist. In one comment about breastfeeding you begin by calling it a tragedy but end by comparing the infant deaths from formula feeding to receiving a scratch on the leg.

    This time you make an even more implausible claim than when you pretended to give a shit about African children dying: Now you want us to believe that you’ve “thought about it”. Adele, the process of thinking is supposed to get you somewhere. Apart from changing your tack from “really obvious fact” (in theory) to “very complicated” (in practice), I see no evidence that all your reading and thinking got you anywhere. You’re still far more interested in your apologetics for Nestle and your jabs at Kevin and Andy than you are in even the briefest tip of a hat in recognition of the tragedy that has happened.

    In the article
    “The rate of HIV among babies born to mothers with the virus fell from 40 percent in 2002 to 6 percent. Demand for the free government formula soared.”
    OK, so first formula helped to cut this rate. No expert denies safe formula cuts transmission.

    So is that science for YOU Adele? Public demand soars for something, so it must be good and helpful – as advertized?

    Of course SAFE formula feeding that doesn’t lead to malnutrition or harm the lining of the gut etc. PER DEFINITION cannot but cut transmission of whatever is in the breastmilk.

    A megadose of AZT cuts transmisson
    The 5 year life expectancy of an HIV+ gay in the mid-eighties cuts transmission
    Early infant death cuts transmission.
    Cutting off a woman’s breasts or a man’s penis will do much the same to transmission.
    No expert denies that either.

    Is that science for you Adele?

  359. #361 Adele
    July 25, 2007

    Michael or whoever you are

    I invite you to read the article. It’s just a newspaper article it would be better if you read the Lancet report and then some other studies but its a place to start.

    The sentence I gave is in context of drugs have cut transmission from 40% to 6% and formula also had some contribution. It’s the drop in transmission not demand for formula proving drugs and formula cut transmission. The Lancet study author Coovadia says this not me.

    Again without antiretrovirals this discussion wouldn’t be possible. The risks of breastfeeding would outweigh any protective effects. We know this from studies from before any drugs were around and in places where there aren’t drugs. No one who has a clue about this topic denies it.

    If you’ve got counter evidence let’s see it. But it’s easier and funner to call me names I know so if that’s what you want go ahead.

  360. #362 Nestle
    July 25, 2007

    Adele,

    I see now that you didn’t claim to have thought about anything at all. You just said it’s been on your mind. But I do appreciate your sudden non-combative approach; It’s as heart warming as “gently heating mother’s milk”, if you’ll allow.
    http://scienceblogs.com/aetiology/2007/07/tripoli_sixhome_and_free.php#comment-512818

    But dear me, Adele, reading through all those studies on breastfeeding and the best you can do is,

    The sentence I gave is in context of drugs have cut transmission from 40% to 6%

    I guess it’s silly me who thought the context was infants dying from a horrible, easily avoidable, thoroughly disgusting medical scandal killing real babies.

    If you’ve got counter evidence let’s see it.

    You betcha, Adele of the noble heart, (you do know the meaning of your own name don’t you?) I’ve got counter evidence! But do you really think it has escaped anybody’s notice that you ‘forgot’ to actually present the ‘evidence’? Is that how you do science Adele?

    Again without antiretrovirals this discussion wouldn’t be possible

    At last a true statement. This was never about the children, the mothers or the breastfeeding. Without the antiretrovirals this wouldn’t have you or your masters’ interest.

    Sweet dreams.

  361. #363 Michael
    July 25, 2007

    Dear lying AIDS DENIALIST Adele. Whats the matter girl? You can dish it out but you can’t take it?

    You deserve vitriolic ad hominem and verbal attack even more than most of your fellow thugs and denialists, because that is all that 95% of what you write is composed of.

    By the way, I am not Nestle. I am Michael. Who Nestle is, I do not know.

    But I do know you are a lying denialist Conspiracy theorist, with your crap about Dr. Maniotis that he “just hangs with the ultra right AAPS neanderfolk”.

    If you don’t have anything intelligent to add to the conversation, Adele, then perhaps you should consider shutting your denialist pie hole!

    Even better, perhaps you should spend your time a bit more wisely and go see a psychotherapist for your obvious discomfort with sex and the human body, especially your own!

    Your obvious discomfort with your own mammary glands was more than evident in your statement about breast feeding:

    “People who just say well breast is natural so breast is best and who cares what happens to your baby it makes me feel better”.

    You are one sick little AIDS and reality denialist Adele! Now quit staring at your lab monkeys sexual organs and get back to work!

  362. #364 Michael
    July 25, 2007

    It really is fairly obvious to me that so many of the real HIV believing AIDS denialists are very uncomfortable with human sexuality and the human body. They only thing they can do is to consider such things soley from clinical points of view that lack any semblance of humanity or reality. They are freaked out over sex and it is no wonder they believe so rabidly that AIDS is a sexual disease and that human reproduction must be stopped because it is too scary and dangerous and the only way of reproducing should be done invitro from a test tube.

    What a bunch of sick repressed freaks of nature!

    It is always so obvious that many sexually dysfunctional and warped personalities are often behind the belief that HIV causes AIDS.

  363. #365 Michael
    July 25, 2007

    Speaking of blatantly obvious sexually repressed human beings, the big daddy of all of the AIDS denialists, John P. Moore himself, breaks out in a cold sweat if anyone discusses something sexual around him. The man is totally paranoid of sex and sexual desires.

    No wonder he spends his time trying to invent microbicides to spread on his lab monkeys dicks and vaginas! No wonder he is trying to come up with microbicide anal and vaginal goo rings. No wonder he is obsessed by gays and obsessed by circumsizing the well endowed Africans.

    The man is a total sexual repression case.

    Speaking of sexual repression and dysfunction, I would love to hear the AIDS denialist Robster, Roy, Adele, DT’s, Richard Jefferies, and Chris Nobles experiences and attitudes with sex. But I can just picture it. They would all be very clinical about it and insist on the quadrupling of condoms.

    Nahhhh, they would most likely NEVER even remotely consider having sex at all, let alone consider simply enjoying it as a natural expression of human intimacy and sharing and playing and reproducing.

    I would bet a dollar to a doughnut they are all extremely sexually repressed!

    I wonder if any of them have ever even had sex. They were probably all taught that it is wrong and bad and dirty and if they masturbate their hands will fall off or grow hair. I seriously doubt that any of these fools have ever considered the role that sexual repression takes in all of their lives!

    The belief that sexually transmitted HIV causes AIDS just makes such total sense to such sexually repressed people as these. No wonder they are so freaked out over it all! The very mention of the word breast or penis or vagina in anything but the strictest of clinical use, and they WOULD JUST FREEEEEEEEEEEEEEEEEEEEEEEEEEEEAAAAAAAAAAAAAAAKKKKKKKKKKK OOOOOOOOOOOOOOOOOOOOOUUUUUUUUUUUUUUUUUUUUUUUUUUTTTTTTTTTTTTTTTTTTTTT!!!!!!!!!!!!!!!!!!!!!

  364. #366 Michael
    July 26, 2007

    Dear HIV-OPHOBES, please do the world a favor and go get some counseling.

    WARNING: only someones own filthy and guilt and shame filled and judgemental mind could conceive of anything “filthy” in the following)

    FOR ALL OF YOU SEXUALLY REPRESSED HIVOPHOBIC BELIEVERS who yet believe the slogan that “HIV IS THE VIRUS THAT CAUSES AIDS”:

    Freud noted that, at different times in our lives, different parts of our skin give us greatest pleasure. Later theorists would call these areas erogenous zones. It appeared to Freud that the infant found its greatest pleasure in sucking, especially at the breast. In fact, babies have a penchant for bringing nearly everything in their environment into contact with their mouths. A bit later in life, the child focuses on the anal pleasures of holding it in and letting go. By three or four, the child may have discovered the pleasure of touching or rubbing against his or her genitalia. Only later, in our sexual maturity, do we find our greatest pleasure in sexual intercourse. In these observations, Freud had the makings of a psychosexual stage theory.

    The oral stage lasts from birth to about 18 months. The focus of pleasure is, of course, the mouth. Sucking and biting are favorite activities.

    The anal stage lasts from about 18 months to three or four years old. The focus of pleasure is the anus. Holding it in and letting it go are greatly enjoyed.

    The phallic stage lasts from three or four to five, six, or seven years old. The focus of pleasure is the genitalia. Masturbation is common.

    The latent stage lasts from five, six, or seven to puberty, that is, somewhere around 12 years old. During this stage, Freud believed that the sexual impulse was suppressed in the service of learning. I must note that, while most children seem to be fairly calm, sexually, during their grammar school years, perhaps up to a quarter of them are quite busy masturbating and playing “doctor.” In Freud’s repressive era, these children were, at least, quieter than their modern counterparts.

    The genital stage begins at puberty, and represents the resurgence of the sex drive in adolescence, and the more specific focusing of pleasure in sexual intercourse.

    Of course, Freud was very influenced by the religiosity and subsequent demonizing of sex in those Victorian times, and felt that masturbation, oral sex, homosexuality, and many other things we find acceptable in adulthood today, were immature.

    Of course, today we know better, and those of us who are not caught up in projecting our own fear of sexuality onto others or projecting it in the fear of HIVophobia are much more comfortable with ourselves and our bodies and the bodies and sexuality of others.

    And of course, this is the true stage theory, meaning that Freudians believe that we all go through these stages, in this order, and pretty close to these ages.

  365. #367 DT
    July 26, 2007

    The more the AIDS “rethinkers” like Michael and Kevin spew their vitriol, the more idiotic the “rethinker” arguments appear (though I must admit they continue to surprise me, as I thought the stupidity ceiling had been reached a while ago).

    If they think their utterances are a good advert for their cause, they had better think again. With every post, the “rethinkers” are exposed for what they truly stand for, and its not pretty, is it?

  366. #368 Michael
    July 26, 2007

    Hello Dt. Thank you for your kind words and vote of support.

  367. #370 Roy Hinkley
    July 26, 2007

    Philly Boy,

    Ever heard of human herpes virus 8?
    http://en.wikipedia.org/wiki/Kaposi's_sarcoma

  368. #371 Michael
    July 26, 2007

    Hey Roy. The HHV8 virus is a very common virus to a large percentage of the population that remains perfectly healthy.

    The hosts affected by HHV8 HAVE ALWAYS HAD QUITE OBVIOUS additional co-factors for HHV8 to have had a deleterious effect. And by golly, poppers and AZT fit the bill, right beside high stress lives, such as those experienced 20 years ago by a gay population living under constant threat of attack by police, homophobes, and rejecting families.

    Or did you, Roy, think for some strange reason that drug abuse, stress, and chemicals that are not found in nature were always healthy for a human body?

    Get a clue there Roy, will yah?

  369. #372 Roy Hinkley
    July 26, 2007

    “Get a clue there Roy, will yah?”

    God! You have NO idea how amusing that is coming from you!

  370. #373 Andrew Maniotis
    July 27, 2007

    July 23, 2007
    Low-Key Recall of AIDS Drug Hits World’s Poor
    By ELISABETH ROSENTHAL

    ROME, July 21 — A total recall of an important AIDS drug widely used in developing countries has disrupted treatment for tens of thousands of the world’s poorest patients, with no clear word from the manufacturer on when shipments will resume.

