Wrong again

Once again, I’m wrong. I said yesterday that HIV deniers accused scientists of thinking of Robert Gallo as a deity. Silly, silly me–my mistake. Turns out he’s just a high preist:

We point to this phenomenon of how easily religious belief triumphs over the most irrefutable evidence to the contrary, in order to challenge all critics of HIV/AIDS to answer this question:

How does this kind of thought-resistant religiosity differ in the slightest from the twenty year adherence of believers in HIV to their favored dogma in the face of similar overwhelming evidence against the belief?

We suggest that there is an exact equivalence, as follows:

Science – Religion
Theory – Dogma
Conference Hall – Church
HIV – The Devil
David Ho – Son of God
AZT, ddI, Protease Inhibitors, Nevirapine – Holy Water
David Baltimore – Pope
Anthony Fauci – Bishop
Robert Gallo – High Priest
NIH Granting Process – Inquisition
Activists – Missionaries
Patients – Penitents
Taxpayer support – Vatican holdings and collections
Paradigm critics – Heretics
Canceled funding – The stake
Evidence overwhelmingly against – Evidence overwhelmingly against.
All objections converted to supporting evidence – All objections converted to supporting evidence.

We cannot discern any difference at all between the two paradigms in nature or shape. However, we have no doubt those cleverer than us will be able to find some difference, however small.


“Irrefutable” evidence that HIV doesn’t cause AIDS, eh? With apologies to Inigo Montoya, “You keep using that word. I do not think it means what you think it means.”

Image from http://media.lawrence.com/img/photos/2005/04/07/inigomontoya.jpg

Comments

  1. #1 Dave S.
    June 6, 2006

    I’ve always wondered about the fascination of the AIDS deniers [and the deniers that deny they are deniers, even though they don’t know what a denier is (like our Hank Barnes)] with Gallo. It appears to be related to their focus on the first appearance of evidence, or the first paper providing support for X. To them, every other advancement since then is clearly tainted by the “assumption” that HIV causes AIDS based on these first papers. The idea seems to be that if you can discredit the “source” of the knowledge, then everything afterwards is irrelevant since it depends on those initial papers being absolutely correct. Strange lawyer-like approach to thinking about science, but that seems to be the case.

  2. #2 Dale
    June 6, 2006

    They like Gallo because they can truthfully assert that Gallo was discredited. Of course they tend to gloss over the fact that Gallo’s conclusions weren’t discredited just Gallo’s claim to have isolated HIV in his own laboratory.

  3. #3 DDS
    June 6, 2006

    Bruce Alberts actually made an interesting comment at his opening talk during the ASM meeting last month. He said that scientists do carry some blame for the continuing science=relgion debates by allowing science to be taught as if it were a religion. Most elementary and High School science text books are little more than a bound compendium of facts with little discussion of where those facts came from. That is, the science/experiments behind the facts. Without this there is little to differentiate textbooks from the Bible as just two different, dogmatic, belief systems.

    BTW, I would have made Gallo the prophet (ie John the Baptist) and Fauci the Cardinal.

  4. #4 Ginger Yellow
    June 6, 2006

    “I’ve always wondered about the fascination of the AIDS deniers [and the deniers that deny they are deniers, even though they don’t know what a denier is (like our Hank Barnes)] with Gallo.”

    This personalisation is a common thing among anti-science types – creationists are obsessed with Darwin and Haeckel, and assume that evolutionary biologists are too. Presumably it’s because it’s a lot easier to just say “You worship Gallo” than it is to actually address the evidence. Also, for people whose objections are religiously motivated, their epistemology is based on authority, which comes from priests and texts, rather than evidence.

  5. #5 Hank Barnes
    June 6, 2006

    Tara,

    It’s hard to sort out all the strawmen from your silly post — the connection between Gallo and “Deity” is a bit stretched.

    I do know a few things about Gallo:

    1. He committed scientific misconduct.

    2. His data didn’t support his conclusions: He only found the virus in about 36% of AIDS patients. So, what accounted for the other 64%?

    This would be a purely academic matter, but for one thing. The drugs prescribed to AIDS patients are highly toxic, and cause more severe or life-threatening illness than the underlying disease, particularly liver failure. (See Reisler paper in JAIDS)

    I can’t speak for other folks, but for me, this seems like a serious bungle — where people are getting hurt.

    HankBarnes

  6. #6 Tara C. Smith
    June 6, 2006

    2. His data didn’t support his conclusions: He only found the virus in about 36% of AIDS patients. So, what accounted for the other 64%?

    A number of reasons. Low viral load at the time. Poorly preserved samples. etc. etc. etc. That’s why the antibody test was used–it was a more reliable indicator of infection.

  7. #7 DDS
    June 6, 2006

    Again, Hank, you misread the paper. As the author’s themselves state:

    “In summary, morbidity and mortality for patients with HIV infection have been substantially reduced with HAART. However, morbidity remains high in the era of HAART.”

    HIV/AIDS will kill you. If you take HAART you will live much longer. But, HAART is a toxic drug regimen. There are side effects. The side effect of not taking the drugs is death (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5521a2.htm). HIV causes AIDs (http://www.niaid.nih.gov/factsheets/evidhiv.htm).

    D

  8. #8 Hank Barnes
    June 6, 2006

    Addendum:

    There is also a huge problem in the medical industry of “making up” diseases.

    The newest example is Intermittent Explosior Disorder.

    New diseases = new drugs = new tests = new research $$.

    Gallo, for example, patented the test for HIV anti-body — based on his fraudulent research –which made him a wealthy man.

    His science was compromised by financial gain.

    Hank Barnes

  9. #9 Hank Barnes
    June 6, 2006

    DDS,

    No, I didn’t. Focus on the data, not the conclusion.

    During follow-up, 675 patients experienced a grade 4 event (11.4 per 100 person-years); 332 developed an AIDS event (5.6 per 100 person-years);

    675 is greater than 332.

    But, HAART is a toxic drug regimen.

    Glacial progress, I’ll take it.

    Hank B

  10. #10 DDS
    June 6, 2006

    I did see the data. It supports exactly what I said. The number of AIDs events was lower because HAART treatment prevents AIDS events. Without HAART treament those 675 patients would have died from AIDs long before any of the reported grade 4 events.

    I await you detailed response to the papers (that contain data) to which I provided links. I especially await your detailed response to the data from the NIAID site(http://www.niaid.nih.gov/factsheets/evidhiv.htm).

    I do agree with your comment.

    “There is also a huge problem in the medical industry of “making up” diseases.” But, I don’t think it applies to AIDs. It is not a made up disease.

    D

  11. #11 Hank Barnes
    June 6, 2006

    DDS,

    Without HAART treament those 675 patients would have died from AIDs long before any of the reported grade 4 events.

    Pure unscientific speculation. Would like to see a controlled study: (1) cohort of HIV+ who don’t take HAART and (2) cohort of HIV+ who do take HAART.

    “There is also a huge problem in the medical industry of “making up” diseases.”

    Hey, we have agreement! I’ll take it:)

    But, I don’t think it applies to AIDs. It is not a made up disease

    I agree, too. Immune deficiency is harmful. But it’s multi-factoral, not caused solely a virus, unknown prior to 1983. Clinically, AIDS is merely a collection of old diseases (tuberculosis, pneumonia, yeast infection, dementia etc, etc.)

    With respect to the anonymous Government website you cite, isn’t this merely an appeal to authority? Who cares what the Government thinks? I prefer the peer-reviewed published literature. Don’t you?

    Hank B

  12. #12 tonyl
    June 6, 2006

    Hank since you’re so fond of questions,

    1) Since AIDS pre-dates the drugs used to cause AIDS, how can they cause AIDS?

    2) Why does the condition of AIDS patients dramatically improve when they start taking HAART tratment?

    3) Why did all of those hemopheliacs develop AIDS? Why did the number of hemopheliacs getting AIDS drop dramatically after we started screening blood for HIV?

    4) Why do you ignore most of the available data and continue to spout off mischaracterizations of a few hand picked studies?

  13. #13 Dale
    June 6, 2006

    Pure unscientific speculation. Would like to see a controlled study: (1) cohort of HIV+ who don’t take HAART and (2) cohort of HIV+ who do take HAART.

    If there were an appropriate animal model for HIV/AIDS you would see such a controlled study. But since there isn’t and since the available evidence (comparing pre HAART with HAART mortality rates) indicates that HAART is better than nothing it would be unethical to refuse to treat HIV+ individuals with HAART if they request it. I note from Internet postings that even dissidents often request HAART when they start developing AIDS.

  14. #14 Hank Barnes
    June 6, 2006

    Bean-Counter Alert!!!!

    Tonyl, your first question is 3-dimensional babble:

    Since AIDS pre-dates the drugs used to cause AIDS, how can they cause AIDS?

    I’ve read is slowly 3 times — it still makes no sense.

    First, AZT was developed in 1964. So, AIDS (1981)doesn’t pre-date AZT (1964).

    Second, your first “cause” is gibberish. Do you mean “treat”?

    Third, strawmen. Show me where I said that AIDS drugs “cause” AIDS.

    According to the Riesler paper:

    The most common grade 4 events were: liver related (148 patients; rate = 2.6 per 100 person-years); neutropenia (89; 1.5/100 person-year); anemia (64; 1.1/100 person-year); cardiovascular (51; 0.89/100 person-year); pancreatitis (50; 0.85/100 person-year); psychiatric (44; 0.75/100 person-year); kidney-related (34; 0.58/100 person-year); thrombocytopenia (32; 0.54/100 person-year); and hemorrhage (25; 0.42/100 person-year)

    Some of these illnesses may or may not overlap with AIDS-defining diseases, but ……WHO CARES?

    Hank B

  15. #15 DDS
    June 6, 2006

    Hank,
    The site isn’t anonymous. It clearly states that it is an NIH website. You can see this by reading the URL. The site has links to the original peer-reviewed data so that you can judge it for yourself. I didn’t ask you to believe the site. I wanted you to provide clear refutation of the data within it. If you can’t or don’t want to just say so.

    On what do you base your hypothesis that AIDS is simply a compendium of other diseases? You are always asking Tara for citations and yet you do not provide any.

    As for your proposed experiment with HAART the comparison has been done. Here is a link to one of many many many papers (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11071184&dopt=Abstract)

    HIV causes AIDs. If you have AIDs take HAART and live longer.

    D

  16. #16 Hank Barnes
    June 6, 2006

    DDS,

    The site isn’t anonymous. It clearly states that it is an NIH website

    Who is the scientist who wrote it?

    You are always asking Tara for citations and yet you do not provide any.

    A lie. I cited the Riesler paper above. I’ve cited Padian numerous times.

    As for your proposed experiment with HAART the comparison has been done

    That’s funny. My friend, Dale, above just wrote:

    If there were an appropriate animal model for HIV/AIDS you would see such a controlled study. But since there isn’t and since the available evidence (comparing pre HAART with HAART mortality rates) indicates that HAART is better than nothing it would be unethical to refuse to treat HIV+ individuals with HAART if they request it.

    So, has the study been done or not — due to ethical concerns?

    HB

  17. #17 Dale
    June 6, 2006

    The comparison has been done using historical data – a matched control study can’t be done for ethical reasons.

  18. #18 DDS
    June 6, 2006

    Hank,
    If you would look at the paper you would see that it is a prospective study. That is they compared people who didn’t have HAART treatment (for whatever reason) with a matched control group who did. Read the paper then respond. Dale is correct, it is unethical to do the experiment now because we know that HAART works. When that study was done we didn’t know that.

    I didn’t lie, you don’t read. I said you didn’t cite any work to support your statement “But it’s multi-factoral, not caused solely a virus, unknown prior to 1983. Clinically, AIDS is merely a collection of old diseases”. Niether of the papers in your last post address this hypothesis. I want to see the citations to back up what you say.

    If you want some names attached to the data go here: http://www3.niaid.nih.gov/news/focuson/hiv/resources/macs_and_wihs.htm

    You ask for a lot but provide nothing in return.

    D

  19. #19 Hank Barnes
    June 6, 2006

    DDS,

    I didn’t lie, you don’t read.

    Well, here’s what you said.

    You are always asking Tara for citations and yet you do not provide any.

    Note the words “always” and “any.” Note the introduction of “Tara” into our dialogue. Sounds like a lie to me.

    I said you didn’t cite any work to support your statement “But it’s multi-factoral, not caused solely a virus, unknown prior to 1983. Clinically, AIDS is merely a collection of old diseases”. Niether of the papers in your last post address this hypothesis. I want to see the citations to back up what you say.

    Totally false. I’ve cited Duesberg many times. Go read his first paper on this issue and/or his last.

    Hank Barnes

  20. #20 DDS
    June 6, 2006

    What does mentioning Tara have to do with it sounding like a lie? I see we have a problem with the English language here.

    I said “On what do you base your hypothesis that AIDS is simply a compendium of other diseases? You are always asking Tara for citations and yet you do not provide any.” Clearly, the word “any” was referring to the sentence that immediately preceded it. That is what I meant by read the post.

    And, you still haven’t refuted any of the citations I mentioned in my previous posts.

    I am waiting…or maybe you can’t? I know, just call me a liar and ignore everything else in the post. I cited a study that shows that HAART works and yet you say nothing. Why not?

    In any case I don’t believe that I will ever change your mind. I post mostly to provide an accurate couterpoint.

    D

  21. #21 Hank Barnes
    June 6, 2006

    DDS,

    Look genius, perhaps we should cut the discussion short, because it is becoming non-fruitful (if that is a word.)

    I cited Reisler for HAART. You agree that it is a toxic regimen. Fine, so let’s move on.