    The recall of the drug, Viracept, by Roche Pharmaceuticals of Switzerland, went largely unnoticed in the developed world when it was announced in early June, after the company had discovered that some batches made at its Swiss plant contained a dangerous chemical. But the recall has caused growing concern among global health officials and in AIDS programs in many poor nations. They say the company did an inadequate job of informing patients and officials about the potential risks and helping them find affordable access to newer alternative drugs.

    Roche said that it had been actively working with health officials across the globe and that the risk from the affected batches was low.

    The scope of Roche’s recall is extraordinary, if not unprecedented, in the battle against the human immunodeficiency virus that causes AIDS, global health officials say. Dr. Lembit Rago, an official at the World Health Organization, said tens of thousands of people take Viracept worldwide, many of them poor people with H.I.V. in developing countries. The recall has left those patients with the painful choice of discontinuing a lifesaving medicine, or using a drug that might contain a dangerous contaminant.

    Officials at the W.H.O. in Geneva and the European Medicines Agency in London said Roche had not provided information they consider essential for safeguarding public health: which countries the tainted medicine was shipped to, the concentration of the contaminant and what the company will do for its patients. The European agency, which regulates drugs for the European Union, has canceled Roche’s license to market the drug.

    Dr. Rago called the recall “sort of a disaster” for patients in very poor countries. He said of Roche, “They failed in communication.” Roche has denied the accusation. The company, which had revenue of $35 billion last year, said it promptly notified health providers in the affected countries to discontinue use of the drug, which is dispensed in both pill and powder form. It also said it would cover the “reasonable costs” of the recall. It did not define “reasonable costs.”

    So far, in some countries like Panama, patients or treatment programs have had to make up the difference in cost between Viracept and far more expensive alternatives. For some patients in other countries, like Venezuela, alternatives to Viracept are unavailable.

    Roche said the recall affected “Europe and some other world regions” but has not been more specific. The recall does not affect the United States, Canada or Japan, where a version of Viracept is made by Pfizer. Roche has been in discussions with Pfizer about supplying Pfizer’s version to some affected countries, but regulatory and licensing issues could take “some time,” said Martina Rupp, a Roche spokeswoman.

    Roche sells Viracept for use in low-income countries at the discounted median price of about 28 cents a dose, according to the W.H.O.’s 2006 global price reporting system for AIDS medicine. The drug, also known as nelfinavir, is a member of the class of AIDS drugs known as protease inhibitors. It is considered an important defense against H.I.V., but it has fallen out of favor in Europe in recent years compared with newer medicines that are more convenient and cause fewer side effects.

    In some places, newer substitutes are not available to patients, either because they are not licensed or are much more expensive, said people with H.I.V. and international health experts. In Panama, for example, a substitute drug, Kaletra, costs three times as much as Viracept.

    “Roche has provided information, but there has been much less support in terms of who is going to pay the additional cost,” said Dr. César Nuñez, the United Nations AIDS program’s coordinator for Latin America, who is based in Panama.

    A more limited recall might have been possible had Roche been more forthcoming about the countries affected and the lots that were suspect, said Dr. Rago, the W.H.O. coordinator of quality assurance and safety for medicines. “It’s fine for Roche to say ‘withdraw and replace,’ but there may not be much else at hand to substitute” in many places, he said. “This is not just about Europe.”

    In response to questions sent by e-mail, Ms. Rupp said Roche had shipped “at least one packet of Viracept with high levels of the impurity to 35 countries.” But she declined to say which countries because Roche regards such information as proprietary. High levels of the contaminant “were observed in batches of Viracept that had been released to countries since March 2007,” she said.

    The company made the recall worldwide “in order to avoid confusion,” she said. Roche estimates that about 45,000 patients were affected by the recall. Ms. Rupp said the toxic substance, ethyl mesylate, should be called an “impurity” rather than a contaminant because it was created in the manufacturing process and because that type of chemical can be found in very low levels in other medicines, although it was not supposed to be present in Viracept.

    The company was performing studies on the issue, but the results would not be available for “some months,” she said. At high doses, ethyl mesylate has been shown to cause cancer in animals, and at lower levels it can cause genetic mutations, which means children and fetuses are particularly vulnerable.

    Asia Russell, the coordinator of international advocacy for Health Gap, a nongovernmental organization based in New York and Philadelphia that focuses on medical care in the developing world, said, “It seems that Roche has abandoned these patients, since in many places there aren’t ready alternatives.”

    In Venezuela, 3,000 people were on Viracept, paid for by the national health service, and the effect of the recall was “severe,” because many had no other options, said Edgar Carrasco, an advocate on issues relating to AIDS in Caracas.

    Alberto Nieve, another advocate, said Roche had promised to make a donation of another medicine. “Most people are still waiting,” he said. “They have not switched yet, especially outside Caracas.”

    In the month since the recall, officials at the European Medicines Agency and the W.H.O. said that they, too, would like more information from Roche about the dose of the contaminant and where exactly the medicine was sent.

    “We have not gotten information, not even an order of magnitude,” said Martin Harvey-Allchurch, a spokesman for the European agency. “I understand sales figures are confidential, but I would have thought by now we would have this information.”

    Viracept was sold in 49 countries since 2004, according to the W.H.O., with more than 12 million units sold in 2006 and 2 million in 2007. Tido Von Schoen-Angerer, director of the essential medicines campaign at Doctors Without Borders, said about half of the 400 patients who received therapy supplied by the group in Africa were on Viracept. The alternate from Abbott is not yet available, he said.

    Cheers!

    Andy

  371. #374 Adele
    July 27, 2007

    Andrew drops by for a quick pasting! Yes the same Andrew who just disappears when he gets tough questions. Someone should tell him how to put a link in. You know, link, maybe a little quote, then your commentary. That’s what a blogs about.

    This way we don’t know what Andy thinks they should of done,
    shipped the tainted drug and kept their mouths shut?
    ended making the drug because one batch didn’t pass QC?
    made sure people who take the drug had an alternative?

    WEll we don’t need a conclusion from Andy we already know it, if something doesn’t got through qc, the whole company should get shut down and put on trial and all HIV drugs made illegal and all there money to Alive and Well.

    My conclusion is, people need this drug their health relies on it and there’s gotta be a way to put some redundancies in the supply system so people aren’t left without.

  372. #375 Andrew Maniotis
    July 27, 2007

    Dear Adele,

    Regarding those mutants you keep in your freezer, what relevance do your in vitro studies on non-PHA stimulated cells with heat inactivated virus and plasmids to the following?

    The little buggers mutate every 19 seconds and therapy always fails because it mutates so fast, and we can’t get a consistent sequence because the virus hasn’t been isolated, so we tell the public and our peers that there is constant mutation-which violates the idea of hereditary material.

    You must stretch the rules of genetics to accommodate the “HIV-AIDS” paradigm. From A. LAU et al. (Suppression of HIV-1 infection by a small molecule inhibitor of the ATM kinase. Nature Cell Biology 7, May 2005, 17 April 2005).

    “HIV treatment: targeting host proteins.”

    Question: Why is “the host” being targeted? I thought “HIV” was an exogenous retrovirus. Please don’t continue to target the host proteins? OK?

    “Chemotherapy to treat human immuno-deficiency virus 1 (HIV-1) infection, targets virally encoded proteins, but tends to select for drug-resistant variants of the virus. An alternative strategy is to identify and target host proteins that are essential for the virus but not the host. In Nature Cell Biology, Alan Lau and colleagues make use of an ATM-kinase-dependent cellular response to genomic damage. By inhibiting this non-essential kinase, the authors are able to suppress HIV-1 replication.

    Translation:

    First sentence: Toxic discarded and non-FDA-approved toxic cancer chemotherapy compounds to “treat” “HIV” infection, target “virally encoded” proteins that haven’t yet been identified because nobody has isolated that virus, but sometimes these drugs don’t work because some of those “viral particles” that are resistant to the toxic drugs that preferentially kill bone marrow, will squeak through because they are drug resistant- variants of the virus. The reason we know they are mutants is because their “sequence is different from patient to patient.”

    Second sentence: The authors are targeting a kinase, and they are following the paradigms of cell signaling science which is fashionable.

    Third sentence: By taking advantage of a theoretical construct regarding how non-essential kinases work in eukaryotic cells, the authors will now use this information to interfere with “HIV” replication and thereby solve “AIDS.” Well…..

    From: The Body Covers (41st Interscience Conference on Antimicrobial Agents and Chemotherapy ICAAC 2001):

    “Prevention of HIV Infection, Epidemiology and the Changing Face of HIV/AIDS (Poster Session 020)”

    “Coverage provided by Andrew T. Pavia, M.D.”

    “Comparison of Nevirapine Resistance (NVPR) Mutations in Women vs. Infants Receiving Single Dose NVP Prophylaxis to Prevent HIV-1 Vertical Transmission (HIVNET 012).”

    “Abstract 234
    Authored by Susan H. Eshleman (The Johns Hopkins Med. Inst., Baltimore, MD), M. Deseyve (Fred Hutchinson Cancer Res. Ctr., Seattle, WA), L.A. Guay (The Johns Hopkins Med. Inst., Baltimore, MD), M. Mracna (The Johns Hopkins Med. Inst., Baltimore, MD), M. Furtado (Applied Biosystems, Foster City, CA), P. Musoke (Makerere Univ., Kampala, Uganda), F. Mmiro (Makerere Univ., Kampala, Uganda), J.B. Jackson (The Johns Hopkins Med. Inst., Baltimore, MD).”

    “The HIVNET 012 study was a landmark study, demonstrating that a single dose of nevirapine given to a pregnant woman in labor, combined with a single dose for the neonate within 48 hours of birth, was about twice as effective as a short-course AZT regimen at preventing mother-to-child transmission. The promise of a simple, practical and inexpensive treatment raised hopes for making a dramatic impact on mother-to-child transmission.”

    “The reality has been more complex, as usual. Political and organizational hurdles have made it hard to begin programs. Relatively few women have had access to programs using nevirapine, even though the drug is available for free to programs in developing countries.”

    “Resistance is an issue that requires careful attention as well. In the HIVNET 012 study, nineteen percent of the women who had received nevirapine, and who were tested at six to eight weeks post partum, had evidence of nevirapine-resistant mutations.”

    “At 48 weeks, these mutations could not be detected in any of the women, but we would expect them to be archived. Only 24 infants were infected and available for resistance testing at four to six weeks, but 49% had resistant virus. (If nevirapine prevents transmission in 67%, as the Times article claims, and resistance mutants occur at 49% frequency, then in fact the 1 dose nevirapine has only saved 18% from the jaws of AIDS death! Check out this math!) Although many women and infants in Africa currently have no chance of receiving HAART therapy, the emergence of nevirapine resistance could compromise their chance of responding to treatment when it becomes available.”

    “Dr. Eshelman reported on the genotypic resistance patterns in the mothers and children with nevirapine resistance in HIVNET 012. Remarkably, the mothers and infants had different patterns of resistance mutations, demonstrating that resistance evolved independently in mother and child. Of 18 women, 15 had the K103N mutation, either alone or with other mutations. In contrast, most of the infants had Y181C.”

    I guess the genetic background of the host influences how the virus mutates. Amazing! Such startling new information! Different organisms respond to the same disease differently. Good reason to do chemotherapy experiments on them I would say…

    “The implications of this are not yet clear. (They should be!!!) It is likely that the different selection pressure based on persistence of drug levels leads to different resistance patterns (EVERY VIRUS HAS A DIFFERENT SEQUENCE-AT LEAST 15 OUT OF 18). Because the drug is metabolized slowly, infants maintain nevirapine levels for up to two weeks. This may provide some protection against transmission through breast milk, but seems to increase the selection for resistance.”

    (IMPOSSIBLE!).

    “For physicians in the developed world, it means that if nevirapine is to be used for a woman with no prenatal care or with a persistent viral load, it should be combined with additional drugs to prevent the emergence of resistance. AZT, 3TC and nevirapine might be a reasonable choice when therapy is begun during labor.”

    GREAT TIME TO HIT A WOMAN WITH 3 TOXIC ANTI-CANCER CHEMOTHERAPY DRUGS-WHEN SHE IS IN LABOR! A REASONABLE CHOICE INDEED!

    “In the developing world, it means that trials combining nevirapine with other agents for short, effective therapy are urgently needed. We need to be able to preserve the mother’s chance of response to therapy. Candidate regimens might include nevirapine and AZT begun at the onset of labor and continued for three days (see abstract 232) or AZT and 3TC. The use of tenofovir, which has been remarkably effective in a monkey model of mother-to-child transmission, needs to be evaluated.”

    FOLLWING THIS LOGIC, IF MUTATIONS ARE DIFFERENT IN INFANTS AND MOTHERS, THEN DON’T YOU THINK THEY WILL BE WAY DIFFERENT IN MONKEYS? MONKEYS DON’T GET AIDS-CHIMPS ARE LIKE HUMANS AND DON’T GET AIDS DESPITE INJECTION WITH “AIDS-PATIENT SERA.”

    “The problem of breast-feeding HIV transmission is not addressed by these regimens. (NO ITS NOT). In many ways, the obvious solution is to treat the mother with HAART after birth. This would give the uninfected child a healthy mother, perhaps the most important therapy of all.

    SEND HER OVER TO US FOR A MASTECTOMY SO THAT SHE WILL COMPLY WITH NON-BREAST FEEDING!

    Yet another:

    “December 16, 2001

    Maternal resistance to nevirapine can develop after single intrapartum dose

    Last Updated: 2002-08-02 13:45:10 -0400 (Reuters Health)

    By Will Boggs, MD

    NEW YORK (Reuters Health) – Nevirapine resistance mutations commonly develop in pregnant women receiving standard antiretroviral treatment after single-dose nevirapine treatment for the prevention of perinatal HIV transmission, according to a report in the July 15th issue of The Journal of Infectious Diseases.

    A single oral dose of nevirapine given at the onset of labor significantly decreases mother-to-child HIV transmission, the authors explain, but new nevirapine resistance mutations develop in 19% ???? (I thought it was 49%?????? According to the article by Esheleman above??? Hmmmmm….) of women who are not receiving other antiretroviral drugs. Whether such mutations develop in women receiving standard antiretroviral treatment had not been studied.

    As part of a study testing the effectiveness of nevirapine for prevention of perinatal transmission of HIV-1 in women and infants receiving standard antiretroviral therapy, Dr. Coleen K. Cunningham from State University of New York Upstate Medical University in Syracuse, New York and colleagues evaluated the risk factors associated with the development of nevirapine resistance.

    Five of 217 women (2.3%) had nevirapine resistance mutations present at the time of delivery and 6 months postpartum, the authors report, though none of them had received nevirapine previously.

    An additional 14 of 95 nevirapine-treated women (15%) without detectable nevirapine resistance at the time of delivery had virus with resistance mutations (most commonly the K103N mutation) by 6 weeks postpartum, the report indicates.

    Mutations associated with resistance to nucleoside analogue reverse transcriptase inhibitors were also common, the results indicate, and resistance mutations in the protease gene less so.

    DAMN! AND I THOUGHT ADLELE’S MUTATIONS CONSISTED OF A VERY TINY PORTION OF THE “HIV” GENOME! JUST THINK, YOU CHANGE THE RULES OF GENETICS, MUTATE REVERSE TRANSCRIPTASE IN HUMANS, AND PRESTO! THE VIRUS STILL WORKS IN HUMANS AND KILLS THEM BUT ADELE GETS NO RADIOACTIVE COUNTS IN HER SUPERNATANTS WHEN SHE TRANSFECTS WITH HER “MUTANT” VIRUS. INTERESTING KIND OF SCIENCE YOU ARE DOING THERE, ADELE!

    The development of new nevirapine resistance mutations was not related to the CD4 cell count or HIV-1 load at the time of delivery, (Does this mean the mutant HIV particles don’t bother the T-cells??????????????????) the researchers note, and such mutations did not vary with the type of antiretroviral regimen used before or during the current pregnancy or with the presence of resistance mutations to other antiretroviral agents.

    MUTATIONS DON’T VARY WITH THE TYPE OF DRUG USED! INTERESTING.

    “This would suggest that any patient with active viral replication incurs some risk for the development of detectable nevirapine-resistance mutations if given a single dose,” the investigators warn, “even if he or she has susceptible virus and nevirapine is given concurrently with other medications.”

    “For women who are on standard antiretroviral therapy, there is no demonstrable benefit to adding the single dose of nevirapine for mother and baby,” Dr. Cunningham told Reuters Health, “and this substudy shows the downside of using it: the potential for nevirapine resistance mutations in Mom’s virus.”

    ISN’T THAT SPECIAL! THE POTENTIAL FOR RESISTANCE MUTATIONS IN “MOMS” VIRUS. I GUESS BABY’S VIRUS HAS A DIFFERENT SEQUENCE OF RT OR SOME OTHER “HIV” GENE EVERY TIME IT ESCAPES THE DRUG AND THE BABY DIES OF AIDS, BECAUSE IT DOESN’T MUTATE ON THE SAME NUCLEOTIDE, AND IF IT DID, HOW WOULD IT STILL WORK THE SAME, OR AT ALL, LET ALONE 49% OF THE TIME MUTATING TO A DRUG-RESISTANT FORM THAT IS NOW IMPERVIOUS TO THAT DRUG THAT CAUSED ITS MUTATION, AND IF YOU BELIEVE CUNNINGHAM, IT DOESN’T MATTER WHAT DRUG CAUSED THE MUTATION-IT ALWAYS WILL MUTATE THE VERY GENES THAT WILL ALLOW IT TO GET AROUND THE MUTATION DEFECT, AND THE PRESENCE OF THE DRUG, BY THE USE OF ITS MUTATED GENE PRODUCT. AMAZING MOLECULAR BIOCHEMICAL CYBERNETICS GOING ON HERE. MONOD, JACOB, LWOFF WOULD BE PROUD!

    This “may lead to difficulty in treating the woman in the future.,”

    THIS IS NOT GOOD!

    Dr. Cunningham continued. “So, in areas of the world where treatment is available, except in very rare circumstances, single-dose maternal nevirapine should not be recommended.”

    SHOULD NOT!

    TRANSLATION.

    SHOULD NOT!

    J Infect Dis 2002;186:181-188.//

    HIV Treatment Bulletin Volume 5 Number 6 July 2004
    Persistent nevirapine resistance following mother to child transmission interventions

    Polly Clayden, HIV i-Base

    Three studies presented at this meeting evaluated resistance in women having received single dose nevirapine to reduce mother to child transmission.

    Patterns of selection and “fading” of Y181C and K103N in women with subtype A vs D:

    A resistance substudy of the HIVNET 012 trial from Susan Eshleman and colleagues examined the impact of subtype A vs D on the selection and “fading” of nevirapine associated mutations K103N and Y181C in a group of women following a single dose of nevirapine to reduce mother to child transmission [1].

    Genotypes were obtained at 7 days and 6-8 weeks and paired data were available for 159 women. Of this group 83 women had subtype A and 57 subtype D.

    The investigators found a significantly higher overall rate of resistance (ie any nevirapine mutation) at 6-8 weeks than at 7 days, 47/140 (34%) and 31/140 (22%) respectively, in women with either A or D subtypes (p=0.013; OR 1,916; 95% CI: 1.287, 2.854). There was a higher rate of accumulation of mutations for subtype D vs A (OR 2.519; 95% CI: 1.136, 5.587).

    The K103N mutation was detected at a higher rate in the 6-8 week samples: 41/140 (29%), than the 7 day samples: 18/140 (13%), (p=0.0001; OR 2.926; 95% CI: 1.287, 2,854) across both subtypes. Again the investigators noted a higher rate of accumulation for subtype D vs A although this was not statistically significant.

    Conversely the detection rate for the Y181C mutation was higher at 7 days than at 6-8 weeks overall, 26/140 (19%) and 15/140 (11%) respectively (p=0.0145; OR 0.509; 95% CI: 0.297, 0.872. The investigators added: “Furthermore Y181 faded quickly in subtype A with little or no fading in subtype D.”

    These findings demonstrate HIV-1 subtype to influence patterns of emergence and “fading” (from detection)
    for the K103N and Y181C mutations The investigators also looked at G190A but the number of mutations detected were too small for meaningful statistical analysis (they also noted other nevirapine mutations eg V106 and Y 188C in a small number of women). They report that for all three mutations, the results suggest that nevirapine mutations are better tolerated in subtype D than subtype A viruses and conclude that these findings suggest that HIV-1 subtype should be considered in the design and interpretation of studies to determine whether single dose nevirapine compromises subsequent NNRTI containing treatment.

    Surveillance of nevirapine resistance in Kwazulu-Natal, South Africa

    The startling scale of 75% nevirapine resistance at two weeks following single dose nevirapine, reported in women with subtype C at this meeting last year provoked much speculation around the longer term consequences of selecting nevirapine resistant virus [2]. Will NNRTI containing drug programmes be effective if women have access to treatment for their own HIV?

    In their surveillance report Gordon and colleagues write: “It is essential that the rate and pattern of drug resistance development is closely monitored.

    (Did Tremont closely monitor this??? I doubt it! He was busy changing the safety data reports against the advice of his staff)!

    This is especially true for South Africa, in the light of the initiation of its national antiretroviral programme [3].” They examined nevirapine resistance patterns in 30 mother and infant pairs (including one set of twins) with HIV-1 subtype C who had participated in a single dose (to mother and infant respectively) mother to child transmission (MTCT) programme at a clinic in Hlabisa, South Africa.

    At six weeks following the nevirapine prophylaxis, 12/30 (40%) of women and 40% of infants had detectable resistance. The K103N mutation was the most common mutation in 10/12 (83%) of the mothers. Other mutations reported in the mothers included: Y181C in 3/12 (25%), Y188C in 3/12 (25%), V106M in 2/12 (17%) and G190A in 1/12 (8%) Two or more mutations were found in 4/12 (33.3%) mothers.

    SEE THERE ADELE! HOW MANY TIMES DOES YOUR VIRUS MUTATE IN 6 WEEKS OF CULTURING? WHY DOESN’T IT EVER MUTATE TO EVADE DRUGS YOU MIGHT PUT INTO YOUR DISH TO “EVOKE” MUTATIONS? EVENTUALLY, WOULD YOU EXPECT YOUR MAGIC LITTLE VIRUS TO DEVELOP RESISTANCE TO NEVIRAPINE IF YOU SPRINKLED SOME IN YOUR CULTURE DISH? THEREFORE, YOU WOULDN’T GET SUPPRESSED COUNTS OF RADIOACTIVITY, YOU’D GET ENHANCED COUNTS EQUALING THOSE OBTAINED WHEN YOU INFECT WITH YOUR WT VIRUS.

    Of the group of infants, the Y181N was the most common mutation and was present in 11/12 (92%) of the children (including one of the twins). Additionally 2/12 infants (17%) had the K103N and another 1/12 (8%) had a subtype C associated V106M mutation.