    I cited Gallo’s misconduct. You are silent. Tara gives more misdirection.

    If you cannot grasp that Gallo, contrary to his claims, failed to establish that HIV caused AIDS, then so be it.

    But, nearly every paper following Gallo’s fraud in 1984, simply presumes that HIV causes AIDS. Massive, repetetive confirmation bias.

    Very few papers set out to test whether HTLV-III
    was a passenger virus or a pathogenic virus. Except, of course, for all the animal studies which showed no pathogenesis.

    Finally, I cited Duesberg for the global proposition that AIDS is multi-factoral. Surely, you knew about Duesberg before you posted on this thread. So, if you are interested, you will read his work and if not, you won’t.

    Hank Barnes

    p.s. As for the NIH website you cite, well it is pathetic. Triple Play!

  22. #22 Dale
    June 6, 2006

    Hank, Duesberg is not an appropriate citation for evidence of anything pertaining to HIV or AIDS as Duesberg has published no clinical or laboratory studies that contain original data.

  23. #23 Dale
    June 6, 2006

    Hank,
    Gallo was cited for scientific misconduct; his conclusions weren’t at issue only who deserved credit for isolating the virus.
    I would also note that although the vast majority of current studies start with the assumption that HIV causes AIDS, many (i.e. any of those that include HIV- controls) also indirectly test the hypothesis.

  24. #24 Viji
    June 6, 2006

    Hahaha, Hank, you’re ridiculous. You cite only selective few references that seemingly support your views, yet clearly these papers are just argumentative papers with little technical data or just information that can be broadly interpreted; yet when the nice folks around here present well studied clinical papers or even technical papers indicating views that deviate from your own, you clearly don’t read them, and try to deflect them by indicating language flaws in their response? just ridiculous

    If you like to believe that HIV is not the causal agent of AIDS, until some sort of detailed study is done to compare HIV VS. HAART contribution to AIDS (which I think is a waste of time and resources), you seem to be immensely curious or the outcome, and very doubtful of HIV causing AIDS, why not you volunteer to take in a dose of HIV as a experimental model, you’ll serve well to clear up the questions about HIV causing AIDS or not.

    I’ve got plenty of concentrated HIV aliquots stored away in the lab, from M strains to O strains, all genetically and positively identified and classified. Care to inject a dose of these and see if you ever acquire full blown AIDS? I’m happy to donate one aliquot or two.

    P.S. Don’t mind my language, English is not my first language. this response is probably pock marked with plenty of grammatical errors and mannerisms misused

    Viji

  25. #25 tonyl
    June 6, 2006

    Bean-Counter Alert!!!!
    Thank you for the compliment. I try to pay attention to the totality of the evidence. Which means I have to count all those beans and not just pick out the two that are the shape I’m looking for.

    Tonyl, your first question is 3-dimensional babble:

    yes, I made a typo, my most humble and sincere apology. But since I was mistaken and you do not claim AIDS drugs cause AIDS, you just claim they are bad, I’ll withdraw the question.

    but first,
    First, AZT was developed in 1964. So, AIDS (1981)doesn’t pre-date AZT (1964).
    AZT isn’t the only AIDS drug, and although it was developed in 1964, it proved ineffective for its initial purpose and wasn’t widely used as a treatment for anything until 1985. So yes, AIDS predates the USE of AZT.

    Now, do you have any answers to the remaining questions.

  26. #26 Viji
    June 7, 2006

    Hank, I presume this would be your response. QUOTE “3. Well, since hundreds of chimpanzees have been injected with HIV and not one has died, I doubt anything will happen to me. By the way, you do understand that it is nearly impossible to find and culture any infectious HIV from an AIDS patient, don’t you? Hence, the controversy.” END QUOTE

    Hahaha, you clearly have absolutely no idea about research on HIV or even the biology of HIV, if i may add

    Indeed, chimpanzees can be infected by HIV, and HIV can replicate and persist in chimpanzees, but chimpanzees do not develop the human equivalent of AIDS, current research have yet to assign all the broad mechanisms behind this phenomenon (As studying HIV pathogenesis in humans are the priority of research funds, rather than in chimpanzees), but we do have some observations that can explain some part of it, here is one example http://jvi.asm.org/cgi/content/abstract/70/9/6502

    “I doubt anything will happen to me.” Thats wishful thinking. Hey Hank, I’m offering you a free trial, no strings attached. Whats more, you will become famous for offering yourself for the understanding/ or in your case refuting that HIV is the causal agent of AIDS. Its your dream come true. Of course you will have to shy away from HAART at anytime after you’ve injected yourself with HIV

    As for the last part of your response regarding the difficulty of culturing HIV from patients, I think many of the above comments have adequately address this issue, if you care to look. And if you’re still no convinced, fly over to Australia and I’ll show you how to detect low levels of HIV replication in AIDS patients using the HIV-1 RNA detection technique

    Viji

  27. #27 Chris Noble
    June 7, 2006

    If Hank is still claiming that it is “nearly impossible to find and culture any infectious HIV from an AIDS patient” he is now simply a liar rather than just ignorant.

    I have cited this article several times already.

    Human Immunodeficiency Virus Type 1 Detected in All Seropositive Symptomatic and Asymptomatic Individuals

  28. #28 Chris Noble
    June 7, 2006

    The same pseudoscientific pattern of attacking a scientist rather than the science is also seen with anti-vaccination kooks.

    If you read the internet you’ll find out that Louis Pasteur was a fraud and therefore the entire germ theory of disease is flawed.

    You don’t have to read any of the science that was done after Pasteur’s death because Pasteur was a fraud, fraud, fraud!

    A Faulty Medical Model: The Germ Theory

  29. #29 DDS
    June 7, 2006

    Sorry I didn’t get a chance to check the boards before everyone else chimed in with res pones to Hank’s non-answers.

    Let me just say that I have read Duesberg’s AIDs work but none of it has been backed up by significant data. He had a hypothesis, others have proven it wrong or falsified it as we say.

    The Science of AIDs and HIV has moved forward and provided treatments that extend life and prevent infection. Duesberg’s work on AIDs has provided no treatments or prevention strategies. Duesberg’s work has not helped a single AIDs patient. Duesberg is wrong and his opinions deadly.

    You still haven’t given me a strong refutation of any of the scientific articles or science containing websites that I have questioned you on. Your comment that the site is pathetic without a reasoned explanation is poor form on your part. If by pathetic you mean you can’t muster a good response then I would agree.

    I am not sure about a triple play. I have not called you a denialist. I provided links to other authored papers and commentaries. The sites I gave also cited the peer-reviewed literature. They have links and citation lists to the actual peer-reviewed articles. I could copy and paste those links and citations into a post but, since you won’t read them anyway it is no use.

    D (Hank’s Genius Friend)

  30. #30 DDS
    June 7, 2006

    As for Gallo. He did unethical things to achieve a laudable scientific end. Gallo’s ethics though don’t invalidate the scientific end.

    HIV causes AIDS. HAART saves lives. Condoms can help prevent spread.

    D

  31. #31 Hank Barnes
    June 7, 2006

    Viji wrote:

    …why not you volunteer to take in a dose of HIV as a experimental model, you’ll serve well to clear up the questions about HIV causing AIDS or not.

    Triple Play!

    DDS:

    We disagree, but you are fairly reasonable, so we’ll just leave it at that. Repeating this mantra:

    HIV causes AIDS. HAART saves lives. Condoms can help prevent spread doesn’t make it so.

    HI Chris Noble!

    Hank Barnes

  32. #32 simon s
    June 7, 2006

    2. His data didn’t support his conclusions: He only found the virus in about 36% of AIDS patients. So, what accounted for the other 64%?

    A number of reasons. Low viral load at the time. Poorly preserved samples. etc. etc. etc. That’s why the antibody test was used–it was a more reliable indicator of infection.

    Please provide evidence that this is true.

  33. #33 Hank Barnes
    June 7, 2006

    Viji, you crazy aborigine!

    Hey Hank, I’m offering you a free trial, no strings attached. Whats more, you will become famous for offering yourself for the understanding/ or in your case refuting that HIV is the causal agent of AIDS. Its your dream come true. Of course you will have to shy away from HAART at anytime after you’ve injected yourself with HIV

    This ain’t a bad idea! I’ve never been to Australia — G’day mate!

    How about a comparison experiment, though:

    1. Viji injects Hank with HIV. No medication.
    2. Hank gives daily dose of AZT to Viji

    Then, we see what happens!

    After 1 year, I’ll be healthy as a horse and you’ll be on death’s doorstep with anemia, neutropenia, wasting disease, bald-ass head, and lymphoma.

    I’m intrigued by this proposition, Viji. Is there a way to get sponsorship for this, though? Mebbe a grant from the Bill & Melinda Gates Foundation?

    HankB

    p.s. Oooh. Logistical problem. 10-year latency period of said deadly virus. We’d have to sustain public interest for a decade. Might be tough.

  34. #34 Dan
    June 7, 2006

    Hank,
    why are you spending your time here, “debating” these wolves?

    You, myself and anybody else that questions the holy house of “AIDS” becomes their whipping boys. Why? Because they don’t want to look inward, and see what they’re doing. Otherwise they might feel extremely bad about it, possibly even responsible. So they need to beat up others to rid themselves of their psychic pain. It’s pretty simple stuff. They know they’re wrong, but this is what they need to do until they can begin the healing process. Don’t be their whipping boy, Hank.

    Hi, Chris!

  35. #35 Hank Barnes
    June 7, 2006

    Hey Dan,

    Yeah, your actual experiences hit much closer to the bone on this hideous tragedy, so I respect you views.

    On an aside, have you heard of this novel about AIDS by Stephen Davis?

    It’s interesting. Who is this dude?

    I reiterate my earlier observation:

    I do know a few things about Gallo:

    1. He committed scientific misconduct.

    2. His data didn’t support his conclusions: He only found the virus in about 36% of AIDS patients. So, what accounted for the other 64%?

    This would be a purely academic matter, but for one thing. The drugs prescribed to AIDS patients are highly toxic, and cause more severe or life-threatening illness than the underlying disease, particularly liver failure. (See Reisler paper in JAIDS)

    I can’t speak for other folks, but for me, this seems like a serious bungle — where people are getting hurt.

    HB

  36. #36 Dan
    June 7, 2006

    Hank,
    we’ve mucked through Gallo with these folks over and over…

    He’s quite the sore spot for them. Without Gallo’s pronouncement (much less “research”) we wouldn’t have HIV as the cause of AIDS. But with his finding of “HIV” in roughly one-third of his patients, it’s looking like some pretty weak science. So you can see why they like to toss him off of the boat. He’s a major embarassment.

    Here are the basics…
    Gallo claims to have found the cause of AIDS…HIV.
    Gallo’s research proves anything but HIV as the cause of AIDS. Ooops.
    Rather than admit grave error, Dr. Tara and her friends abandon Gallo and furiously attack those who question Gallo’s involvement in laying claim to HIV as the cause of AIDS…and of course all the science thereafter resulting from that basic premise (established by Gallo).
    Dr. Tara and company should try out for the Olympics in the event of mental gymnastics. They’re attempts to somehow make Gallo a less than primary player in the AIDS paradigm are impressive!

  37. #37 Hank Barnes
    June 7, 2006

    Dan,

    Good points. You know what’s it like?

    If fraudulent Korean Stem-Cell scientist was not discovered, but allowed to dominate stem cell research for 10-15 years.

    Hank

  38. #38 Dale
    June 7, 2006

    ,,, and company should try out for the Olympics in the event of mental gymnastics.
    What is it they say Dan? If the shoe fits … Gallo seems to be a sore spot for you and Hank, not Tara or any of the other supporters of the HIV causes AIDS hypothesis. The latter recognize that the science (which has been validated over and over) is more important than the scientist (who was found guilty of scientific misconduct).

  39. #39 Viji
    June 8, 2006

    Indeed Dale… and they seem to miss the fact the existance of so many AIDS sufferers I’ve seen in the most unfortunate places around the globe which have no access to AZT or HAART but invariably tested seropositive for the
    HIV virus

    YET suffering from the very same symptoms of immune deficiency syndrome of the fortunate “wealthier” people elsewhere in Europe or America, those on HAART or those that do not.

    Hmmmm how then should I account for such an observation… prob Hank and his lot will attribute it as divine intervention perhaps, or some novel alien intervention, hahaha

    its a waste of time trying to explain science and testable facts to Hank and his lot of friends, clearly they do not understand the scientific approach, do not appreciate empirical esearch, and seemingly base all their “facts” on mere speculation, one or two disproved papers, or some dodgy website written by equally deluded individuals (equivalent to cuckoo Soothsayers of the days past). I think they’ve watched too much X-files for their own good, so many conspiracy theories and the such. Rather, they should try to spend 24/7 caring for afflicted persons and observe first hand how advancements in AIDS treatments help improve lives. And not waste time reiterating the same pseudoscience crank and mud-slinging like a broken gramaphone, promoting disinformation.

    Just by reading at their rude comments, particularly Hanks, that they are just a bunch of ruffian crybabies which dreads using their grey matter to critically appraise the wealth of research being done.

  40. #40 Chris Noble
    June 8, 2006

    Here’s another irony.

    “Dissidents” go on and on about the various tests for being completely unreliable. They do this by citing studies that show that false positives do occur and extrapolate this to “totally unreliable”. A false dichotomy.

    Now they insist that Gallo’s first antibody tests had to be %100 reliable. The first tests were relatively crude. The specificity and sensitivity of these early tests were not high. Why expect the first tests to be perfect?

    Like all other tests specificity and sensitivity have improved over time.

    Why does Hank neglect later work such as.

    Human Immunodeficiency Virus Type 1 Detected in All Seropositive Symptomatic and Asymptomatic Individuals

    Even if we assume (falsely) that Gallo’s earliest tests were %100 accurate why were 36% of AIDS patients infected with a virus that is present in only very low levels in the general population? Coincidence?

  41. #41 Wilhelm Godschalk
    June 8, 2006

    Good God! DID YOU READ THAT? The paper that Chris Noble cited? Have these people no shame? To begin with, there are 9 authors again, the hallmark of crappy science. You’ll only find this phenomenon in today’s biomedical corner. In other fields, researchers still write their papers alone, or in collaboration with one other colleague.
    But let’s talk about the paper itself. Read the “Materials and Methods” section:

    Briefly, PBMC were separated from 30 ml of heparinized blood on a Ficoll-Paque (Pharmacia, Inc., Piscataway, N.J.)gradient, and 1 x 107 cells were placed in a 50-ml tissue culture flask containing 15 ml of RPMI 1640 medium-20% fetal calf serum-5% interleukin-2-Polybrene (Sigma Chemical Co., St. Louis, Mo.) (5 lig/ml)-penicillin (200 U/ml)-streptomycin (200 ,ug/ml) and cocultured with 5 x 10’phytohemagglutinin-stimulated PBMC from an HIV-1 antibody-negative blood donor.

    Wel, well… a complete witches’ brew. Sure, you may argue that this is all standard procedure, but that’s exactly what worries me. That culture has everything thrown in but the kitchen sink. I have no idea what’s going on in there… and sad to say, neither do the people who did this work.
    But they have no difficulty explaining the results, because the conclusions were fixed before the experiments were performed. See here an illustration:

    To confirm the presence of HIV-1 infection in the antibody-positive, culture-negative subjects, a rapid lysis-extraction technique and a PCR assay were used to detect HIV-1 gag sequences.

    Ah, I see! When the co-culture soup didn’t give the results they wanted, they committed PCR on eh… something that they have (by Papal decree?) declared to be an HIV-1 gag sequence. Without ever having seen, heard or smelled an HIV particle. And please let’s not forget that we’re talking about DNA now. That has nothing to do with a retrovirus directly (they contain RNA), but folklore has it that HIV produces a proviral DNA first through the action of a reverse transcriptase (yes indeed, that’s what retroviruses do), and this DNA is integrated into the host cell genome (so far so good). But from this position it produces a lot of new virus particles, so goes the story, and they destroy all the lymphocytes. – A crazy story! Did Stephen King write it?

    Look at the conclusion of this study:
    HIV-1 infection is present in all HIV-1 antibody-positive adults, regardless of clinical status, by using a sensitive culture or PCR assay for detection of the virus.

    This takes balls, especially since the previous paragraph reads:
    It should also be noted that PCR analysis as done in this study does not distinguish active from latent infection or defective from nondefective virus.

    No, indeed it doesn’t. It doesn’t even distinguish a virus from no virus at all, you swampheads! (I mean all 9 or you).
    You’re doing a roundabout experiment on DNA (supposedly part of “Viral Load, whatever that is) to “prove” that there’s an infection with an RNA-containing virus, for catsake!

    Let’s look at what we really have here:
    409 Subjects, all showing a positive Western Blot. They have antibodies against something, but I don’t know what, and neither do you. A number of them are sick (must be, because they are declared to have AIDS). From all of them it’s possible to grow something in a stimulated cell culture. That works fine with the subjects who are already sick (with something), but I sense some uneasiness in the case of the asymptomatic ones. So they go the extra mile with PCR, because they want to prove so bad that all 409 subjects have that same something.

    Well, I’m ready to believe that sick people under certain circumstances have something,/I> in their blood that you choose to call “Viral Load”. But when you, without valid grounds, call that “something” a retrovirus named HIV, I have to object. On peer review, I wouldn’t have passed this paper.

    Nice to run into you again, Mr. Noble. Please try to get that Shygetz character in here, too, so we can have a ball.
    Unfortunately, just when I intended to get rough with Shygetz’s ideas last time, Tara pulled the plug on that thread. But shucks… It’s her blog.

  42. #42 Dan
    June 8, 2006

    The first tests were relatively crude. The specificity and sensitivity of these early tests were not high. Why expect the first tests to be perfect?

    So, what’s the real story then, Chris? If those tests weren’t so crude, might Gallo have scored 100%? Should we just assume that? Let me know, is this how science works?

    Or do we go with your other line of reasoning?
    …why were 36% of AIDS patients infected with a virus that is present in only very low levels in the general population? Coincidence?

  43. #43 Dale
    June 8, 2006

    Ah, the mocking. Much easier, albeit more intellectually sloppy, than actually critiquing a paper.

    It’s called a retrovirus because, as Peter Duesberg has pointed out, you can amplify those DNA sequences, purify them away from any cellular proteins, put them back into cells and generate retroviral particles that are then capable of infecting other cells. Cute trick that, don’ cha think?

  44. #44 Wilhelm Godschalk
    June 8, 2006

    How nice to find all of you gathered here again! I feel as happy as a dog who sees a fire hydrant. It’s good to be among all the pharma phlunkies again. Sure, I know most of you claim not to get paid a penny by the pharma industry. And you know, I believe you. But… how about that scholarship that made it possible for you to study?

    But let me greet some of you personally:

    Tara:
    How does this kind of thought-resistant religiosity differ in the slightest from the twenty year adherence of believers in HIV to their favored dogma in the face of similar overwhelming evidence against the belief?

    You are baiting us, aint-cha? Well, happy to oblige. But please don’t close the thread abruptly when things get hairy.

    Dave S.
    The idea seems to be that if you can discredit the “source” of the knowledge, then everything afterwards is irrelevant since it depends on those initial papers being absolutely correct.

    A paper doesn’t have to be 100% correct, but if the central theme is wrong, the paper is useless. The problem with Gallo’s (and also Montagnier’s) papers is that the conclusions were not even plausible. Let me explain this in a form even you can understand:
    If Euclid had written a paper saying “The shortest distance between two points is a parabola”, then any subsequent paper based on this assumption would have been suspect.
    Neither Montagnier nor Gallo found any virus particles. So on what grounds do later investigators base their assumption that there is a virus?

    Dale:
    Of course they tend to gloss over the fact that Gallo’s conclusions weren’t discredited

    The story about Santa Claus traveling in a flying sleigh pulled by reindeer has never been discredited either.
    There was nothing to discredit, because Gallo (among others) never backed up his conclusions with evidence.
    And now you expect us to prove a negative?

    DDS
    But, HAART is a toxic drug regimen. There are side effects. The side effect of not taking the drugs is death
    What “side effects”? The toxicity is the main effect. Only, they don’t call the effect of HAART “death”. They call it a “grade 4 event”. How nice of them.

    tony
    Why does the condition of AIDS patients dramatically improve when they start taking HAART tratment?

    Because these people are sick with something. The HAART drugs are also toxic to bacteria. So they have some effect on whatever disease the patient really has. The problem comes with the long term: The patient kicks the bucket from liver failure. Well, at least he doesn’t die from AIDS, because liver failure is not an AIDS-defining disease.

    DDS
    On what do you base your hypothesis that AIDS is simply a compendium of other diseases?

    On the CDC, of course. (Jeez, these questions are getting dumber and dumber)

    Dale
    …indicates that HAART is better than nothing it would be unethical to refuse to treat HIV+ individuals with HAART if they request it.

    I know people (personally) who find that “nothing” is better than HAART. But don’t read that sentence wrong (LOL). They were on HAART, but quit, and are now taking nothing and feeling a lot healthier.
    I agree that individuals who request HAART, should get it. But in this country we have no problem with euthanasia.

    Viji
    why not you volunteer to take in a dose of HIV as a experimental model, you’ll serve well to clear up the questions about HIV causing AIDS or not.

    Oh, there he goes again! Sooner or later somebody comes up with this ridiculous proposal. You are bluffing, mate. You have no idea what’s in those preparations you have in the lab. Nobody does. So why should anybody agree to take a dose of that crap? The only thing we know for sure it’s NOT is “HIV”. And by the way: It has been done. By Dr. Robert Willner.

    Viji
    Here’s a quote from that abstract you cited:
    Chimpanzees infected with HIV-1 show viral replication resembling early infection in humans but do not show T-cell depletion or progression towards AIDS.

    I have the perfect explanation: Today’s clinical virologists are incompetent, and their viral replication methods in heavily stimulated co-cultures are not worth a damn. They would get the same results if they inoculated their cell cultures with juice squeezed from a teddy bear.
    And of course chimpanzees do not show T-cell depletion or progress to AIDS. The poor animals wouldn’t even know how to use poppers or inject heroin.

    Chris Noble
    I have cited this article several times already.

    Yes, you did. And it’s the S.O.S. I dissected this paper already in my previous post.

    DDS
    Let me just say that I have read Duesberg’s AIDs work but none of it has been backed up by significant data.
    First of all, Duesberg’s funding was cut off abruptly, because he is branded as an infidel. He has advanced a hypothesis that is infinitely more plausible than the fairy tales about a retrovirus causing this whole package of diseases. And about retroviruses Duesberg knows a thing or two. He is the world’s major expert on them. The crap that the HIV/AIDS orthodoxy is peddling to the mass media is so off the wall, virologically speaking, that any undergraduate student can see straight through it. But shucks… if Glaxo-Smith-Kline offers to pay for your graduate studies…

    The Science of AIDs and HIV has moved forward and provided treatments that extend life and prevent infection.

    Now that’s a bald-faced lie, plain and simple. You money wasters have been at it for 25 years, and you can’t even come up with one unequivocal isolation of the virus you have dreamed up, and a cure for the disease you have invented.
    Yes, you have provided treatments, and all the patients are raving… R.I.P.

    Dale
    The latter recognize that the science (which has been validated over and over) is more important than the scientist (who was found guilty of scientific misconduct).

    Eh… What science exactly, Dale? I’ve read a lot of papers on the subject, but I find precious little science in them. What Gallo claimed was highly improbable, and almost certainly wrong. He never backed it up with evidence. And all the other prophets after him just repeat the same noncense without any of them ever proving it. Really, we don’t just indulge in Gallo-bashing. The ones who came later (Fauci, Ho, Wainberg, Tramont, and countless others, are at least as bad.

    Viji
    its a waste of time trying to explain science and testable facts to Hank and his lot of friends, clearly they do not understand the scientific approach, do not appreciate empirical esearch, and seemingly base all their “facts” on mere speculation, one or two disproved papers, or some dodgy website written by equally deluded individuals

    Why don’t you stop crying on Dale’ shoulder, Viji. Show some spunk and come out with some real scientific facts. But all you’re doing is running with the herd, because you’re uncapable of doing anything else. So if you understand scientific methods so well, please come up with something more convincing than an attitude. I’ve been doing science when you were still in short pants, chasing wallabies. The people who are looking for HIV in AIDS patients are mostly the same who wasted many years and billions of dollars searching for viruses that cause cancer. Some people are just not cut out for science. They should learn a useful profession instead, such as carpentry or bartending.

  45. #45 Chris Noble
    June 8, 2006

    Wilhelm wrote:

    I have no idea what’s going on in there

    Only in Denialist circles is a statement declaring ones own ignorance considered to be a valid argument.

    … and sad to say, neither do the people who did this work.

    Not content with his own ignorance Wilhelm has the gall to insist that everbody else must be as clueless as himself. Brilliant!

    As Wilhelm knows HIV is a retrovirus that inserts its proviral DNA into the human genome. Wilhelm neglects to even attempt to explain why it is that HIV DNA is found in the cells of people that have antibodies to HIV but not in antibody-negative patients. A wild coincidence?

    On peer review, I wouldn’t have passed this paper.

    As you have admitted to your ignorance of the subject I somehow doubt that you would be asked to review a paper like this seeing as you also claim that RNA viruses don’t mutate and other nonsense. Even implying that you are a peer is laughable.

  46. #46 Wilhelm Godschalk
    June 8, 2006

    Dale
    Ah, the mocking. Much easier, albeit more intellectually sloppy, than actually critiquing a paper.

    Are you talking to me, Dale? I took that paper apart, shred by shred. It sucks. Unfortunately, it’s typical for what’s being written about HIV/AIDS these days. I recently saw one written by 20 (!) authors. You would think that the contents would be earth-shattering. (Hahahahahahahaaaa!)
    Yes, the mocking. That’s the only thing that gets me through an experience like that. Otherwise I might become hostile, and we don’t want that.

  47. #47 Chris Noble
    June 8, 2006

    I took that paper apart, shred by shred. It sucks.

    No, you simply demonstrated that you cannot even understand the paper. Not only that you are actually proud of it.

    Your critique based on the number of authors shows your desperation to find an excuse for ignoring inconvenient experimental results.

  48. #48 Wilhelm Godschalk
    June 8, 2006

    Ah, that’s the way I know you again, Chris:

    Not content with his own ignorance Wilhelm has the gall to insist that everbody else must be as clueless as himself. Brilliant!

    Yes, they are clueless. They make up their mixtures, because everybody does it that way. I’ve known lots of them. Completely devoid of originality, but well-trained, like a circus elephant.

    Wilhelm neglects to even attempt to explain why it is that HIV DNA is found in the cells of people that have antibodies to HIV but not in antibody-negative patients.

    Why should I attempt to explain something that is simply not true? Sure, there may be something different in people who are seropositive (for what, by the way?). So if they find some piece of DNA that they can’t find in seronegative people, does it follow automatically that it must be HIV-related DNA? A little far-fetched, I think.