    ITS AMAZING HOW NATURE MAKES MUTATIONS A RANDOM THING-THE GRIST FOR THE MILL OF NATURAL SELECTION, BUT HERE, IN HIV SCIENCE, YOU GET THE SAME MUTAION 92% OF THE TIME! THAT’S REALLY LANDING A NICKEL ON ITS EDGE (92% OF THE TIME) AFTER THROWING IT OFF THE SEARS TOWER, IF YOU GET MY MEANING?

    The investigators also reported that the K103N mutation resulted in the loss of a protein kinase phosphorylation site at codons 102 to 105 in reverse transcriptase. This was replaced with myristoylation site at codons 99 to 104 and a glycosylation site at 103 to 106. All infants with nevirapine resistance lacked a tyrosine kinase phosphorylation site at codons 174 to 181.

    SIMPLY AMAZING THAT THE MUTATION OR FRACTIONATION OF THE GENETIC MATERIAL ALWAYS HAPPENS AT THIS SITE ON THE REVERSE TRANSCRIPTASE GENE (BETWEEN SITES 102-105), AND THE ENZYME ALWAYS WORKS BETTER THAN IT DID BEFORE BECAUSE AIDS KILLS THE INFANT BECAUSE THE VIRUS IS NOW “RESISTANT DUE TO THIS CHANGE IN THE STRUCTION, AND FUNCTION, OF RT!

    The investigators concluded: “Given the high rate of resistance in mothers and infants after single dose nevirapine, the search for safer regimens to prevent MTCT should be intensified.” ]

    MORE MONEY FOR SURE!

    But what should we do in the mean time to distribute the life-saving meds to all those pregnant African Women, while we “intensify our search” for new toxic drugs to give to the pregnant or birthing African women?

    LET EM BREAST FEED WILL YA!@@#$#@@#$$#

    Persistence of nevirapine resistance: the Ditrame Plus study:

    A resistance substudy of the Ditrame Plus trial – in which women received single dose nevirapine in addition to short course zidovudine to reduce MTCT and the infants short course zidovudine and single dose nevirapine syrups – evaluated nevirapine resistance at four weeks post partum.

    Baseline and four week samples were available for 63 women, of this group 21 had infected and 42 uninfected infants. Samples from the 26 infected children were also evaluated (21 children whose mothers had and 5 children whose mothers had not received nevirapine, but who had received the infant dose.

    The investigators reported 21/63 (33.3%) of women having developed nevirapine resistance at week four, with the K103N being the most common mutation. They also reported the mothers with infected and uninfected infants developed resistance at the same rate (33.3%), 7/21 and 14/42 respectively. No zidovudine resistance was detected in this group. Additionally DNA-PBMC nevirapine mutations were detectable in 15/20 (75%) of women for whom DNA samples were available at week four.

    21 out of 63 women developed resistance in week four? Looks like they need to take 15 different drugs at a time. I hope Bush’s 3 by 5 program knows about these MUTATIONS AND statistics! (The 3 by 5 program is slated to distribute toxic drugs to 3 million persons by the year 2005).

    Analysis of nevirapine plasma concentrations revealed wide inter patient variability with a median concentration of 648 (range 417-954) ng/ml. Resistance was significantly associated with a higher plasma concentration of nevirapine and among women who received two doses of nevirapine 3/4 (75%) acquired resistance. (This is going the wrong way…..it should reduce viral load of all “non-resistant viruses because it is so effective at preventing mother to infant transmission BECAUSE IT PREVENTS THE VIRUS FROM REPLICATING TO FORM MASSIVE POPULATIONS IN WHICH A RARE MUTATION CAN OCCUR ACCORDING TO THE RULES OF GENETICS-why do two doses of nevirapine increase the “resistant strains to 75%??????????????????????????????????).

    75% resistance? Wow! But isn’t this good news on account of the fact that these drugs should be given to persons with threats about their personal freedom and with death sentences imposed if they don’t take their meds on schedual?

    The investigators described predictive factors for nevirapine resistance for the mothers as: median viral load 4.93 log10 copies/ml (nevirapine resistance) vs 4.54 log10 copies/ml (no nevirapine resistance) (95% CI: 3.11[1.04-9.29], p=0.020); median nevirapine plasma concentration 851 (633 – 1063) ng/ml (nevirapine resistance) vs 598 (315-885) ng/ml, p=0.014 and CD4 <350 cells/mm3 81% nevirapine resistance vs 19% >350 cells/mm3, p=0.06. Multivariate analysis revealed two factors to be independently predictive of development of resistance: viral load OR 95% CI: 4 (1.13 – 14.09) p=0.12 and plasma concentration 2 days post partum OR 95% CI: 1.05-1.50, p=0.31.

    Additionally 6/26 (23%) of the infected infants developed nevirapine resistance detectable in plasma and DNA-PBMC at four weeks post partum, and follow up samples in two children – one at 3 and one at 12 months old – detected archive mutations in the DNA-PBMC.

    Summarizing their findings the investigators note that the association between high level nevirapine plasma concentrations suggests, “That a high level of nevirapine concentration induced a prolonged viral replication under suboptimal drug selective pressure which promote the emergence of resistant strains.” Concerning the infants they write: “Recent studies have reported a negative impact of nevirapine resistance on a subsequent treatment including nevirapine; our results raise anxiety for those very young children presenting with resistant viruses.”

    Comment:

    More bad news for highly active drugs with long half-lives, given as monotherapy. Although nevirapine resistant variants “faded” from detection in women in HIVNET 012 by 12-24 months using population sequencing methods, resistant variants will surely still persist as minority variants and rapidly return when drug pressure is reintroduced. “Fading” is an incongruous term in a room of viroloists that have warned of the risks from archived resistance for many years now.

    Jourdain et al showed dramatically reduced response in women receiving NNRTI containing regimens following acquisition of nevirapine resistance after receiving single dose nevirapine to reduce MTCT (at six months 75% unexposed, 53% of exposed but with no detectable mutations and 34% of exposed with detectable resistance were below 50 copies). Additionally when Mellors et al evaluated the role of minor NNTRI mutations, failure to achieve viral suppression was associated with previous NNRTI experience and NNRTI mutations at baseline. However, genotyping failed to detect NNRTI mutations in 50/216 (23%) baseline samples in the NNRTI experienced patients, yet this group performed no better than those with detectable NNRTI resistance, and much worse that the NNRTI-naïve group who similarly showed no mutations.

    Utter non-sense! “This group performed no better than those with detectable NNRTI resistance.”

    SO MUTATIONS REALLY DON’T MATTER AFTER ALL. WHERE DID THE RULES OF GENETICS GO! THEY HAVE BEEN PLUNGED INTO THE DANK HOLE OF SCIENTIFIC WHOREDOM.

    Furthermore, as in the Thai study, adding nevirapine to background zidovudine is not associated with significantly less nevirapine resistance. The early emergence of the Y181C in the Uganda study (HIVNET 012) may help to explain the different rates of NNRTI mutations in mothers compared to infants, as previously reported and as seen in Kantor’s study. The more rapid “fading” of the Y181C would seem to suggest that this mutation is “less fit” relative to both K103N and wild-type virus at least in sub-type A virus.

    Better news is that no resistance was reported for zidovudine as prescribed in the DITRAME study and this should equate with less of an impact on future therapy.

    These data, and emerging pharmocogenomic data, highlight the need for more thorough investigation of antiretrovirals, new and old, and their resistance patterns, paying attention to clade, gender, age and ethnicity.

    THEY HARKEN FOR A NEED FOR MORE HUMAN EXPERIMENTATION ON BLACK PREGNANT WOMEN.

    References

    1. Eshleman SH, Wang L, Guay LA et al. Distinct patterns of selection and fading of K103N and Y181C are seen in women with subtype A vs D HIV-1 after single dose nevirapine: HIVNET 012. XIII Intl Drug Resistance Workshop, Tenerife 8-12 June 2004. Abstract 50. Antiviral Therapy 2004; 9:S59.
    2. Kantor R, Lee E, Johnston E et al. Rapid flux in non-nucleoside reverse transcriptase inhibitor resistance mutations among subtype C HIV-infected women after single dose nevirapine. XIII Intl Drug Resistance Workshop, Tenerife 8-12 June 2004. Abstract 78. Antiviral Therapy 2004; 9:S89.
    3. Gordon M, Graham N, Bland R et al. Surveillance of resistance in KZN South Africa, including mother-infant pairs six weeks after single dose nevirapine. XIII Intl Drug Resistance Workshop, Tenerife 8-12 June 2004. Abstract 71. Antiviral Therapy 2004; 9:S80.
    4. Dabis F, Ekouevi DK, Rouet F et al. Effectiveness of a short course of zidovudine and lamivudine and peripartum nevirapine to prevent HIV-1 mother-to-child transmission. The ANRS 1201 DITRAME Plus trial, Abidjan, Cote d’Ivoire. 2nd IAS Conference. France. 8-12 July 2003. Abstract 219.
    5. Chaix ML, Ekouevi DK, Peytavin G et al. Persistence of nevirapine resistant virus and pharmacokinetic analysis in women who received intrapartum NVP associated to a short course zidovudine (ZDV) to prevent perinantal HIV-1 transmission: the Ditrame Plus ANNRS 1201/02 Study, Abidjan, Cote d’Ivoire. Abstract 160. Antiviral Therapy 2004; 9:S176.
    6. Jourdain G, Ngo-Giang-Huong N,Tungyai P et al. Exposure to intrapartum single-dose nevirapine and subsequent maternal six-month response to NNRTI-based regimens. Abstract 41LB.
    7. Mellors J, Palmer S, Nissley D et al. Low frequency NNRTI-resistant variants contribute to failure of efavirenz-containing regimens. 11th CROI 2004, Abstract 39.

  373. #376 Adele
    July 27, 2007

    4,126 words. Impressive! Annoying thought I can’t tell what he wrote here and what he wrote somewhere else and what hes quoting.

    Oh well I can’t respond anyway now I’m working unlike Dr. Maniotis who must be on vacation for four months or something.

    I just want to say, this is really disturbing and Maniotis or Semon or someone going by Nestle already said it a few days ago,
    SEND HER OVER TO US FOR A MASTECTOMY SO THAT SHE WILL COMPLY WITH NON-BREAST FEEDING!

    Disturbing and disgusting.

  374. #377 Andrew Maniotis
    July 27, 2007

    ADELE,

    THANKS FOR ANSWERING MY QUESTION ABOUT THE RELEVANCE OF YOUR MUTANT EXPERIMENT IN THE CONTEXT OF THE ABSTRACTS I POSTED ABOVE. YOU SHOULD BE A PROFESSOR WITH THE CLARITY OF YOUR RESPONSES.

    BUT SADLY, I MUST ADMIT,

    I knew it DAmnit! Its all the fault of those BLACKS!!!! CAN’T WE DO SOMETHING ABOUT THOSE BLACKS!

    MONTAGNIER IS A RACIST.

    “…Dr. Luc Montagnier, the French virologist whose team discovered HIV, concluded that the AIDS virus was present in the hospital before the nurses arrived, probably brought to Libya by guest workers from countries in sub-Saharan Africa.”

    GUEST WORKERS FROM SUB-SAHARAN AFRICA MY ASS-THOSE PEOPLE WERE BLACK,BLACK, BLACK I TELL YOU! THEY SHORE DID A WHOLE LOT OF TRANSFUSIONS AWEFUL QUICK THERE, YA KNOW? MUST HAVE ALL BEEN WHOLE BLOOD FROM BLACKS THEY INFUSED INTO THOSE 426 CHILDREN.