    So they have sequenced that DNA, and placed it in the gene bank. Fantastic! They sequence everything they can get their hands on. Because that’s what they have learned in grad school. Like the butcher’s apprentice who learns how to operate the sausage machine.

    Hey! Wanna hear a real conspiracy theory? You know why the stores give you those S&H Green Stamps? After you lick them, put them in the boolet, and cash them in, they go to the FBI, so they have your DNA on file.

  49. #49 Dan
    June 8, 2006

    Gallo seems to be a sore spot for you and Hank, not Tara or any of the other supporters of the HIV causes AIDS hypothesis.

    Umm, did you happen to notice that it was Tara that started this blog about Gallo?

    Gallo’s good for a laugh (like his research), but I find so many more aspects of this “AIDS” debacle much more interesting.

  50. #50 Wilhelm Godschalk
    June 8, 2006

    No, you simply demonstrated that you cannot even understand the paper. Not only that you are actually proud of it.

    Eh… do you mean only the true believers can understand a paper like that? Would it help to put on a beanie with a propellor while reading it?

  51. #51 Dale
    June 8, 2006

    Wilhelm, no matter what you want to think those ‘sequences’ represent, people get them through exposure to people or the blood products of people who already have them, and the people who get them are far more likely to get sick than the people who don’t get them. Those ‘sequences’ behave in every way like an infectious pathogen.

    And you can put that in your ultracentrifuge and spin it.

  52. #52 Alan Kellogg
    June 8, 2006

    I’ve noticed one difference between creationists and HIV deniars; the latter have yet to motorize the wheels on their goalposts.

  53. #53 Chris Noble
    June 9, 2006

    Why should I attempt to explain something that is simply not true?

    For people that get offended when labelled as Denialists you do a lot of denying of evidence. A succesful critique would be to provide an alternative example for the evidence rather than simply denying that it exists.

    Sure, there may be something different in people who are seropositive (for what, by the way?). So if they find some piece of DNA that they can’t find in seronegative people, does it follow automatically that it must be HIV-related DNA? A little far-fetched, I think.

    It must just be wild coincidence that DNA sequences that code for retroviral proteins are found in people that have antibodies for the same proteins.

    The same sequences share homology with other retroviruses. they are obviously retroviral. You can take the gene coding for RT and express this enzyme which shows reverse transciptase activity.

    You can transfect cells with these sequences and they produce retroviral particles with gp120 knobs and conical cores.

    These retroviral particles can be cultured. The keep on replicating.

    You can take part of these sequences and generate SIV/HIV chimeras. Infection of macaque monkeys with these hybrids (cell free isolates) reproducibly leads to CD4 cell depletion and simian AIDS. I am yet to hear an even remotely plausible alternative explanation for the easily demonstrable simian AIDS produced by SIVmac or SIV/HIV hybrids.

    All wild coincidences for which Denialists have no alternative explanations other than to deny the evidence.

    Reasons for denying the evidence can be one of the following: the number of authors, funding from industry or funding from any government agency. These “reasons” can be used to ignore effectively any scientific evidence and are equivalent to putting your fingers in your ears and repeating “Nananananananananananana”.

  54. #54 Viji
    June 9, 2006

    ” I’ve been doing science when you were still in short pants” by Wilhelm Godschalk

    hahaha I seriously doubt that and I do agree on the bartender part, as I think you’re the bartender trying to pass off like a scientist.

    Simply, a person that touts to have so much experience as a scientist would never speak in such an boorish manner, more so belittling your peers

    and you clearly have little idea what cell culture is at all

    “15 ml of RPMI 1640 medium-20% fetal calf serum-5% interleukin-2-Polybrene,(5 lig/ml)-penicillin, (200 U/ml)-streptomycin (200 ,ug/ml) and cocultured with 5 x 10’phytohemagglutinin-stimulated PBMC from an HIV-1 antibody-negative blood donor.”

    witches brew you said, hmmm I’m curious, I’ve never heard of any science referrals to witches before, you aren’t a scientist, are you?

    look closely at these ingredients, its closely modelled after the very human equivalents you have in yourself, silly, apart from the antimicrobials of course, but you take antibiotics too, does that make you less natural?

  55. #55 Viji
    June 9, 2006

    Wilhelm, Who is this Dr. Robert Willner? I’m really curious. I’ll like to critically appraise his work if you would provide some links, if you may. It would be very interesting to look at his study if he had infected himself with HIV and found no progression to AIDS.

    “inoculated their cell cultures with juice squeezed from a teddy bear.” you said, enlighten me Wilhelm, is this “teddy bear” an organism I missing out or is it a active ingredient of some sort, I’ve never come across a teddy bear in scientific literature.

    Hmmm, what about those many people who is HIV seropositive , has no access to AZT or HAART yet show remarkably the same symptoms you find with AIDS? Enlighten me with your many years of scientific approaches, Wilhelm.

  56. #56 DDS
    June 9, 2006

    I guess I should respond to Mr. Godschalk’s responses to my statements.

    “First of all, Duesberg’s funding was cut off abruptly, because he is branded as an infidel.”

    Duesberg lost his funding because his science was bad…His hypothesis wasn’t even that original (see Duesberg’s own FAQ). It was proposed by several scientists early in the epidemic. The difference is that they realized that the hypothesis was wrong and moved on. Duesberg didn’t.

    “He has advanced a hypothesis that is infinitely more plausible than the fairy tales about a retrovirus causing this whole package of diseases.”

    Exactly how is his hypothesis infinitely more plausible? The HIV hypothesis is very simple. It destroys part of your immune system and therefore you get sick from other bugs and die. That is simple. According to Duesberg’s own work retroviruses can cause cancer so why not an immunodeficeincy type disease.

    “And about retroviruses Duesberg knows a thing or two. He is the world’s major expert on them.” The first part is true, although I would give him more credit and say he knows at least 10 or 12 things about retroviruses. Unfortunately, most of what he knows is from the 80s and there are thousands of things to know about retrovirsues. I think few experts consider Duesberg an expert in retrovirology anymore.

    “The crap that the HIV/AIDS orthodoxy is peddling to the mass media is so off the wall, virologically speaking, that any undergraduate student can see straight through it. ” Explain this to me exactly. I am not familiar with your version of virology. Perhaps it is from the 1980s?
    It is very clear and simple. HIV destroys an important part your immune system. You get sick easier and die. For evidence check out the links I gave to Hank in the posts above.

    “But shucks if Glaxo-Smith-Kline offers to pay for your graduate studies…” I have never received money from any drug company.

    “Now that’s a bald-faced lie, plain and simple. You money wasters have been at it for 25 years, and you can’t even come up with one unequivocal isolation of the virus you have dreamed up, and a cure for the disease you have invented.
    Yes, you have provided treatments, and all the patients are raving… R.I.P.”

    How did you know that I shave (i.e., Bald Face)? In any case, your statement is clearly wrong. The virus has been unequivocally isolated and grown in culture hundreds of times. We do not have a cure but we do have very effective treatments. Where ever HAART treatment has been started the death rate of AIDs declines. That is a simple fact. (For evidence check out the links I gave to Hank in the posts above.) You might not want to believe it but it is true nonetheless.

    You wouldn’t happen to be this person?
    http://www.theonion.com/content/node/49180

    D

  57. #57 DDS
    June 9, 2006

    I just read this comment from Godschalk and had to comment.

    “Hey! Wanna hear a real conspiracy theory? You know why the stores give you those S&H Green Stamps? After you lick them, put them in the boolet, and cash them in, they go to the FBI, so they have your DNA on file.”

    Wow, this really dates you. Especially since S&H greenstamps have gone virtual. “http://www.straightdope.com/mailbag/mgreenstamps.html”
    “http://www.greenpoints.com/account/act_default.asp”

    I hope you are not still saving them up for that new toaster.

    D

  58. #58 Tara C. Smith
    June 9, 2006

    Two quick notes:

    Wilhelm wrote:

    Tara:
    How does this kind of thought-resistant religiosity differ in the slightest from the twenty year adherence of believers in HIV to their favored dogma in the face of similar overwhelming evidence against the belief?

    You are baiting us, aint-cha? Well, happy to oblige. But please don’t close the thread abruptly when things get hairy.

    Note that those aren’t my words–I’m quoting from the post I linked, authored by “truthseeker.”

    Next, from Dan:

    Umm, did you happen to notice that it was Tara that started this blog about Gallo?

    First, I most certainly didn’t start this blog about Gallo. This post, sure. But the reason I did so was because you were the one who brought him up in the previous AIDS thread (link in the main post above). Y’all are the ones who always bring Gallo into this, assuming making an ad hominem argument against one of the discoverers of HIV discredits all research done on the virus over the last 20 years. This is, of course, ridiculous, and akin to creationists who assault Darwin in an attempt to discredit evolutionary theory. That one of you went so far as to construct a whole “religion” and “clergy” of HIV researchers just shows how desperate you are. You can’t refute the science, so you try (like evolution-deniers) to reduce it to the level of a religion.

  59. #59 Dan
    June 9, 2006

    Tara,
    you’re right…you started this post about Gallo, not the blog. My mistake.

    But the reason I did so was because you were the one who brought him up in the previous AIDS thread

    Really, you brought him up because of me?

    Well, to start a new post on him, you must think this worthy of more discussion.

    Chris, can you answer the questions I asked you? Here they are again, so you don’t have to go looking for them.

    The first tests were relatively crude. The specificity and sensitivity of these early tests were not high. Why expect the first tests to be perfect?

    So, what’s the real story then, Chris? If those tests weren’t so crude, might Gallo have scored 100%? Should we just assume that? Let me know, is this how science works?

    Or do we go with your other line of reasoning?
    …why were 36% of AIDS patients infected with a virus that is present in only very low levels in the general population? Coincidence?

  60. #60 simon s.
    June 9, 2006

    I find all of this offensive. I find it offensive that a little bitch like blondie up there thinks she knows anything about people who have HIV, becuse she studies epiedemiology! Have you ever worked in a hospice? Have you ever gotten your hadns dirty changing a diaper? I doubt it very much, you’re so smarmy, and you give the denilists so much to work with. You are a disgrace. This blog should be shut down.

    I can’t read all of wilhelm’s writing so maybe I just dont get it, but if you think that HIV doesn’t cause AIDS then you haven’t watched thirty people drop like flies around you in three years. But if Tara and Chris Noble think that the drugs are easy!!! Stupid!!!!!! Don’t fucking kid yorselves, morons. If you think so, youve never taken them, or watched friends try to swallow the cocktail day to day. Wrong!

    I aske dabout the tests, because Tara you wrote that everybody in teh beginning had low viral loads, but that is so stupid. They didn’t even have VIRAL LOAD THEN TARA! You are so dumb. You give these assholes so much room to fire at you. They didn’t have fucking viral load TARA! Maybe some of them were not infected and some were, why can’t you be more honest?

    This is the most offensive blog I have ever read about AIDS and I think yuou should all be ashamed of yourselves, especially the doctors here who should fucking know better.

    I can’t even begin to tell you how embarassing this is to watch. This is not how to solve the problem. AIDS is real TARA, its not a gam,e and if you don’t think that Gall and his henchmen have profiteered from this, you are a dumb bitch. We did die-ins at Glaxo and at city hall (inphiladephia) in 92 because AZT was killing us. What the fuck do you know about it? The cocktail is better, but what you should be really doing is figuring out how to help people who are infected and figouring what it is in our genes that keeps some of us (ME!) from getting sick for 20 years but kills other people in 3 years.

    Thats the question, you stupid bitch. not fucking Robert Gallo.

  61. #61 Dan
    June 9, 2006

    You wouldn’t happen to be this person?
    http://www.theonion.com/content/node/49180

    That’s a hilarious article.

    From his tendency to round off calculations, to his rejection of controlled experiments, Hapner is determined to avoid becoming “one of those cowardly sheep who slavishly kowtows to a tired old methodology.”

    According to “Hapner”, Wilhelm would be “one of those…who…kowtows to a tired old methodology”. Read his posts. That’s what he’s asking those involved in “HIV” research to do.

  62. #62 Tara C. Smith
    June 9, 2006

    Simon,

    I’ve never said the drugs are “easy.” In fact, I’ve written previously acknowledging they’re everything but.

    And no, Simon, I’ve not worked in a hospice–I have no medical degree. I have, however, spent time in one. I’ve changed adult diapers and wiped asses; just because I don’t write about them doesn’t mean I’ve not witnessed some terrible things in my “little bitch blondie” lifetime. I don’t presume to know anything about your situation and history, so please don’t presume to know about mine.

    As far as the science, you write:

    I aske dabout the tests, because Tara you wrote that everybody in teh beginning had low viral loads, but that is so stupid. They didn’t even have VIRAL LOAD THEN TARA! You are so dumb. You give these assholes so much room to fire at you. They didn’t have fucking viral load TARA! Maybe some of them were not infected and some were, why can’t you be more honest?

    You mean they didn’t have the tests to measure “viral load” at that point? I certainly agree–that’s why viral *isolation* was being discussed, which is more difficult to detect. PCR, which is used to measure viral load, is more sensitive than viral culture. And antibody tests are often used because they detect prior exposure regardless of whether the microbe is currently in the body or not–so it gets around all the pitfalls that come with PCR or pathogen isolation. That was my point.

    AIDS is real TARA, its not a gam,e and if you don’t think that Gall and his henchmen have profiteered from this, you are a dumb bitch.

    You’ll not get any argument from me that AIDS is real, nor that Gallo has made a profit from his test. That’s the nature of our economy; I can’t really fault him for it.