    Epilogue in Libya: A spreading AIDS epidemic
    By Elisabeth Rosenthal, INTERNATIONAL HERALD
    Thursday, July 26, 2007.

    ROME: Five Bulgarian nurses and a Palestinian doctor landed in Sofia this week, freed of a death sentence after eight years in Libyan prisons, an apparent victory of diplomacy at long last.

    Officially, two visits to Libya by Cécilia Sarkozy, the French president’s wife, precipitated the release of the six medics who had been found guilty – not once, but twice – of infecting more than 400 children with HIV as part of a plot by the Israeli secret service.

    Sarkozy’s visit was only the latest in countless pilgrimages by diplomats and scientists to the Libyan leader, Muammar el-Qaddafi, to plead the medics’ cause. Recent visitors included the U.S. secretary of state, Condoleezza Rice, the European Union’s external relations commissioner, Benita Ferrero-Waldner, and Richard Roberts, a Nobel laureate, who represented more than 100 Nobel Prize winners.

    But the drawn-out drama also reflects a complex structure of Libya’s internal politics that prevented an obvious solution from being reached, experts in the case said. And the sad epilogue will be in Libya, too: an AIDS epidemic that has never been fully acknowledged and that continues to spread, as well as the 426 children dependent on treatment in a system ill-prepared for the task.

    “It was completely clear scientifically since 2002 that they were not guilty,” said Vittorio Colizzi, a renowned AIDS expert who was invited by the Qaddafi family to study the hospital in Benghazi where the infections took place and was given wide access to wards and medical records. “But the nurses suffered for years from the incapacity of diplomacy and politics to free them in a timely manner.”

    He and another expert, Dr. Luc Montagnier, the French virologist whose team discovered HIV, concluded that the AIDS virus was present in the hospital before the nurses arrived, probably brought to Libya by guest workers from countries in sub-Saharan Africa. In many of these nations more than 10 percent of the adult population is infected. It was spread by the infusion of unscreened blood and blood products, as well as by unsterilized equipment – problems that have been only partly solved, Colizzi concluded.
    A homegrown AIDS outbreak caused by lax practices at a government hospital was not a result the government could acknowledge, medical and other experts say, especially when there was a convenient foreign scapegoat.

    Bulgarians have long provided medical care in Libyan hospitals and “are very unpopular because of racism,” said George Joffe, an expert on Libya at Cambridge University’s Center for International Studies. Palestinians are unpopular, too, he said. “So this group provided an obvious target,” Joffe said.

    Once the medics were blamed, the families of the children had to be placated, which took time and carried special problems. Qaddafi is unpopular in Benghazi, which was the home of Libya’s former regime, Joffe said. Also, Benghazi is a city of extended clans, so many residents were related, if distantly, to a sick child.

    “Qaddafi needed to pacify the community there, while satisfying the international community,” said Joffe. “Of course, he exploited the issue for political and economic gain internationally, but, basically, a domestic issue delayed international resolution.”

    The families also have pressing needs. The children, many of them approaching the teenage years, are carrying a disease that is difficult to treat in a country with poor medical infrastructure. A million dollars – the amount each family got in compensation – “is nothing” for the lifetime treatment of a child with HIV, Colizzi said. “It won’t cover their medical problems, let alone issues of discrimination and their psychological needs.”

    Libya had reported 10,450 cases of HIV/AIDS to the World Health Organization by the end of 2006, but outside experts consider the figure low.

    “There is evidence of increasing HIV infections in Libya, especially among the younger age groups,” with many if not most cases among injection-drug users, the WHO’s annual report says.

    Early on, European negotiators recognized that winning over the families would be crucial in freeing the nurses. “We knew since 2004 that the families were the key to resolving this,” said an EU diplomat who was involved in the negotiations and who spoke on condition of anonymity.
    Once the medics had been sentenced to death, their best hope was to invoke Islamic law and custom, under which injured parties accept compensation and express forgiveness, allowing the sentences to be reduced or overturned.

    “We were constantly working around two axes: to give signs of attention to the families to show them the world cared, vis-à-vis things like equipping hospitals and providing medical care,” the EU diplomat said. “And to see how far we could go in helping with compensation. But in many ways, this was less important.”

    In the end, the families received $1 million apiece, almost all of that paid by the Libyan state, Joffe said, and agreed to the death sentences being dropped. The European Union and its member states have sent tens, if not hundreds, of million of dollars in aid to Libya, to create “a positive psychological and political environment” for the families. Furthermore, the children have been treated in hospitals in Italy, France and Britain.

    Still, said Colizzi, who has seen the children during visits to Benghazi and in Europe, some are “really sick” and are not getting good treatment at home. More than 50 have died.
    “The tragedy for the nurses is finished; now starts the tragedy for the children,” he said. “If there’s no more attention” – and money – “their situation will start to deteriorate.”

  375. #378 Adele
    July 27, 2007

    Sorry Andy, will get to you in time. Some of us have day jobs.

  376. #379 DT
    July 27, 2007

    I’ll try again. Maybe Maniotis would like to respond this time. He brought this subject up, but doesn’t want to answer questions about it. I wonder why not?

    He is on record above as saying the incidence of transfusion-dependent anemia in those on AZT is 50% as shown by product leaflets and published studies.

    Can we have some citations for this claim?

    All he did was quote:
    1. The original Fischl study, which even though patients had advanced AIDS, which causes anemia, showed only a third on AZT had anemia,
    2. The McKinney study (again looking at advanced AIDS) which had 27% with anemia that needed dose adjustment of AZT OR transfusion (Thanks for the true numbers on this one, Adele!), so presumably the percentage actually needing transfusion is somewhat less than 27%.
    3. Another Fischl study where 26% of patients on AZT needed transfusion.
    4. Product leaflets for AZT which do not indicate what percentage of patients on AZT get severe anemia.

    I, on the other hand, referred him to a meta-analysis of 54 different published trials where the incidence of anemia requiring transfusion was 1% in those on AZT (versus up to 0.6% in thoses not on AZT), and I did not need to massage the numbers or leave out data to beef up my claim, like he did.

    My question to him was a simple one: Can you provide a citation for your claim that transfusion dependent anemia occurs in 50% of those on AZT? One paper will do, just one….

    His continued refusal to answer confirms he was lying when he made his original claim.

  377. #380 cooler
    July 27, 2007

    Yeah dt, AZT is good for you, thats why it was never patented because it was deemed to dangerous and useless for cancer. Sprinkle some on your toast, have a birthday party for your kids and give them AZT candy bars. Treat a virus thats in 1 of 1000 blood t cells with a drug that kills all cells. Its good fun.

    Dr. maniotis has posted tons of studies showing AZT’s damagae to mitochondria etc that you ignore, as usual like a corrupt defense lawyer you focus on details and try to get off on technacalities.

  378. #381 Michael
    July 27, 2007

    Hello DT.

    You said: “so presumably the percentage actually needing transfusion is somewhat less than 27%”.

    Whether or not Maniotis is right or wrong about 50% needing a blood transfusion after taking AZT is absolutely beside the point, when you yourself readily admit that at least 26%, MORE THAN ONE FOURTH, of those poor fools who were given AZT needed a blood transfusion……………….

    DT, you DO realize, that YOU, DT, are defending a drug that has AT LEAST a 1/4th blood transfusion rate, not to mention its other myriad destructive effects?

    Think about this DT, just for a fraction of a mommmmmmmmennnnnntttttt………………………..

    By the way, DT, is your last name Kevorkian by any chance?

    I only ask because you certainly seem to be in favor of doctor assisted suicide.

    Or is your defense of such a drug as AZT more about some repressed subconscious death wish of your own, DT?

  379. #382 Andrew Maniotis
    July 28, 2007

    Microchips mulled for HIV carriers in Indonesia’s Papua

    Jul 24 03:57 AM US/Eastern
    http://www.breitbart.com/article.php?id=070724075657.4w2f978g&show_article=1

    Lawmakers in Indonesia’s Papua are mulling the selective use of chip
    implants in HIV carriers to monitor their behaviour in a bid to keep
    them from infecting others, a doctor said Tuesday.

    John Manangsang, a doctor who is helping to prepare a new healthcare
    regulation bill for Papua’s provincial parliament, said that unusual
    measures were needed to combat the virus.

    “We in the government in Papua have to think hard on ways to provide
    protection to people from the spread of the disease,” Manangsang told
    AFP.

    “Some of the infected people experience a change of behaviour and can
    turn more aggressive and would not think twice of infecting others,”
    he alleged, saying lawmakers were considering various sanctions for
    these people.

    “Among one of the means being considered is the monitoring of those
    infected people who can pose a danger to others,” Manangsang said.

    “The use of chip implants is one of the ways to do so, but only for
    those few who turn aggressive and clearly continue to disregard what
    they know about the disease and spread the virus to others,” he said.

    A decision was still a long way off, he added.

    The head of the Papua chapter of the National AIDS Commission,
    Constant Karma, reportedly slammed the proposal as a violation of
    human rights.

    “People with HIV/AIDS are not like sharks under observation so that
    they have to be implanted with microchips to monitor their movements,”
    he told the Jakarta Post on Tuesday.

    “Any form of identification of people with HIV/AIDS violates human
    rights.”

    According to data from Papua’s health office cited by the Post, the
    province has just over 3,000 people living with HIV/AIDS. Some 356
    deaths have been reported. Papua has a population of about 2.5
    million.

    Copyright AFP 2005

  380. #383 DT
    July 28, 2007

    More pap from Maniotis, without answering the question (yet again).

    This issue is not so much about AZT as it is about Maniotis. I am not saying AZT is harmless – it clearly has toxicities and can cause all the problems mentioned above. But Maniotis claimed it caused transfusion dependent anemia in 50% of recipients, and said he had papers to prove this.

    By giving evidence that the anemia rate is far lower than he stated, I am merely correcting what is another of his completely unfounded claims. I am offering him the opportunity to correct me and show us the evidence he says he has. He has turned down this offer several times, so it should be apparent to everyone that he has lied about this.

  381. #384 Andrew Maniotis
    July 28, 2007

    RE: The action of AZT on cells…

    “Telomerase inhibition as a potential new therapy for colorectal cancer”

    “Abstract:
    Colorectal cancer represents the second leading cause of cancer-related deaths. Despite local tumour control, patients die from disseminated disease and improved therapy is clearly required. One possible new approach is inhibition of telomerase, a reverse-transcribing enzyme thought to be essential to prevent senescence of cells by synthesizing chromosomal telomeres, which is reactivated in 85-95% of colorectal cancers. The purpose of this study was to determine the degree of telomerase inhibition by known retroviral reverse-transcriptase inhibitors using concentrations that are not acutely toxic to cells. The concentrations of three drugs (azidothymidine (AZT); dideoxythymidine (ddT); and dideoxyguanidine (ddG)) needed to reduce the proliferation (ID50) of the colorectal cell line HT29 by 50% were determined. Extracts were made of cells exposed for 24-48 h to these concentrations of each prodrug, telomerase activity determined using the Telomerase Repeat Amplification Protocol (TRAP), quantifying polymerase chain reaction products generated by telomerase with a phosphorimager and ImageQuantTM software. The drug treatments reduced the activity of telomerase in these cells by 97% for AZT, 38% for ddT and 47% for ddG, compared with control extracts. In order to confirm that the drugs used were directly inhibitory to telomerase, extracts of control cells were exposed to the active (phosphorylated) drugs and telomerase activity determined: greater than 60% and 80% inhibition occurred at 0.02 mM and 0.04 mM concentration of ddT and ddG, respectively. Control experiments demonstrated that the action of the active drug was not at the PCR stage of the TRAP assay and so was directly exerted on telomerase. We conclude that reverse transcriptase inhibitors can directly inhibit telomerase in cells exposed to prodrug concentrations, which are not acutely toxic, and that the active drug does directly inhibit telomerase. We propose that such inhibitors may have a role in reducing the survival, by inducing senescence, of remaining malignant cells after potential curative surgery, thus reducing recurrence and improving the prognosis of the disease. In addition they may be used in high-risk susceptible patients and in early-stage cancers.”

    Or AZT is used to stop Acute Myogenous Leukemia cells from dividing: (From Mangiacasale R, Pittoggi C, Sciamanna I, Careddu A, Mattei E, Lorenzini R, Travaglini L, Landriscina M, Barone C, Nervi C, Lavia P, Spadafora C. CNR, Institute of Molecular Biology and Pathology, Rome, Italy. Exposure of normal and transformed cells to nevirapine, a reverse transcriptase inhibitor, reduces cell growth and promotes differentiation. Oncogene. 2003 May 8;22(18):2750-61):

    Endogenous, nontelomeric reverse transcriptase (RT) is encoded by two classes of repeated elements: retrotransposons and endogenous retroviruses. Expression of RT-coding genes is generally repressed in differentiated nonpathological tissues, yet is active in the mammalian germ line, embryonic tissues and tumor cells. Nevirapine is a non-nucleoside RT inhibitor with a well-characterized inhibitory activity on RT enzymes of retroviral origin. Here, we show that nevirapine is also an effective inhibitor of the endogenous RT in murine and human cell lines. In addition, progenitor and transformed cells undergo a significant reduction in the rate of cell growth upon exposure to nevirapine. This is accompanied by the onset of differentiation, as depicted in F9 and C2C7 progenitor cells cultures in which nevirapine triggers the expression of differentiation-specific markers. Consistent with this, an extensive reprogramming of cell cycle gene expression was depicted in nevirapine-treated F9 cultures. Furthermore, nevirapine exposure rescued the differentiation block present in acute myeloid leukemia (AML) cell lines and primary blasts from two AML patients, as indicated by morphological, functional and immunophenotypic assays. The finding that an RT inhibitor can modulate cell proliferation and differentiation suggests that RT may represent a novel target in the development of therapeutical approaches to neoplasia.

  382. #385 Andrew Maniotis
    July 28, 2007

    Regarding transfusion-dependent anemia: some numbers for ya DT!

    Good stuff for anemia…

    Dainiak N et al. 3′-Azido-3′-deoxythymidine (AZT) inhibits proliferation in vitro of human haematopoietic progenitor cells. British Journal of Haematology. 1988;69:299-304 wrote:

    …nearly one half of patients treated with AZT for [HIV]-associated disease develop transfusion-dependent anaemia due to bone marrow depression…

    The good news of course is that half of patients don’t experience hematotoxicity!

    Costello C. Haematological abnormalities in human immunodeficiency virus (HIV) disease. J Clin Pathol. 1988;41:711-5 also reported that:

    “Blood transfusion is often necessary in patients with AIDS, especially in those receiving AZT, a drug which produces severe anaemia in a proportion of recipients. Forty nine (36%) of 138 patients treated with AZT … required blood transfusion at least once.”

    Walker RE et al. Anemia and erythropoiesis in patients with the acquired immunodeficiency syndrome (AiDS) and Kaposi sarcoma treated with zidovudine. Ann Int Med. 1988;108:372-6 reported:

    “In the current study, transfusion-dependent anemia occurred in 6 of 15 patients with AIDS and Kaposi sarcoma who were receiving zidovudine therapy. All 6 affected patients required their first blood transfusion between 3 and 9 weeks after starting zidovudine therapy, and each required 4 to 14 units of packed erythrocytes to maintain a hemoglobin level above 100 g/L over a 12-week study.”

    In one article, Gina Kolata from the New York Times health desk wrote: “Imminent marketing of AZT raises problems; marrow suppression hampers AZT use in AIDS victims.” (Science. 1987 Mar 20;235:1462-3) where she argued that:

    “more than half of all AIDS patients may not benefit from the drug because it is more toxic for them than their AIDS infection. The most serious side effect of AZT is to suppress the bone marrow, leaving patients highly vulnerable to bacterial infections”

    Richman DD et al. The Toxicity of Azidothymidine (AZT) in the Treatment of Patients with AIDS and AIDS-Related Complex. NEJM. 1987;317:192-197 reported that:

    “Anemia…developed in 24% of AZT recipients and 4% of placebo recipients (P<0.001). 21% of AZT recipients and 4% of placebo recipients required multiple red-cell transfusions (P<0.001). Neutropenia (<500 cells per cubic millimeter) occurred in 16% of AZT recipients, as compared with 2% of placebo recipients (P<0.001).”

    Fischl MA et al. Prolonged zidovudine therapy in patients with AIDS and advanced AIDS-related complex. JAMA. 1989;262(17):2405-10 in a follow-up study to the 1987 study which ushered AZT through FDA approval concluded:

    “58% of all subjects with AIDS and AIDS-related complex receiving zidovudine experienced granulocytopenia of grade 3 or higher…Serious anemia occurred in 32% of all subjects receiving zidovudine…and could be typically managed by dose attenuation, temporary dose interruption of zidovudine therapy and/or red blood cell transfusions…12% of subjects…had an episode of thrombocytopenia [low platelet count] after the initiation of zidovudine therapy…Ten patients had liver enzyme levels elevated…and were managed with dose attenuations or interruptions of zidovudine therapy…One report of a grand mal seizure, two events associated with cardiac dysfunction, and five reports of myopathy were the only new serious potentially drug-related adverse events reported during extended periods of zidovudine administration.”

    Dournon E et al. Effects of zidovudine in 365 consecutive patients with AIDS or AIDS-related complex. Lancet. 1988 Dec 3;2:1297-1302 concluded that:

    “AZT was started at full dose in 260 patients, 64 with ARC and 196 with AIDS. In 58 of these patients, AZT had to be stopped at least once for a minimum of 7 days. In 142 other patients, dosage was reduced by half because of leucopenia (79), leucopenia and anaemia (32), anaemia (20), rash (3), vomiting (3), headaches and insomnia (2), myalgia (2), or hepatitis (1). 3 patients reduced the dose with no medical reason. Later on, progression of toxicity led to suspension of AZT (for at least 7 days) in 85 of the 142 patients whose treatment had been reduced to half dose. Thus AZT was stopped at least once in 143 (55%) patients who began the full-dose regimen. Because of their initial haematological status 105 (28.8%) patients were treated from the start with half-dose AZT – toxicity led to cessation of treatment in 71 (67.6%) cases”

    Mocroft A et al. Anaemia is an independent predictive marker for clinical prognosis of HIV-infected patients from across Europe. AIDS. 1999;13:943-50 reported:

    “We found that 78.2% of the patients with mild or severe anaemia at baseline had received zidovudine [AZT]”

    Hymes KB et al. The Effect of Azidothymidine on HIV-related Thrombocytopenia. NEJM. 1998 Feb 25;318(8):516-7 reported:

    “The hematocrit [red blood cell count] decreased in the same patients…with three of eight patients requiring red-cell transfusion by the fourth week of treatment.”

    The advertisement for PROCRIT, 1997 solicited that:

    “While effective drug therapy is continued in zidovudine [AZT]-treated HIV-infected patients…PROCRIT Reduces Transfusion Requirements and Helps Lift the Burden of Anemia.”

    Fischl MA et al. A randomized controlled trial of a reduced daily dose of Zidovudine in patients with the Acquired Immunodeficiency Syndrome. NEJM. 1990;323(15):1009-14 and a follow up study reported that:

    “178 subjects (34%) had a hemoglobin concentration below 5 mmol per liter [anemia]…A greater proportion of subjects in the standard-treatment [high dose AZT] group had a first episode of severe anemia earlier in the study, as compared with the proportion in the low-dose group. 134 subjects (26%) received red-cell transfusions (65 in the standard-treatment group and 69 in the low-dose group)…230 subjects(44%) had a [low] neutrophil [infection fighting white blood cells] count…134 (51%) in the standard-treatment group and 96 (37%) in the low-dose group…22 subjects (4%) had a [low] platelet [blood clotting cells] count.”

    Mir N, Costello C. Zidovudine and Bone Marrow. Lancet. 1988 Nov 19;1195-6 reported:

    “Zidovudine is well known to produce haematological toxicity in vitro and in some patients…It is worrying that bone marrow changes in patients on zidovudine seem not to be readily reversed when the drug is withdrawn…These findings have serious implications for the use of zidovudine in HIV positive but symptom-free individuals.”

    Dainiak N et al. 3′-Azido-3′-deoxythymidine (AZT) inhibits proliferation in vitro of human haematopoietic progenitor cells. British Journal of Haematology. 1988;69:299-304 wrote:

    …nearly one half of patients treated with AZT for [HIV]-associated disease develop transfusion-dependent anaemia due to bone marrow depression…

    The good news of course is that half of patients don’t experience hematotoxicity!

    Costello C. Haematological abnormalities in human immunodeficiency virus (HIV) disease. J Clin Pathol. 1988;41:711-5 also reported that:

    “Blood transfusion is often necessary in patients with AIDS, especially in those receiving AZT, a drug which produces severe anaemia in a proportion of recipients. Forty nine (36%) of 138 patients treated with AZT … required blood transfusion at least once.”

    Walker RE et al. Anemia and erythropoiesis in patients with the acquired immunodeficiency syndrome (AiDS) and Kaposi sarcoma treated with zidovudine. Ann Int Med. 1988;108:372-6 reported:

    “In the current study, transfusion-dependent anemia occurred in 6 of 15 patients with AIDS and Kaposi sarcoma who were receiving zidovudine therapy. All 6 affected patients required their first blood transfusion between 3 and 9 weeks after starting zidovudine therapy, and each required 4 to 14 units of packed erythrocytes to maintain a hemoglobin level above 100 g/L over a 12-week study.”

    In one article, Gina Kolata from the New York Times health desk wrote: “Imminent marketing of AZT raises problems; marrow suppression hampers AZT use in AIDS victims.” (Science. 1987 Mar 20;235:1462-3) where she argued that:

    “more than half of all AIDS patients may not benefit from the drug because it is more toxic for them than their AIDS infection. The most serious side effect of AZT is to suppress the bone marrow, leaving patients highly vulnerable to bacterial infections”

    Richman DD et al. The Toxicity of Azidothymidine (AZT) in the Treatment of Patients with AIDS and AIDS-Related Complex. NEJM. 1987;317:192-197 reported that:

    “Anemia…developed in 24% of AZT recipients and 4% of placebo recipients (P<0.001). 21% of AZT recipients and 4% of placebo recipients required multiple red-cell transfusions (P<0.001). Neutropenia (<500 cells per cubic millimeter) occurred in 16% of AZT recipients, as compared with 2% of placebo recipients (P<0.001).”