    The cocktail is better, but what you should be really doing is figuring out how to help people who are infected and figouring what it is in our genes that keeps some of us (ME!) from getting sick for 20 years but kills other people in 3 years.

    People are indeed working on that. They’ve already identified the CCR5 delta 32 mutation. Proportionate to the number of cases in the US, we have more money spent and more scientists working on the disease than any other, but even so, science is never quick and easy.

  63. #63 Hank Barnes
    June 9, 2006

    Wow! Y’all getting heated here.

    Simon S,

    One of my working hypotheses, is that the drugs are often worse than the underlying disease.

    You write:

    We did die-ins at Glaxo and at city hall (inphiladephia) in 92 because AZT was killing us.

    From 1987 -1997, AZT was the primary drug on the market, pushed relentlessly by the scientists/media/Glaxo, because of their utter failure to develop a vaccine.

    This was a terrible idea. AZT is far too toxic.

    Then, they started giving it to pregnant women to “prevent” transmission of the virus to unborn children. Noble intentions, but…..

    In 1997, Olivero et al at the National Cancer Institute performed a similar study on pregnant mice. Here’s what they found:

    At 1 year of age, the offspring of AZT-treated mice exhibited statistically-significant, dose-dependent increases in tumor multiplicity in the lungs, liver, and female reproductive organs.
    (Olivero, Journal of NCI, (1997) 89: 1602-1603.)

    Why on earth they prescribed this carcinogenic drug, AZT, to thousands of AIDS patients, BEFORE trying it out on mice, is mind-boggling.

    It dwarves Gallo’s misconduct and fraudulent work in spades.

    Hank Barnes

  64. #64 DDS
    June 9, 2006

    So Hank, how exactly are you working on your hypothesis?

    D

  65. #65 DDS
    June 9, 2006

    Tara, How long have you been blonde?

    D

  66. #66 Tara C. Smith
    June 9, 2006

    :) It was news to me.

  67. #67 DDS
    June 9, 2006

    Tara,
    Nice response to Simon. I am not sure what he hopes to accomplish by his insult driven diatribe, except maybe to be ignored. I hope that when my turn comes I can muster the same strength-of-character in response to such hate-filled message.

    D

  68. #68 Hank Barnes
    June 9, 2006

    So Hank, how exactly are you working on your hypothesis?

    A few years — hard to dig thru the original papers from Gallo and Montagnier. The Journal of Irreprodicible Results.

    As an aside, Dr. Bialy is mixing it up with Dr. Moore.

    HB

  69. #69 Wilhelm Godschalk
    June 9, 2006

    Thank you, folks, for noticing me. But I see that not all things I brought up are clear to you yet. So I owe you some clarifications:

    Dale
    Wilhelm, no matter what you want to think those ‘sequences’ represent, people get them through exposure to people or the blood products of people who already have them, and the people who get them are far more likely to get sick than the people who don’t get them.

    You make it all sound so easy, Dale. But don’t we need proof that people get these DNA sequences through exposure to other people who already have them? A human being is full of all kinds of biochemically active substances (I personally know a number of people who are full of it).
    The human body can even synthesize most of these macromolecules. So if we isolate DNA sequences from a human, how do we know they come from outside? Now I know there are characters like Chris Noble who think they have a franchise on the “normal” human genome, and have therefore a perfect right to declare any sequence that deviates from it to belong to the virus of their choice. But from previous discussions I know you’re not an unreasonable guy, Dale. Don’t you agree that, before we declare a virus infection, we must first establish that we have indeed an exogenous virus? Now if we could isolate RNA from that virus and sequence that for comparison, then… But I’m dreaming of course.

    Chris Noble
    Your critique based on the number of authors shows your desperation to find an excuse for ignoring inconvenient experimental results.

    Let me explain my criticism. I think I know exactly why publications about HIV, Bird Flu and all that rot have 8 – 20 authors.
    Today’s graduate students, on a scholarship from GlaxoSmithKline, only have time to learn one technique before they get their Ph.D. One only learns how to sequence DNA, a second one is only familiar with tissue culture methods, a third only knows how to shaft monkeys with SHIV, etc. So there is no single individual around who is competent to carry out a whole scientific investigation. But with a group of 12 or so, including one who can write in English, they can do the job.
    I wonder how many of them are needed to screw in a lightbulb…

    For people that get offended when labelled as Denialists…

    Oh, don’t worry about that. I’ve been called worse.

    A succesful critique would be to provide an alternative example for the evidence rather than simply denying that it exists.

    Oh? Is that your requirement? I don’t think that’s customary. When a shaky and decrepit building has to be replaced by a new structure, the first one needed is the man with the wrecker’s ball, to take the old ruins down. That will get the space ready for the new building. I’ve never seen a wrecking company that was also required to undertake the new development.
    In practical terms: Showing up a theory for the load of crap it is, can be done by logical thinking only. To advance – and prove (!) – a new hypothesis takes lots of research money. Who’s going to provide that? Big pharma?

    It must just be wild coincidence that DNA sequences that code for retroviral proteins are found in people that have antibodies for the same proteins.

    Coincidence? No. But what’s so special about it? The biomedical hacks have a real DNA-fixation. They never want to go too far away from DNA. I’m speculating now, but I think that is because the double-helical structure is firmly screwed in their behinds.
    But there’s another important step between DNA and proteins, and the coding information can go both ways. Reverse Transcriptase is an omnipresent enzyme, even though the retrovirus pimps want to claim sole ownership. They’re terribly afraid of everything that lies between genes and proteins. But I admit, it’s rather complicated.
    Is it really strange that the immune system doesn’t recognize a body protein as its own? Of course not; proteins can change conformation by interaction with simple chemicals (mercury compounds for example). And a protein that has changed conformation (shape) cannot be recognized by the lymphocytes. So the situation is quite common. No virus required to explain it.

    The same sequences share homology with other retroviruses. they are obviously retroviral. You can take the gene coding for RT and express this enzyme which shows reverse transciptase activity.

    Homology? There are only 4 bases. That doesn’t allow for all that many variations (compared to the amino acids in proteins).
    Gene coding for RT? Well, of course! It’s a very commonly occurring enzyme. See above what I had to say about retrovirus pimps.

    You can transfect cells with these sequences and they produce retroviral particles with gp120 knobs and conical cores.
    These retroviral particles can be cultured. The keep on replicating.

    You mean in that co-culture soup? I’ve never seen particles with gp120 knobs, but I’m sure you’ll be willing to show them to us. The conical cores I’ve seen, and that shape is exactly the reason I don’t believe they’re virus particles. They look more like transport membrane vesicles. Are you sure they replicate? You might see the exact same particles in a culture that has not been inoculated with the lab artifacts you choose to call retroviral particles.

    You can take part of these sequences and generate SIV/HIV chimeras. Infection of macaque monkeys with these hybrids (cell free isolates) reproducibly leads to CD4 cell depletion and simian AIDS. I am yet to hear an even remotely plausible alternative explanation for the easily demonstrable simian AIDS produced by SIVmac or SIV/HIV hybrids.

    You have presented that SHIV paper before, and I’ve already critiqued it in the Snake Pit. SHIV is a complete lab artifact. It is not surprising at all that some of these monkeys get sick after having been treated to these foreign nucleoproteins. Who wouldn’t?
    There is a ridiculous story making the rounds that HIV originated with monkeys (or apes) in Africa. But this virus wasn’t able to make one single monkey sick, once it crossed the Atlantic, while striking lots of victims among the gay community in N.Y.C. and S.F. In addition to “HIV”, the specific SIV monkey viruses don’t bother the animals either. They carry the viruses, but they don’t experience any discomfort from them.

    All wild coincidences for which Denialists have no alternative explanations other than to deny the evidence.

    Wild coincidences? Look again at that paper you’re holding so dear. Look what they did to those poor animals, which caused me to coin the phrase “shafting with SHIV”.

    Reasons for denying the evidence can be one of the following: the number of authors, funding from industry or funding from any government agency.

    I already explained the reason for having so many authors: Nobody is competent any more to do a study on his own.
    And you have the gall to suggest that these criticisms are the only ones the “denialists” come up with? I’ve taken numerous papers that you and your underprivileged friends in the Snake Pit have presented , apart on scientific grounds.
    And I’m ready to do the same here. I wonder why you still don’t wake up and smell the coffee. But… on the other hand, it must be very sad when you’re not free to do your own thinking. I’ve been interviewed for jobs where they asked me: “Are you a team worker?” I’ve always answered: “Hell, no!”. I wonder why I never got those jobs…
    Nevertheless, I don’t regret anything. It must be hell to be a team player.

    And furthermore…
    …as you also claim that RNA viruses don’t mutate and other nonsense.

    Now that’s just spreading ugly rumors, Chris. I’ve never said RNA viruses don’t mutate. Only that they don’t mutate to the ridiculous extent as the HIV- and Bird Flu jockeys want us to believe.
    They are only trying to cover up their own incompetence with that mutation story. They sequence anything they happen to get their hands on, and as can be expected, their results vary all over the map, because it’s all different muck.
    So they try to explain all these varying sequences by saying they’re different mutants. Oh, great! So if they do 138 experiments on what they think is HIV, and they get 138 different sequences, they try to tell us they have 138 different mutants of HIV. They did that also with that other non-existant virus: Hep-C (the alibi virus).

    Viji
    Simply, a person that touts to have so much experience as a scientist would never speak in such an boorish manner, more so belittling your peers

    I used to be more respectful to colleagues. But considering that most of them are totally unimaginative, only know one lab technique, propagate the wildest theories without any shame, and act as if they possess the ultimate wisdom, I have decided they are not my peers. They wish…

    look closely at these ingredients, its closely modelled after the very human equivalents you have in yourself, silly, apart from the antimicrobials of course, but you take antibiotics too, does that make you less natural?

    No, I seldom take antibiotics. They may have been part of the problem in the first place. The gay crowd during the late seventies took antibiotics as prophylaxis. That’s not a smart thing to do. It kills off bacteria, but fungi get a free run. That’s how Pneumocystis carinii Pneumonia got to run rampant.
    Look, I understand why they make up this kind of witches’ brew for tissue culture. It’s because the guy who taught you did it that way, and the guy before him, and.. etc.
    But don’t you ever think about possible complications caused by these ingredients?
    And then the PHA-stimulated PBMC’s from the blood donor. Is this PHA stimulation natural?

    Who is this Dr. Robert Willner?
    Well, Dr. Willner did not really a study on this which he published. It was more like a stunt. He inoculated himself on Spanish TV with the blood of a seropositive man. You can read about here:

    Dr. Willner has passed away since. Not from AIDS, but from heart disease.

    enlighten me Wilhelm, is this “teddy bear” an organism I missing out or is it a active ingredient of some sort, I’ve never come across a teddy bear in scientific literature.

    Actually, it’s a toy generally owned by children. And what you can squeeze out of it is mostly children’s piss. But I’m sure you would get similar results with it as you get with the stimulated PBMC’s.

    Hmmm, what about those many people who is HIV seropositive , has no access to AZT or HAART yet show remarkably the same symptoms you find with AIDS?

    Well, we have to be more discerning here: Those who live in developed countries (such as the U.S., Europe, or Australia) are doing just fine. I happen to know a number of them, and they are in excellent health. Some of them have been on HAART drugs before, but they were miserable then, so they decided to quit the meds.
    Now for those who live in third-world counties, especially in Africa, the picture is quite different: They suffer from nasty diseases such as malaria and malnutrition. The ones who have access to AZT or the HAART drugs are in a different position. They don’t suffer (anymore). They’re dead.

    You seem like a decent person after all, Viji. Not at all like Chris Noble, for example. Just my impression. You ideas suck, of course, but I’m sure we can work something out.

    DDS
    Duesberg lost his funding because his science was bad…His hypothesis wasn’t even that original (see Duesberg’s own FAQ). It was proposed by several scientists early in the epidemic. The difference is that they realized that the hypothesis was wrong and moved on.

    His science was bad? Gallo and his gang can’t hold a candle to Duesberg. Yes, it’s true that several scientists had the same idea at the time (because it’s logical and plausible) But they “moved on” You may call it “the hypothesis was wrong”. I call it corruption.

    The HIV hypothesis is very simple. It destroys part of your immune system and therefore you get sick from other bugs and die.

    Yes, it’s so simple that only a simpleton would believe it.
    In vitro, the preparations rumored to contain “HIV” don’t destroy a single CD4 cell. The HIV orthodoxy is still at a loss to explain how “HIV” destroys these CD4 cells in vivo.
    And people with low T4 cell counts get only sick from bugs connected with the 29 AIDS-indicator diseases? Not the flu, common cold, typhus, or scarlet fever? Besides, among the 29 AIDS diseses are a few cancers. I’m still absolutely rejecting the idea that any type of cancer is an infectious disease, no matter what Duesberg says.

    Unfortunately, most of what he knows is from the 80s and there are thousands of things to know about retrovirsues.

    I agree that the eighties were the lost decade. I can’t say anything positive about the eighties. But I hope that you don’t mean that scientific results become invalid just because they were obtained long ago. What to do with Euclid’s math? Or newton’t laws of classical mechanics?
    But when I look at what has been accomplished in the field of Virology the past 25 years, I’m not impressed. there is especially a lot of hogwash about retroviruses. I’m beginning to wonder if the whole concept is not just a matter of virus-like material coming out of the human body, rather than an infectious agent infecting us from the outside. The fact that none of these human retroviruses have been isolated doesn’t help either.

    I am not familiar with your version of virology. Perhaps it is from the 1980s?

    Hell, no! Nothing good has come out of the eighties.
    But do the names Stanley, Fraenkel-Conrat, Luria, Dulbecco, and Todaro mean anything to you?