    The Fischl Phase II trial is the trial said to have demonstrated the efficacy and safety of AZT, upon which FDA approval was obtained, and which was the only trial in US history to show in a record 4 months, that a drug (AZT) was “worthy” of FDA approval (From Duesberg et al., J. Biosc, Vol. 28 No. 4, June 2003, 383-412) (Fischl M A, Richman D D, et al and the AZT Collaborative Working Group 1987 The efficacy of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex; N. Engl. J. Med. 317 185-191, 1987):

    “The licensing study of AZT, performed in 1987 by the NIH in collaboration with the drug’s manufacturer Burroughs Wellcome in the US, is the primary placebo-controlled study set-up to test the ability of AZT to reduce the mortality of AIDS. The study showed that, after 4 months on AZT, 1 out of 145 AIDS patients died, whereas 19 out of 139 died in the placebo group. The study interpreted this result as evidence for reduced mortality by AZT. However, this interpretation failed to consider that among the 4- month-survivors of AZT, 30 could only be kept alive with multiple blood transfusions because their red cells had been depleted by AZT below survivable levels. Thus, without lifesaving transfusions 30 more AZT-recipients would have died from anemia. In addition many AZT recipients had developed life-threatening bone marrow suppression, neutropenia, macrocytosis, headaches, insomnia and myalgia, that augured poorly for their future survival (Richman D D, et al and the AZT Collaborative Working Group 1987 The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex; N. Engl. J. Med. 317 192-197). Indeed, the low mortality of 1/145 reported for the first 4 months on AZT, could not be maintained in a follow-up study, which found the “survival benefits” of AZT rapidly declining after the original 4 month period. By 21 months, 42% of the original AZT group had died and 35% of the control group, which by then had also received AZT for 12 months on a “compassionate” basis:

  383. #386 franklin
    July 29, 2007

    Andrew,

    Once again you demonstrate the truth of your admission that you “really don’t understand what’s going on.”

    Having failed at reading the primary scientific literature and a simple virological protocol, you now show that you are incapable of understanding even simplified press coverage of scientific results.

    You quote from the summary by Andrew T. Pavia, M.D., of an abstract authored by Eshleman et al. at the 2001 ICAAC:

    In the HIVNET 012 study, nineteen percent of the women who had received nevirapine, and who were tested at six to eight weeks post partum, had evidence of nevirapine-resistant mutations.

    You then quote from a piece written for Reuters by Will Boggs, M.D., on Cunningham et al. (2002) J Inf. Dis. 186:181-8, and with strings of question marks you reveal your inability to understand straightforward English prose:

    A single oral dose of nevirapine given at the onset of labor significantly decreases mother-to-child HIV transmission, the authors explain, but new nevirapine resistance mutations develop in 19% ???? (I thought it was 49%?????? According to the article by Esheleman above??? Hmmmmm….) of women who are not receiving other antiretroviral drugs.

    Pavia says “nineteen percent” and Boggs says “19%”–yet Maniotis is totally baffled!

    I really don’t understand what is going on.
    Andrew Maniotis, Ph.D. July 6, 2007

  384. #387 DT
    July 29, 2007

    Andrew, I was appreciative that you looked out some studies. I was prepared to revise my opinion of you, but then realised that you just resorted to your usual “cut and paste” spam tactic. The problem with answering by compiling “cut and paste” lists from places like virusmyth is that you don’t actually look at any of the original articles yourself, and just compound their misinterpretations. You also seem to have cut and pasted several studies twice – Did you think I wouldn’t notice? Did you even look at what you wrote, or are you entirely on autopilot?

    Quoting the same study twice which has an anemia rate of 26% does not provide evidence of transfusion dependent anemia in 50%, or do you think we can double the percentage if we read 26% twice?

    In all you have produced about 9 studies for us to see, (including your previous posts). Most quote rates af anemia around 20-30%. Disingenuously, you also slipped in one study to try make us think the rate of anemia on AZT is as high as 78% –

    Mocroft A et al. Anaemia is an independent predictive marker for clinical prognosis of HIV-infected patients from across Europe. AIDS. 1999;13:943-50 reported:
    “We found that 78.2% of the patients with mild or severe anaemia at baseline had received zidovudine [AZT]“

    This of course says nothing about the rate of anemia in everyone on AZT. 78% of the patients who were anemic might also have recieved kisses from the ward sister. In fact, for all you know, 100% of the patients without anemia may have also “recieved zidovudine”. You cannot draw any conclusion from this about the frequency with which AZT does cause anemia.

    The only study which comes close to your mythical figure of 50% is the first study you cite (and also the 9th I think – you quoted it twice)

    Dainiak N et al. 3′-Azido-3′-deoxythymidine (AZT) inhibits proliferation in vitro of human haematopoietic progenitor cells. British Journal of Haematology. 1988;69:299-304 wrote:
    …nearly one half of patients treated with AZT for [HIV]-associated disease develop transfusion-dependent anaemia due to bone marrow depression…

    This phrase is extracted from the introduction to this article on the mechanisms of AZT’s marrow toxicity. The study itself did not look at the incidence of anemia. The phrase actually refers to the original Fischl study where 39% of patients with advanced AIDS (which itself can cause anemia).

    So we are still searching for a paper that shows 50% of recipients of AZT developed transfusion-dependent anemia.

    Care to try again?

  385. #388 Andrew Maniotis
    July 29, 2007

    Dear AIDS Apologists,

    I looked up some studies I had on file in order to make good on your request(s) to provide data for my claim re: 50% transfusion-dependent anemia due to AZT. Actually it was an underestimate from the Fischl trial (1987) where it gained FDA approval fraudulently, and DT agreed on this approximate figure (39% I think she said without checking what she posted), but I wanted to see for myself if I was correct and was providing an accurate number.

    By pasting these studies above as I have, (no I wasn’t aware I pasted one twice)-I thought (incorrectly) that you AIDS apologist denialists may accept the fact that I am trying to connect with you folks to achieve some kind of understanding, after 25 years of anger, insults, name-calling, dismissal, and unproductive exchanges.

    What I learned from this AZT exercise, is that we need to carefully separate transfusion-dependent anemia stats from anemia stats-they are undoubtedly different things that are lumped together, and I’m pretty sure not many investigators have rigorously separated one from the other, because there are no placebo control groups in most of the studies, and a wide variety of medications will induce anemias. Transfusions are dangerous medical procedures in and of themselves-they cause auto-immune diseases in many who receive them (that old self-versus-non-self thing-which is why no “HIV” vaccine has evoked cellular, humoral, mucosal immunity, or activated T-cells-but this is another story you don’t want to address).

    The more important point to me is that some authors have noted 3/8, 6/15, and nearly half requiring TRANSFUSION dependent anemias, not to mention the first Fischl study where it is claimed by a number of investigators that all 30 of the AZT group had received them at some point in order to stay alive, which in the long run didn’t help with survival even though AZT is still called “life saving.”

    I would be far more interested in what insults you have to sling regarding my hypothesis of a drug like AZT’s law of similar’s effect on the immune system and other systems, as opposed to its so-called specific action against “HIV.” As I have indicated above (to earn the title of homeopathologist, liar, I don’t know what’s going on, etc.),
    a dispassionate view of all drugs, and their effects on organisms is not easily achieved by anyone for any compound I have ever worked with, nor is it the case here with AZT, as I have followed many persons on this drug, and those who refused the drug, and those that came off of the drug because it made them too ill, or very occasionally, those who came off the drug because their doctors told them to take a holiday because of the toxicity (especially anemia and neutropenia, throbocytopenias).

    I’m sure many of you have had a lot of experience developing new cancer drugs as I have, designing pre-clinical experiments, and following them through human clinical trials, so I’m sure you have a lot of advice or teaching for me to learn. The desperation to do SOMETHING for immune suppressed individuals early during the AIDS era ushered in some very unfortunate results with AZT, and I’m sure not even you religious folks would deny this fact anymore. In the meta-analysis that was raised a few blogs ago, transfusion-dependent anemia is in perhaps now in the single digits as I remember-earlier studies in double digits, and there have been studies, all imperfect, that go as high as 50% as was the first one I pasted, and when AZT was used at super-gram dosages because the Gay community demanded it so vociferously. Dosages have all been lessened over time, scheduling has also been adjusted, or drug holidays imposed, and the effects of these interruptions, dose diminutions, have either been recorded or not, so to obtain a hard and fast statistic for AZT’s ability to cause transfusion-dependent anemia is dependent on all of these factors.

    The cell biology, and warnings that have arisen, however, have and are still ignored, and with the “standard of care” being the blind, ignorant, and harmful thing it often is in medicine, no concerted opinion ON BOTH SIDES OF THE ISLE has been advanced to help stop the drug-reliance and carnage for either AIDS or cancer patients. Fauzi et al., can publish all they want on vitamin supplements, promising studies with selenium, forced eating schedules in Cuba that showed promise, and legions of folks who stopped taking AZT and HAART and are living productive and healthy lives 20 years later cannot for a moment change the forced drugging going on in this culture.

    The most egregious issue for me was and is the scheduling and threats of compliance that are still forcefully imposed on patients using a DNA chain-terminating compound like AZT, 3Tc, DDI, etc. We sometimes get dozens of calls/ a month from folks who, for instance , developed HCC after 10 years of HAART, and who quit taking their HAART 6 years ago (this happened last week for instance). What do you tell a desperate housewife of an “HIV-positive, 10 year recipient of HAART who quit HAART on his own because of its toxicity, and then began to feel normal until a year ago began to develop liver cancer, and who now can’t receive “the standard of care” for HCC at any hospitals or clinics where he lives (in a major metropolitan American city), because no doc will treat him for his cancer unless he also agrees to go on HAART again. What do you say to the wife? When you see this kind of story, and other similar conundrums again and again, what does a poor scientist to do/think?

    I’d really appreciate Adele answering my question re: the relevance of her mutant’s lack of activity to all of those mutant studies in humans I posted above where mutation is able to overcome the suppressive effects of nevirapine or other ARV’s. I’m not interested in Franklin’s inability to follow what the studies are saying-perhaps his “students” who do not know of his extracurricular activities can help him out here, if he for instance provides them with the Lockman et al., (and Essex)study from earlier this year citing a figure of I believe it is 47.1% mutations after a single dose of nevirapine (I have posted this on this blog at least 4 times without a single comment from you AIDS apologists debunking my inability to post a study verbatim. Franklin, you really should come clean with your students, and tell them that you are not only a teacher somewhere, but a devoted drug-enforcer for the federal government’s forced drugging programs.

    I’d also like a reaction from you folks regarding Montagnier’s proported reason for the infection of the 426 children being due to “an influx of workers from sub-Saharan Africa” (read Blacks) that was quoted in the National Harold by Rosenthal. Also I suppose the breast feeding debacle is something I don’t anticipate you have anything to say about where children have been dying due to lack of breast feeding because of the abhorrance of the human female breast and breast-feeding, or sexuality in general, as the implications of the carnage due to pulling mothers away from their infants because of an impassioned crusade to give toxic drugs to pregnant women is so disgusting that not even folks like you could excuse the ignorance here. In this regard, you might like to look at the following:

    Among the more sober assessments of global health crises by certain mainstream AIDS Establishment doctors and scientists, “AIDS” isn’t even the collection of diseases that poses the greatest challenge. For example, a series of articles was published in the January 6, 2005 issue of the New England Journal of Medicine by Berkley et al. (96), that is accompanied by a short and pointed commentary in the same issue, that introduces the Berkeley et al. study, (by Kim Mulholland, and Richard Adegbola) entitled, “Bacterial Infections-A Major Cause of Death among Children in Africa:”

    ” For the past 25 years, since the United Nations Children’s Fund (UNICEF) has been publishing estimates of mortality among children worldwide, the international medical community has been aware of the appalling burden of early deaths among African children. Early studies indicated that, in the absence of any effective medical care, children born in a rural African village had a probability of death before the age of five years of 30 to 50% (2. Reference 2 given here is from Mosley WH. Primary care: rhetoric and reality. Poluli J UN Fund Popul Act 1983; 10: 41-53, which is from a period of time before the “AIDS era).” From the outset, it was understood that many of these deaths result from the combined effect of poverty and malnutrition (2). Since 1990, mortality rates have fallen but remain high by global standards. Twelve African countries still report official death rates for children under the age of five of more than 20 percent. Community-based studies of death among children have been able to attribute these deaths to a number of common causes, either syndromes or specific diseases (see table I).”

    “Table I. Official Estimates of Mortality among Children under 5 years of Age According to Cause in Sub-saharan Africa and Globally in 2002.

    “Table I. Official Estimates of Mortality among Children under 5 years of Age According to Cause in Sub-saharan Africa and Globally in 2002.
    Cause of Death Africa Global
    Acute respiratory infection 16 18
    Diarrheal disease 14 15
    Malaria 22 10
    Measles 8 5
    HIV or AIDS 8 4
    Neonatal deaths 13 23
    Other causes 19 25
    All causes 4.5 million 10.9 million

    “Data are from the World Health Organization (WHO) and reflect the WHO African region, which excludes most North African countries, Somalia, and Sudan. Many of the deaths that were classified as due to “other causes” may actually belong among the main causes listed. A total of 54 percent of all deaths among children are believed to be associated with malnutrition. HIV denotes human immunodeficiency virus, and AIDS the acquired immunodeficiency syndrome.”

    “In the study, 28 percent of children admitted to the hospital with bacteremia died. Even more important, 26 percent (308 of 1184) of hospital deaths were associated with bacteremia. This finding compares with 22 percent of the deaths that were associated with malaria, suggesting that bacterial disease may be responsible for more deaths in children than malaria in this area where malaria is endemic. Did the children who died at home die from a spectrum of causes similar to that among children who died after reaching the hospital? Both malaria and bacterial illness are amenable to relatively simple therapeutic approaches, but antimalarial drugs tend to be more widely available in African communities than are antibiotics. Therefore, in a rural community, bacteremia may be even more important as a cause of death among children than it is in a hospital setting, since the management of bacteremic illness in the community is likely to be less effective than the management of malaria.”

    The article concludes with:

    “only 18 percent of children admitted with bacteremic illness were infected with HIV, whereas severe malnutrition was present in 37 percent, suggesting that the latter is a more important cofactor.”

    “During the past six years, the world of international health care has been dominated by high-profile efforts to control HIV infection, malaria, and tuberculosis. Of these, malaria is seen as the most important contributor to death among children in Africa. This study (Berkeley et al) gives us cause to question whether this very narrow, disease-based approach is indeed appropriate and whether the most important causes of death among children have been appropriately targeted. Even in an area of rural Kenya with high rates of HIV infection and malaria, there appear to be more deaths of children associated with bacterial infection than with malaria, with malnutrition still the main cofactor. Global health strategies, like any other public health activities, should be based on evidence.”

    If you want to see some real African statistic kept by Africans themselves, you also might want to look at the statistics that were painstakingly arrived at over a 35 year period that were presented in a piece I wrote this year with Charles Geshekter, which can be found here.

    http://barnesworld.blogs.com/barnes_world/2007/01/a_global_strate.html

    Cheers,

    andy

  386. #389 Michael
    July 29, 2007

    Franklin, the REAL AIDS DENIALIST, seems to think that 19% of patients developing mutations makes for a good “life saving” drug.

    AIDS denialist Franklin also conveniently ignores that Nevirapine was never compared to a placebo to get a real finding of how effective the drug is for reducing HIV transmission, but was only tested against toxic AZT!

    He also conveniently forgets that the study done formerly to compare AZT treatment to nontreated women came up nearly the same for both groups. Did AZT actually even have any effect on HIV transmission.

    The denialist Franklin doesn’t know and really doesn’t even care, as long as he continues his slogan of propaganda of “RahRah lifesaving drugs”.

    AIDS denialist Franklin also conveniently ignores that all of the investigators on these drugs had conflicts of interest with the drugs manufacturers.

    Franklin the AIDS DENIALIST has nothing at all to comment on the fact that the HIVnet 012 investigators claim to have “lost the log book in a flood” that just so happened to verify all of the other destructive effects of Nevirapine.

    Why is that Franklin? Why is it that you blindly and ignorantly believe the head investigators claim that the logbook was lost in a flood, when the investigator himself was being paid directly by the drugs manufacturer for his study?

    Why does Franklin have no healthy sensce of critical thinking and why does he even blindly accept the results of many of these pharma directed and pharma controlled and pharma paid studies whose sole purpose was to gain marketing approval?

    You are one sick puppy Franklin, and you are the Real AIDS Denialist!!!

    Did the denialist Franklin just fall off of a turnip truck.

    Or is he also a paid off shill for pharma companies?

    Which is it Franklin?

    Are you a lying AIDS denialist simply due to your own ignorance or due to financial motives?

  387. #390 franklin
    July 29, 2007

    Andrew,

    You asked us to check out your math. I have, and once again you prove that (as you put it yourself) you “really don’t understand what is going on.”

    When quoting from Pavia’s summary of an abstract authored by Eshleman et al. at the 2001 ICAAC, you tried to reason through the statistics on your own, with typically confused results:

    “Only 24 infants were infected and available for resistance testing at four to six weeks, but 49% had resistant virus. (If nevirapine prevents transmission in 67%, as the Times article claims, and resistance mutants occur at 49% frequency, then in fact the 1 dose nevirapine has only saved 18% from the jaws of AIDS death! Check out this math!) Although many women and infants in Africa currently have no chance of receiving HAART therapy, the emergence of nevirapine resistance could compromise their chance of responding to treatment when it becomes available.”

    Huh? Andrew, is simple arithmetic beyond your skill level?

    The identification of nevirapine-resistant HIV in 49% of the children who became infected despite nevirapine prophylaxis has no bearing on the reduction of the infection rate brought about by nevirapine.

    If, as Andrew suggests, nevirapine prevents 67% of the cases of HIV transmission, then 67% of the children who would have developed AIDS have been spared. This remains true even if 49% of the children who did become infected have nevirapine-resistant HIV.

    Let’s check out Andrew’s math by applying his numbers to an illustrative case. Assume a population in which, in the absence of Nevirapine, 100 children would acquire HIV. According to Andrew, nevirapine would reduce this number to 33 children (ie., “nevirapine prevents 67% of the cases of HIV transmission”), but 16 of these 33 infected children (49% of infected children) are now expected to have nevirapine-resistant HIV.

    So according to Andrew’s numbers: without nevirapine–100 infected children (with an unknown fraction having nevirapine-reisistant HIV), and with single-dose nevirapine–33 infected children (with 16 having nevirapine-resistant HIV). Yet somehow Andrew calculates that that nevirapine would only save 18% from AIDS.

    Keep posting Andrew–you just keep proving the truth of your statement:

    I really don’t understand what is going on.
    Andrew Maniotis, Ph.D. July 6, 2007

  388. #391 Michael
    July 29, 2007

    Hey Franklin, you damned AIDS denialist. You, Franklin, are the one who “Really Does not understand”.

    You sound like a broken record. Why are you ignoring my post Franklin?

    The details of the following as well as the study cites were presented publicly by Celia Farber in her March 2004 Harpers Article: “OUT OF CONTROL-AIDS, AND THE CORRUPTION OF MEDICAL SCIENCE”!!!

    The REAL AIDS denialist Franklin also conveniently ignores that Nevirapine was never compared to a placebo to get a real finding of how or even IF the drug is effective for reducing HIV transmission. IT WAS ONLY TESTED AGAINST PROVEN DEADLY TOXIC AZT!

    Franklin also conveniently forgets that the study done formerly to compare AZT treatment to nontreated women came up nearly the same for both groups. Did AZT actually even have any effect on HIV transmission.

    The denialist Franklin doesn’t know and really doesn’t even care, as long as he continues his slogan of propaganda of “RahRah lifesaving drugs”.

    Hey Franklin, enough with the babbling denialist nonsense. Wake up!!!

  389. #392 Michael
    July 29, 2007

    I really don’t understand what is going on.

    A quote by

    FRANKLIN, the Prize Winning REAL LYING AIDS DENIALIST

    Unanimously elected into the “Denialists Hall Of Infamy” on July 29th 2007

    Dohhhhhhhhhhhhhhhhh!

  390. #393 Michael
    July 29, 2007

    DT, you AZT addicted bonehead! I see you are still rambling on that AZT is deadly poison, but not as deadly poisonous as Dr. Maniotis says.

    Oh, you really are a case DT. You really are a very special case.

    However, it was very nice to see you finally admit a couple of posts above:

    “AZT clearly has toxicities and can cause all the problems mentioned above. But………”

    Well, DT, you can but,but,but,but,but,but, all you want. BUT THIS DT: It does not change one simple fact:

    All of your “but but butts” clearly show you to be either psychopathic or insane, because you are still arguing for the use a a proven very deadly toxic poison to be used on your fellow human beings.

    I suppose you thought that The Hippocratic Oath” to FIRST DO NO HARM, taken by doctors that you have sold this stuff to actually meant:

    HYPOCRITIC OATH!

    Well DT, it may come as news to you, but Hippocrates and Hypocrites are actually two very different and opposite things:

    The Hippocratic Oath is an oath traditionally taken by physicians pertaining to the ETHICAL practice of medicine.

    On the other hand…….

    HYPOCRITE-Definition:

    Noun.

    1) a person who professes beliefs and opinions that he does not hold

    2) dissembler, phoney, phony, pretender, beguiler, cheater, deceiver, trickster, slicker, cheat –

    3) someone who leads you to believe something that is not true

    4) charmer, smoothie, smoothy, sweet talker – someone with an assured and ingratiating manner

    5) a person who is inwardly evil but outwardly professes to be virtuous

    Now which of those two definitions would DT, the AZT and Nevirapine advocate be a follower of?????

  391. #394 DT
    July 29, 2007

    There are what – 20 licensed HIV drugs now? And the denialists still get hung up on AZT and nevirapine, big time.

    Nevirapine seems to be the bete noir for the reason that the single dose given to mothers to prevent MTCT of HIV can select resistance to nevirapine. This is through a K103 mutation, which would also rule out efavirenz. But there are plenty of other drugs available, should the mother require treatment sometime in the future (and why are rethinkers getting so worked up about drug resistance if they think that the drugs don’t work in the first place?)

    One way to look at the rethinker POV is to compare HIV MTCT like bacterial meningitis. Imagine these two scenarios (the first being equivalent to giving nevirapine, the second being to withold it.)

    OPTION 1: Give people antibiotic A, which will prevent the meningitis in 2/3 of recipients. However, of the third who do get meningitis, half will have resistance to antibiotic A in the future, so if an antibiotic is ever needed again, you will have to use a different antibiotic, of which there are at least a dozen available.

    OPTION 2: Give nothing, and let 100% get meningitis. Comfort yourself in the knowledge that although this will result in significant morbidity and mortality, if the patients do survive and ever need an antibiotic in the future, you could give them antibiotic A, even though this may not be necessary considering all the other antibiotic options there will be available to you.

  392. #395 DT