    It is very clear and simple. HIV destroys an important part your immune system. You get sick easier and die.

    See my comments above. No, you don’t get sick and die. I know too many people who are seropositive, don’t take the toxic drugs, and live a healthy life. The “latent” time between “infection” and “full-blown AIDS” has been contnuously lengthened by the CDC. It used to be 2 years or so, now it’s at least 10 years. Do they really think we’ll believe anything? No, I won’t let you get awy with this simple-minded picture.

    I have never received money from any drug company.

    That’s what they all say. So why don’t you declare your independence, and start thinking?

    The virus has been unequivocally isolated and grown in culture hundreds of times.

    Really? That reminds me… I asked, a few posts ago, if somebody would present a paper (just one) describing a successful isolation of HIV. Are you trying to postpone the moment, Mr. DDS, when you have to admit to me that you cannot produce such a paper?

    Where ever HAART treatment has been started the death rate of AIDs declines. That is a simple fact.

    Nobody lived even a day longer with HAART. They are no longer considered dying from AIDS, but they die from liver failure. Must make the victims feel a lot better…

    You wouldn’t happen to be this person?

    No, I’m not the person The Onion describes. I’m just me. But you could Google my name, of course.

    Tara
    You can’t refute the science, so you try (like evolution-deniers) to reduce it to the level of a religion.

    Now wait a minute! We’re refuting the science all the time. But the HIV/AIDS orthodoxy is moving the goalposts so often, and the theory has become so patchy, to explain the unexplainable, that nobody could believe it out of free will. Nobody is THAT stupid. So don’t be shy. I know there must be other motives to run wih that crowd. I promise I’ll try to understand…

    P.S. Try to get those other unspeakable characters in here, Richard TAG Jefferys and Shygetz. I’m smelling blood.
    Hatchet Day is near.

  70. #70 Wilhelm Godschalk
    June 9, 2006

    I see that the Willner link did not come through. here is another try:

    Willner

  71. #71 simon
    June 10, 2006

    They’ve already identified the CCR5 delta 32 mutation. Proportionate to the number of cases in the US, we have more money spent and more scientists working on the disease than any other, but even so, science is never quick and easy.< \blockquote>

    Quick and fucking easy? just shut up Tara. AZT was bullshit and nobody did anything right until crix and then that got everybody fucked up after a year anyway. Hank i wasn’t talking to you. And DDS or whatever your name is – go fuck yourself. I don’t need to be “handled”. Who are you? what do you do? Are you gay? then shut up. do you have any fucking idea waht youre talking about?

    Do you have AIDS? Do you know anybody who does? Did you ever care for anybody who did? Then shut the fuck up. Im sick of hearing from you academic types who makes excuse after excuse for all the money that goes down the hole into YOUR POCKETS while people are DYING. I’m not respondign to anything else here. Don’t answer anything, i’m not interested in your sorry ass point of view. I told you what I thought that this is THE most offensive thing I’ve ever seen on AIDS, this whole Gallo bullshit. You know the fuckking denialist dissidents are right about one thing and one thing only: you don’t know what the fuck you’re doing.

  72. #72 simon s
    June 10, 2006

    PS I’m sorry if you think I’m so rude. I tried to be polite at first and I asked a question as politely as I could that nobody answered, and then it was just ignored. When you don’t know stuff , you lie, that’s the way its always been with this and it is insane and it makes me fucking insane and angry. Tara you lie when you don’t know stuff like with that answer about v.l. You don’t know and you dont know why some of those men had HIV and some didn’t, you dont know and you just make up an answer like Viral load!!!!!! YOU DIDN”T KNOW and you just make stuff up, instead of being honest, which we all would REALLY APPREICIATE INSTEAD because WE ARE TIRED OF THE LIES. IF you dont know something then tell the truth, just tell the fucking truth and give us a chance to know ahead of time what we dont know, because most people WOULD NOT HAVE TAKEN AZT IF YOU HAD TOLD THE TRUTH and we could have tried SOMETHING ELSE THAT WORKDED BETTER at least we could have SAVEd TEN Years!!!!!!!! until the P.I.s came, and maybe they would have come FASTER if you people would have been MORE HONEST. You are not honest and I’m sorry if you think I’m rude but it’s been a long time and a lot of years. I’m sorry if you think Im rude here but I have to be honest because after awhile you just cant take the BULLSHIT anymore. I’m sorry I called you a name Tara, but you have to be more honest all of you do AND GIVE US A BETTER CHANCE TO FIGURE THIS OUT

  73. #73 Viji
    June 10, 2006

    Simon, you’re starting to become incomprehensible, and being miserable and vengeful doesn’t justify being rude and impossible towards the very people who are giving their life’s time and effort working on attempts and trials to alleviate the suffering of people from the many diseases that afflict many people in the world

    And despite you thinking us grad students, scientists, and post docs as blood sucking people exploiting vultures, we’re a bunch very far from that. Inspite of the many years and money spent on training, education, and endless hours working in the labs, on the field, in the medical facilities, we remain the bottom rung of the economy everywhere in the world, so don;t do us a disfavour by spitting on us. Who else would you suggest to have so much passion and dedication to even try to tackle your problems and everyone elses in this miserable world?

    As far as I understand from my fairly recent reading of Tara’s blog, I have never seen her lying, and she’s done a fine job highlighting recent developments, critically appraising these developments, and describing the many scientific jargons in plain english so that the common people can at least comprehend information that would otherwise be unaccessible to them. Your blind branding Tara and everyone else in our profession as liars and insanes just lets people to look at you with disdain.

    I was yet born during the AZT years, and I believe neither has Tara anything to do with that, so why do your integrity this disfavour with such slander. As Tara has correctly pointed out, this is how human knowledge progresses, thru experimentation, trials, and learning from mistakes. You think the very medical care we have today came about without its equal sets of misteps? Its easy for you to complain about everything when you have the best treatment and care options for your use, care to think about the people that has none of these in Asia and Africa?

    learn to control your emotions before you start rambling and complaining about the people who are giving their best working on a better solution for your woes

    Viji

  74. #74 Viji
    June 10, 2006

    To Wilhelm Godschalk,

    I do not understand your rationale that a paper or a study that is conducted/collaborated between a panel of experts from their respective fields of expertise, is a sign of inferiority or weakness. Care to enlighten me on this

    And to think that the complexity today’s scientific questions and pursuits are as simple as screw in a lightbulb, you’re sadly mistaken.

    Perhaps during your time, it was all quick and dirty, but the scope of studies undertaken almost everywhere nowadays are multifactorial. For example, my current study of resistance in MDR bacteria already take me to various technical expertise, from simple microbiology, developing HPLC methods, MALDI-TOF, AFM to classic molecular biology methods like mutagenesis, all the way up to animal PKs PDs and clinical phases of developing optimal dosage regimens, yet I can/and will never profess to be an expert in all of these fields of study. I take on talented individuals who are experts in these fields and work in collaboration with them, thus having their names on publications as an appreciation of their contributions. May I ask you what is so inferior about that?

    In fact, such inter-discipline mingling and cooperation facilitates the exchange or ideas and further innovations, which serve well to discourage unilateral preoccupation with certain theories and techniques or static/stubborn interpretation of results.

    In this day and age, the information age, we can never aspire to be a jack of all trades, thats just silly, as you’ll just spend too much time learning the many techniques available and the new ones being introduced constantly, in the end being an expert of none, and contributing little to the advancement of knowledge.

    As for Hank Barnes, I am eagerly waiting for the publication of your study and critical review of the HIV research, your “working hypothesis” if you may, to hear what you have to say about this rather than shorts comments than seem to look like little more than rantings and lacklustre conspiracy allegations (probably due to the lack of content, a result of keeping comments concise). If you’re so disastified with our current understanding of HIV-AIDS, stop something, and do something to contribute to knowledge, rather than ranting and complaining. At least we are spending all our effort 24/7 doing the research required to understand HIV-AIDS (even if you think our research is misdirected, at least we are trying to solve the problem, while you’re not even lifting a finger)

  75. #75 Viji
    June 10, 2006

    Hey Wilhelm, you seem to question the intelligence of other people apart from your own .. with this comment you wrote

    “I used to be more respectful to colleagues. But considering that most of them are totally unimaginative, only know one lab technique, propagate the wildest theories without any shame, and act as if they possess the ultimate wisdom, I have decided they are not my peers. They wish…”

    that’s gratuitous at the very least,

    first, because you are assuming everyone around you knows less and you know better ,

    second, no matter how many techniques I myself may be profficient in, I can never profess to know about everything, and similarly, I wouldn’t expect you to know every technique or know-how under the sun. So why insult other persons without first reflecting on yourself.

    Third, hypothetically, if you are at the receiving end of this comment by yourself, i.e. “you* are totally unimaginative, only know one lab technique, propagate the wildest theories without any shame, and act as if you* possess the ultimate wisdom”, it doesn’t sound like fair judgement, does it? especially if its being directed at people you do not know very well.

    DO not upon others that you wish not upon yourself

    Cheers
    Viji

    Viji

  76. #76 Frodo
    June 10, 2006

    I am new here and new to this discussion. What I see here so far is two sides equally unimpressed with each other’s arguments and equally unwilling to listen. I cannot make heads or tails of the argument based on what I’ve read so far, so am keeping an open mind. I have no problem believing that mistakes are made in institutions; on the other hand, I’m not a conspiracy theorist so I’ll continue to read until something convinces me overwhelmingly of one side’s veracity. If you wouldn’t mind, however, I would like to pose a question that may help me understand the issue from a different perspective: Are you more Left-leaning (liberal) or Right-leaning (conservative)? (I am Liberal, though open-minded to ideas from both sides)

  77. #77 Dan
    June 10, 2006

    An open letter to Simon (since he told us not to respond to him):

    I find myself agreeing with some of your rants, at least on an emotional level. These people “playing scientist” have been doing so for more than 20 years on this issue. They’ve squandered billions and billions of dollars, and what do they have to show for it?

    AZT is a nightmare. I watched two close friends die from taking it. But they still promote this crap like it’s a godsend…and even worse, they give it to pregnant women and their babies. Joseph Mengele would be smiling if he were alive today.

    Why do you give your power away to these people, Simon? Why do you give your power away to the doctors, scientists and especially the pharmaceutical companies? Why do you expect them to help? I’m being a bit cynical here, as I’m aware that there are many dedicated, caring researchers and scientists out there who believe they’re helping. But I certainly don’t see the pharmaceutical companies as bastions of altruism. Just turn on the TV, you’ll see their true nature…and they don’t seem the least bit ashamed!

    As a gay man in his forties who’s lived through this nightmare, I was never able to understand why we were so quick to give our power away to the drug companies. All those protests, with the screaming, why?

    Which do you think is more motivating to the drug companies, altruism or profit?

    You seem to be aware of what a profit-machine AIDS is. With ALL of that money moving around…kind of makes you question if they really want this gravy train to come to a stop. Remember Margaret Heckler’s announcement, that there would be a vaccine available within two years?…which would have been in 1986. With so much money going on…might they be dragging their feet on purpose?

    Simon, you may want to consider taking your power back. You’ve been going through this for so long, giving away your power, and where has it gotten you? Now, I don’t know you of course, this is the impression I’m getting from reading your posts. But that’s what it looks like to me, that you want “them” to solve this. They don’t seem to be anywhere near as motivated as you are on this issue. You LIVE it. For some of them, it’s just a fascinating microbiological drama…and/or a steady source of income. For you, it’s reality.

  78. #78 Dan
    June 10, 2006

    P.S. to Simon,

    did you notice that one of the categories Dr. Tara chose to place this post under is HUMOR?

  79. #79 Hank Barnes
    June 10, 2006

    Viji,

    I was yet born during the AZT years, and I believe neither has Tara anything to do with that, so why do your integrity this disfavour with such slander

    AZT is still being prescribed under the brand name Retrovir or Combivir. Few scientists are even keen on recognizing it as a highly toxic carcinogen.

    Why not make up for lost time, Viji, and DO something about this.

    Hank

  80. #80 Thom
    June 10, 2006

    Frodo, I am an old Democrat fighting for the party. (and damn, I hope that’s not your real name). I am not a scientist, but I do read and I do use the thing on top of my neck, eyes, ears, brain and all, you AIDS mechanics will have to forgive me for that.

    Dale you wrote

    Wilhelm, no matter what you want to think those ‘sequences’ represent, people get them through exposure to people or the blood products of people who already have them, and the people who get them are far more likely to get sick than the people who don’t get them. Those ‘sequences’ behave in every way like an infectious pathogen.

    Now what are you thinking about? A strand of something is not infectious. I’ve been bumping up against AIDS and every other kind of patient for all my life and I’ve never gotten an infectious strand of DNA lodged in me. I have followed this argument (where it was cogent) and Wilhelm has given good answers to this about strands and the PCR tests, and you just ride roughshod over them without pausing to even look down. You have got to unmake your mind for one moment and look at it without the smirk and judgement.

    viji and Noble
    It is very clear and simple. HIV destroys an important part your immune system. You get sick easier and die.

    Well say it again, Swami. I never had any idea why doctors would say this. When Simon says that thirty fellows dropped dead in 3 years, I’ll say yes that happened, but the men I knew who passed were almost to the man the poppers slaves and sex slaves, and that meant that they were always pumping something in themselves that did not belong there, whether it be drugs by the nose and mouthful, or benzene in the colon and rectum (I have long since passed on that and found other materials for that purpose, though it’s not usually me but my partner, who is fine as well).

    But to say this, I can only think of what they always say on tv shows about medicine, that line they got from that old Greek, First Do No Harm. And it seems to me an abrogation of duty to inflict the death sentence before the patient has a chance to get better. Now I have seen people die and the doctors like to say AIDS when its a gay man, but I also watched those patients demoralized and beaten down by the very doctors they went to for salvation and I have seen their veins run dry on bactrim and pentamadine, and on radiation, which is what they used to do for those poor souls who went in with the sarcoma. I have not looked for the medical establishment to fix one of my ills and ailments for the last 30 years, and I’m all the better for it. I pity the boys who didn’t learn this lesson early or didn’t grow up having to fend for themselves and learn the healing arts of the body and of herbs and of good old common sense.

    Frodo, I don’t know if that will help you, and I don’t think it will help Simon, I’ve seen his type and it is heartbreaking. I hope God can ease his burden and lighten his soul.

    Viji you wrote
    Simply, a person that touts to have so much experience as a scientist would never speak in such an boorish manner, more so belittling your peers

    That is pure horseshit. This whole blog line is based on bashing your peers who are trying to inject some sensible thought into this death cult of yours. Tara posts blog after blog bashing and provoking her peers, who she calls denialists, because they have a separate hypothesis. Try opening your mind and honoring honoring your profession.

    Wilhelm, you fight that good fight for the rest of us. I stay away, but I just wanted to make it plain once, because most of the time I stay out of this madness. We all tried in the begining to make some sense and to work with the doctors, but then the AIDS mafia (that’s what I call it and that’s what it is) and Larry the K and all those boys took it over and layed down right in front of those bulldozers and let it run right over them. I’d never seen such a thing in my life. We were finally a little bit freer in a sense, and then it was all over. You doctors who really believe you are fighting for my “gay rights” or my “human rights” by fighting this AIDS war can rest assured that I would prefer you figured out how to keep the hormones out of my food, the mercury out of my tuna and salmon, or how to get us out of oil, and not worry about making sure that we all get our heads full of this nonsense.

  81. #81 Dan
    June 10, 2006

    This whole blog line is based on bashing your peers who are trying to inject some sensible thought into this death cult of yours. Tara posts blog after blog bashing and provoking her peers, who she calls denialists, because they have a separate hypothesis. Try opening your mind and honoring your profession.

    Well put!!

  82. #82 DDS
    June 10, 2006

    Hank,
    I would post a link to dozens of papers where HIV has been isolated. I would even post links to EM pictures of the virus. But, it would do no good. Every time I have posted a paper in support of what I say you ignore it and start another rant. Just look over the papers I have linked to in the first few posts of this thread. You are wrong. HIV causes AIDs. Your working hypothesis is wrong. HAART saves lives. The data is unequivocal.

    As for the angry mob that attacks those you are actually helping. I feel pity for your pain. Whether you want me to or not I still do. No matter what vile words and screaming anger you post, I’ll just feel more pity. I hope you spend as much time screaming at your uninfected friends to wear condoms and stop this epidemic in its tracks.

    D

  83. #83 Hank Barnes
    June 10, 2006

    DDS:

    Huh? What are you talking about?

    I would post a link to dozens of papers where HIV has been isolated.

    Feel free to post them.

    I would even post links to EM pictures of the virus.

    Post these too — I hope they are at 1.16 density gradient, but I would defer to Wilhelm.

    But, it would do no good. Every time I have posted a paper in support of what I say you ignore it and start another rant.

    What rant are you talking about? I ain’t ranting. I’m watching the show. There’s been some very interesting developments on this thread. I think its critical to hear from gay men, who have been most victimized by this bad science. Their stories need to be told — particularly about AZT.

    Just look over the papers I have linked to in the first few posts of this thread.

    The NIH website was your best shot. Sorry. Weak.

    You are wrong.

    Well, hypotheses aren’t wrong — they are either proven or unproven.

    HIV causes AIDs. Your working hypothesis is wrong. HAART saves lives. The data is unequivocal.

    Broken record, no citation. Broken record, no citation. Broken record, no citation.

    Look DDS, you have glimmers of reasonability and humor,which separates you from some of the wackos and AIDS cultists who merely parrot the party line. So, if ever there can be a fruitful discussion of this, I’m game.

    As for the angry mob that attacks those you are actually helping.

    Don’t follow you, here.

    I feel pity for your pain. Whether you want me to or not I still do.

    Again, don’t follow. Are you conflating me with simon s or Thom? Trust me, I’m not them. Tara can confirm this with IP Addresses.

    No matter what vile words and screaming anger you post, I’ll just feel more pity. I hope you spend as much time screaming at your uninfected friends to wear condoms and stop this epidemic in its tracks.

    Again, don’t follow. Yes, generally condoms are fine. Although, the largest epidemiological study, Padian (Am. J. Epid 1997), found “no seroconversions” with or without condoms.

    HB

  84. #84 DDS
    June 10, 2006

    Hank,
    The last paragraph of my post was for Simon et al not you. Sorry, I should have been more explicit.

    I’ll post some links to pics and papers to support the HIV has been isolated assertion, although I am sure you can find them yourself. But, if I do you have to promise to look them over and give a reasonable critique not just a “these are a bunch of crap papers” comment. Deal?

    I’ll have to post them later tonight or tomorrow. I am otherwise occupied for the next several hours.

    D

  85. #85 Hank Barnes
    June 10, 2006

    But, if I do you have to promise to look them over and give a reasonable critique not just a “these are a bunch of crap papers” comment. Deal?

    Yes, if its a two-way street. You have to promise to look over and give reasonable critique to Duesberg’s Cancer Research Paper and Duesberg’s PNAS paper.

    Deal or No Deal?:)

    Hank

  86. #86 Dan
    June 10, 2006

    Simon:
    aske dabout the tests, because Tara you wrote that everybody in teh beginning had low viral loads, but that is so stupid. They didn’t even have VIRAL LOAD THEN TARA! You are so dumb. You give these assholes so much room to fire at you. They didn’t have fucking viral load TARA! Maybe some of them were not infected and some were, why can’t you be more honest?

    Tara:
    You mean they didn’t have the tests to measure “viral load” at that point? I certainly agree–that’s why viral *isolation* was being discussed, which is more difficult to detect.

    Hank:
    His data didn’t support his conclusions: He only found the virus in about 36% of AIDS patients. So, what accounted for the other 64%?

    Tara:
    A number of reasons. Low viral load at the time. Poorly preserved samples. etc. etc. etc. That’s why the antibody test was used–it was a more reliable indicator of infection.

    It looks like Dr. Tara has done what Simon is accusing her of, lying…or at least stretching the truth to the breaking point.
    Hank made a reasonable point about Gallo, for which Dr. Tara makes excuses for her esteemed colleague. I especially like the excuses called etc., etc. etc.
    So, Dr. Tara, do other scientists make excuses for Gallo finding HIV in only 36% of his patients as well? Like I asked Chris (who seems to have vanished), is this how science works? When the evidence is less than convincing, we make excuses? Let me know.

  87. #87 Wilhelm Godschalk
    June 10, 2006

    DDS
    I’ll post some links to pics and papers to support the HIV has been isolated assertion, although I am sure you can find them yourself.

    Glory bee! Hallelujah! Am I looking forward to that! You know you’ll be writing world history, DDS (dentist?). No, I couldn’t find them myself, and neither could Kary Mullis.
    I’ve been taunting several of you to present these papers, but to no avail thus far. But now it’s really gonna happen!
    Although… You won’t be feeding us the Gelderblom paper again, won’t you? (Ho-hum). And a bunch of papers where it’s supposed to be understood that HIV exists and has been isolated?
    Oh well, at least you know your stuff where it come to S&H Green Stamps.

    Viji
    I do not understand your rationale that a paper or a study that is conducted/collaborated between a panel of experts from their respective fields of expertise, is a sign of inferiority or weakness. Care to enlighten me on this

    Do you know the old joke about a camel? That’s a horse designed by a committee.
    It may be expected from a scientist that he or she is able to handle all the laboratory techniques that are necessary to do a certain study. A panel of experts never gets any useful results. Would you like a dinner prepared by 20 gourmet cooks? Have 12 medical specialists look after your health? I wouldn’t. A specialist on some lab technique is somebody you consult, and then you mention him in the “Acknowledgements” section, when you publish your paper. But a lab project carried out by a dozen people is like a quilt, or a clown’s suit. Yes, it’s inferior and it has no focus.
    I hope that, if I piss against it enough, they will abandon this practice. A publication by 8 authors used to indicate some monumental piece of work, such as the chemical synthesis of insulin. Now it’s a manifestion of incompetence by a bunch of losers.

    Perhaps during your time, it was all quick and dirty, but the scope of studies undertaken almost everywhere nowadays are multifactorial. For example, my current study of resistance in MDR bacteria already take me to various technical expertise, from simple microbiology, developing HPLC methods, MALDI-TOF, AFM to classic molecular biology methods like mutagenesis, all the way up to animal PKs PDs and clinical phases of developing optimal dosage regimens

    Well, I’m glad to hear that you’re willing to put in some work. If you think that in earlier times everything was quick and dirty, you’re mistaken. On the contrary, it is the other way around. Painstaking quantitative measurements used to be the rule. Now it’s just counting bands on an acrylamide gel. Lab research has always been multifactorial, but we never made such a fuss about it. We just did the work.
    So you’re doing a study on bacterial resistance? Excellent! But are you aware that these HIV-hucksters are talking all the time about “resistance of HIV”? That’s hilarious! I’m laughing my ass of each time I hear about it. They just transplant a phenomenon observed in bacteria (which are real organisms, with a metabolism) to viruses (which are not organisms at all). Those drugs “HIV” is supposed to have acquired resistance to, never interact with a virus at all; they just kill the host cells. There is no such thing as a resistant virus.

    I wouldn’t expect you to know every technique or know-how under the sun. So why insult other persons without first reflecting on yourself.

    Of course I don’t know everything. But whenever I needed a technique for my lab project, I learned enough about it, so that I could use it and interpret it. I see very little of that now.

    Third, hypothetically, if you are at the receiving end of this comment by yourself, i.e. “you* are totally unimaginative, only know one lab technique, propagate the wildest theories without any shame, and act as if you* possess the ultimate wisdom”, it doesn’t sound like fair judgement, does it?

    Don’t worry about me. I’ve seen it all, heard it all. From elementary school on, I’ve always been surrounded by people with big mouths who knew all about everything. It took some years of quiet development to make me realize that these bigmouths knew absolutely nothing. So I won’t be bullied by anybody. That doesn’t mean there are no people I respect; there are plenty of them. But they have to earn it first.

    You wrote to Hank: If you’re so disastified with our current understanding of HIV-AIDS, stop something, and do something to contribute to knowledge, rather than ranting and complaining. At least we are spending all our effort 24/7 doing the research required to understand HIV-AIDS.

    Right. And in 25 years of 24/7, all your club has achieved is terrifying people and bumping millions of them off with toxic drugs, at a cost of many billions of dollars.
    Don’t you know there are many cientists who would be extatically happy to start research on other aspects of the problem? Without some virtual virus that seems to have learned all kinds of circus tricks (like hiding, dodging, “getting resistant” and killing without being there)?
    And these researchers would need only a small fraction of the money that is spent on the misdirected HIV-research.
    But there’s absolutely no funding for alternative AIDS research; not one penny. And even those who do some work in that direction, don’t get their papers published.
    Now I know there’s no big money coming your way. The average lab scientist does his slave work faithfully, so that the big shots can rake in the millions or billions.
    So why the hell do they keep doing it?

    Simon
    I can understand you’re angry. But I see that Dan has already reacted to your post. And I happen to know he’s far more qualified to do so, because he has “been there”.
    But please, don’t be too hard on Tara. Otherwise you give her an excuse to pull the plug on this discussion.

    Dan
    did you notice that one of the categories Dr. Tara chose to place this post under is HUMOR?

    So why is nobody laughing?
    But I did ask: “Tara, you’re baiting us, ain’t-cha?”

    Thom
    We all tried in the begining to make some sense and to work with the doctors, but then the AIDS mafia (that’s what I call it and that’s what it is) and Larry the K and all those boys took it over and layed down right in front of those bulldozers and let it run right over them.

    Yes, future historians will have trouble explaining this course of events. I never stopped being surprised that, whenever I speak about HIV/AIDS, I get the toughest opposition from gay men, who still don’t see they are being deceived, and what’s worse, being murdered with AZT (which still is an integral part of HAART).

    But thanks for the words of support. I’ll keep on fighting this madness and gross injustice. I hope to see Hatchet Day soon.

  88. #88 Dale
    June 11, 2006

    … do other scientists make excuses for Gallo finding HIV in only 36% of his patients as well? Like I asked Chris (who seems to have vanished), is this how science works? When the evidence is less than convincing, we make excuses?

    You call them ‘excuses’, many people consider them reasonable explanations. They are considered reasonable because compared with isolating other pathogens there’s nothing either suspicious or unusual about Gallo’s findings. Initial tests for the presence of pathogens are often far less sensitive than later tests. And as anyone with any experience with detecting things in human blood can tell you, sample quality is often a problem.

  89. #89 Dan
    June 11, 2006

    Dale,

    thanks for your reply.

    I’m waiting for Chris and Tara to answer my questions.

  90. #90 Dan
    June 11, 2006

    Here’s one of the problems I’m having with this 36% issue…maybe Chris can clarify these statments of his on the issue that are at odds with each other.

    First, he says:
    The first tests were relatively crude. The specificity and sensitivity of these early tests were not high. Why expect the first tests to be perfect?

    Simple enough. He’s saying the tests are crude and imperfect.

    Then, he says:
    …why were 36% of AIDS patients infected with a virus that is present in only very low levels in the general population? Coincidence?

    This would imply that the tests AREN’T crude and imperfect.

    Which is it, Chris? Help us out here.

    And after that, I’d like to hear more about this scientific standard where a pathogen need only be found in 36% of people with the disease to be proclaimed as the cause of this disease. That sounds very interesting.

  91. #91 McKiernan
    June 11, 2006

    Wilhelm,

    Given AIDS being used first as a term in October 1982 and the Gallo papers 1984, are you aware of any important molecular biologists that opposed Dr. Gallo’s findings publically prior to (Cancer Research article) March of 1987 ? Or the Pasteur Institute gentleman from France ? Given the epicenters of San Francisco, LA and NYC and their daily reportage of HIV/AIDs in the Chronicle, LA Times and NYT, numbering in 1000’s of newspaper articles between 1982 and 1987, that the wee, itty, bitty, harmless ? retrovirus which has been around for millenia that found its home as a human parasite intracellularly that co-incidentally causes the human body to produce anti-bodies towards it and often renders previously sero-negative persons to become sero-positive in a primarily co-finding of hiv positive sexual partners, and the question is:

    wouldn’t you think the retro-virus scientific community could have not spread some pre-emergent weed seed killer on the budding paradigm as they say in the home gardening community ? Do you have any explanation for the initial years of silence ?

    It is a serious question one answer to which isn’t HIV doesn’t exist.

    What say you ?

  92. #92 Wilhelm Godschalk
    June 11, 2006

    McKiernan:

    The only hard facts that we really have are the gay men who started getting sick and dying, even during the seventies. Only in 1981, Michael Gottlieb gathered up 5 of those cases, and found a common factor: Low T4 lymphocytes. So these 5 men became the first epidemiological cluster. But as there had already been many others dying in the years before that, the choice was somewhat arbitrary and opportunistic.
    Nobody paid much attention at the time; certainly not the government. Gays were not the Reagan administration’s favorite citizens.
    Of course, the gay community in the big cities was keenly aware of the problem, especially those who had lost friends and lovers. But cries for help fell upon deaf ears. Nobody outside the gay world had any interest in solving the problem. There was no money in it. It’s a callous world.
    At that time, Gallo was not in the picture yet. He was still searching frantically for viruses that cause leukemia.
    There were several hypotheses as to what could cause these deaths. The idea that it might be a virus was not even the most popular one. Retroviruses have been known since 1911, and they are always benign.
    But in 1984 it all changed. I don’t think it was Gallo who set it all up. Rather, it was the government that started to realize that there was money to be made and power to be gained if people could be made to believe that this was an epidemic that could hit anybody, not just a bunch of gays in S.F. Like many others, Gallo was just about at the end of his rope with his cancer virus research. He was a crook, but also an opportunist, and they needed him. So he switched effortlessly from cancer viruses to an AIDS virus.
    Peter Duesberg was a staunch opponent of the AIDS-virus theory from the start. He knew all there is to know about retroviruses, and he didn’t buy the paradigm. But the famous press conference of April 23rd, 1984 had been well prepared. The press had been primed, and came out in force. With all the press coverage that followed, alternate theories didn’t stand a chance anymore.
    But Duesberg stood his ground. As he was an authority in the retrovirus field, they tried to discredit him. A special presidential committte was set up especially for this purpose. You can read a report of the hearing where Duesberg was giving his testimony:

    Katie Leishman

    Duesberg stood his ground, and you know what happened to him. David Rasnick, the expert on protease inhibitors, has been with Duesberg almost from the start.

    I think that the packed press conference was instrumental in the repression of all other ideas except the virus hypothesis. A free press doesn’t exist; that has been convincingly demonstrated. Most journalists are spineless cowards who just write what the orthodoxy wants them to write.

  93. #93 Tara C. Smith
    June 12, 2006

    I’ve been out all weekend and am catching up. Since most of the comments directed at me are nothing but more insults on my character, I’m glossing over them but do want to address this one from Dan:

    It looks like Dr. Tara has done what Simon is accusing her of, lying…or at least stretching the truth to the breaking point.

    based on these snippets:

    Simon:
    aske dabout the tests, because Tara you wrote that everybody in teh beginning had low viral loads, but that is so stupid. They didn’t even have VIRAL LOAD THEN TARA! You are so dumb. You give these assholes so much room to fire at you. They didn’t have fucking viral load TARA! Maybe some of them were not infected and some were, why can’t you be more honest?

    Tara:
    You mean they didn’t have the tests to measure “viral load” at that point? I certainly agree–that’s why viral *isolation* was being discussed, which is more difficult to detect.

    Hank:
    His data didn’t support his conclusions: He only found the virus in about 36% of AIDS patients. So, what accounted for the other 64%?

    Tara:
    A number of reasons. Low viral load at the time. Poorly preserved samples. etc. etc. etc. That’s why the antibody test was used–it was a more reliable indicator of infection.

    The confusion here comes from the term “viral load.” Simply put, it’s a measure of the virus in the blood. Currently, this is measured via PCR, which is very sensitive. So this is the test I’m talking about when Simon says, “they didn’t even have viral load then.” Of course they had “viral load,” there was virus in the blood. What they didn’t have in 1984 was the PCR test to measure it as we do now; as such, viral isolation (and antibody tests, as I explained) were used. The problem I was discussing with viral isolation is that it’s not as sensitive as the PCR test. If one has a low viral load–a low amount of virus in the blood–when the aliquot of blood is taken and used to inoculate tissue culture cells, there may not be enough virus present in that sample to infect the cells–thus giving a false-negative result. That was what I was getting at in my response to Hank. Even if this is the case, the antibody test can still be positive, as antibodies persist.

    I hope this is a bit clearer.

    did you notice that one of the categories Dr. Tara chose to place this post under is HUMOR?

    Indeed. I found “truthseeker”‘s characterization amusing.

    Finally, for Frodo:

    I am new here and new to this discussion. What I see here so far is two sides equally unimpressed with each other’s arguments and equally unwilling to listen. I cannot make heads or tails of the argument based on what I’ve read so far, so am keeping an open mind. I have no problem believing that mistakes are made in institutions; on the other hand, I’m not a conspiracy theorist so I’ll continue to read until something convinces me overwhelmingly of one side’s veracity.

    Hi Frodo,

    It’s always hard to jump into the middle of something like this, without the background. If you check out previous HIV posts here, you’ll see that I and others have spent a lot of time explaining the evidence to the likes of Hank et al. here, and they keep returning with the same refuted arguments. It does tend to get old, and I apologize that I seem “unwilling to listen.” It’s simply a by-product of hearing the same things dozens of times, and refuting them as many to no avail. If you’re interested in some background information on HIV, drop me an email and I can catch you up a bit further.

  94. #94 Hank Barnes
    June 12, 2006

    Hey Frodo,

    Check out this thread today by Dean Esmay, if you wanna get a feel for the issue. It gets wild!

    Hank Barnes

  95. #95 Dan
    June 12, 2006

    you’ll see that I and others have spent a lot of time explaining the evidence to the likes of Hank et al. here, and they keep returning with the same refuted arguments.

    Reading this bit from Tara, you’d think that poor Hank and his friends just don’t get it. The truth is that most of us accepted what we were told back in ’84, but as time went on, things just weren’t adding up. We ask questions of those who place themselves in a position of scientific/medical authority. Where we find gaping holes and fatal flaws, they find “anomalies”.

    It does tend to get old, and I apologize that I seem “unwilling to listen.” It’s simply a by-product of hearing the same things dozens of times, and refuting them as many to no avail.

    Tara, you don’t “refute to no avail”. That’s simply your method of attempting to establish that there’s nothing more to discuss. And when that tactic fails you either close the thread or add your trademark *sigh*.

  96. #96 Frodo
    June 12, 2006

    Tara, Thank you, I will definitely read the link that you posted!

    Hank, I will also read “Dean’s World,” which is what appears when I click the link. That site looks more Right-wing to me, which won’t stop me from reading it, I promise, but it goes back to my question. I tend to be interested in most issues, but especially issues of science debate, from a Left-Right perspective.

    I have been told that this can be a false dichotomy, and so I am careful to look for details. But I would still like to know, Tara seems more popular Left in some of her posts, but it is not possible to know just from that. Hank, how would you describe yourself? Dan, how would you describe yourself in a political sense?

    I promise that I will not make my assesment of the science based on these answers, I am more interested in knowing about which groups are active in the sciences and on which issues.

    For example, when you look at the stem-cell issue, you find that the research is not as promising as is sometimes claimed by the Left, though not so useless as some groups on the Right counter-claim. Both groups have made reasonable claims about the research however. The Left is often reported as being more truthful in media, but the Right often seems to have more control of the research (ie in the limiting of research).

    I am now wondering if the same is true about AIDS? That is, are many issues about AIDS reported from the Left agenda, but the research is limited by the Right? Or is it the reverse?

    Tara, I will read your links but it will take me a long time to absorb it all, so don’t expect much commenting from me on the technical aspects! Hank, I will also read your links, but again, I’m primarily interested in the social agendas that promote research and limit research. Thank you for your responses in advance!

  97. #97 Hank Barnes
    June 12, 2006

    …. I and others have spent a lot of time explaining the evidence to the likes of Hank et al. here, and they keep returning with the same refuted arguments.

    That’s a laugh!

    You didn’t even KNOW about the “largest” epidemiological study of heterosexual transmission of HIV, which found no seroconversions! (see Padian, Am. J.Epidem. (1997) — and you’re an epidemiologist!

    I like the old Tara better, who once wrote:

    Here’s the exchange:

    Hank: Ok, Tara, prove me wrong: Are you skeptical of any aspect of the current HIV=>AIDS paradigm?

    Tara: Sure, I’m skeptical of all of it. Does HIV really cause AIDS? Does it work alone? Are there other factors necessary? Is our treatment strategy the best method to go currently? Is advising all HIV+ people to take drugs optimal, or should some kind of screening–such as for the CCR5 delta 32 mutation–be provided first? I’ve mentioned all this on here previously, Hank. Despite what you say, my mind certainly is open to other alternatives–but as I’ve mentioned, show me the evidence.

    Hank

  98. #98 Hank Barnes
    June 12, 2006

    Frodo,

    I am now wondering if the same is true about AIDS? That is, are many issues about AIDS reported from the Left agenda, but the research is limited by the Right? Or is it the reverse?

    It’s a strange political amalgation:

    The Pro-AIDS side is part right-wing (Pharmaceutical $$) and part left-wing (gay activism)

    The Dissident side is mostly left-wing, but a few libertarians, contrarians, non-conformists.

    Me, I’m slightly left of center — but I don’t know much about politics. Dean Esmay is a little more right wing. Pro gay marriage, pro-Iraq war. It’s hard to pigeon hole him.

    All the money and power is on the AIDS side, though.

    HankB

  99. #99 Dan
    June 12, 2006

    Frodo,
    for the record: I’m a thinking Liberal/progressive (I’m listening to the Thom Hartmann program as I write).

    What I mean by that, is that I don’t simply go with (what I see as) the “groupthink” that’s nearly a pathology amongst the progressive crowd.

    I’m left of center, but I think for myself. I suppose if I didn’t think for myself, I’d spout such popular liberal mantras as “AIDS drugs save lives”.

  100. #100 Tara C. Smith
    June 12, 2006

    Reading this bit from Tara, you’d think that poor Hank and his friends just don’t get it. The truth is that most of us accepted what we were told back in ’84, but as time went on, things just weren’t adding up. We ask questions of those who place themselves in a position of scientific/medical authority. Where we find gaping holes and fatal flaws, they find “anomalies”.

    And again, this comes back to having more experience with the larger picture of the biomedical literature. These “fatal flaws,” as you call them, apply not only to HIV research, but to every type of infectious disease. Luckily, most people realize how absurd it would be to throw the whole germ theory of disease out the window, but somehow HIV is the exception.

    I also love the characterization of scientists as folks who don’t think for themselves, even as Hank quotes me from an old thread noting my skepticism. Thing is, evidence overcomes skepticism. The “dissidents” have nothing but old arguments and Gods of the gaps. Since you don’t like *sigh*, Dan, how about *yawn* ?

  101. #101 Hank Barnes
    June 12, 2006

    Tara wrote:

    Thing is, evidence overcomes skepticism

    Totally agree. Like most, I accepted the party line that HIV was a sexually transmitted disease (albeit skeptically), but after reading the evidence in the Padian paper, showing it wasn’t, I overcame it:)

    Hank Barnes

  102. #102 Tara C. Smith
    June 12, 2006

    Totally agree. Like most, I accepted the party line that HIV was a sexually transmitted disease (albeit skeptically), but after reading the evidence in the Padian paper, showing it wasn’t, I overcame it:)

    To the lurkers, this is a perfect example of someone spouting those rebutted claims I mentioned. Hank continues to try and use the Padian paper as some kind of evidence for his views, when I showed it doesn’t support his claims at all.

  103. #103 Dale
    June 12, 2006

    Hank,
    That’s what happens when you try to pin your analysis of a scientific hypothesis on a single piece of cherry picked data – you end up getting the wrong end of the stick.

  104. #104 Dan
    June 12, 2006

    Hank continues to try and use the Padian paper as some kind of evidence for his views, when I showed it doesn’t support his claims at all.

    YOU showed?! Well, Dr. Tara is a little short in the humility department. How about what Padian showed? Hank’s right for continuing to point out this study.

    I also love the characterization of scientists as folks who don’t think for themselves

    I find it interesting that you should say this.

    Who among us non-scientists have accused you of not thinking for yourself?

  105. #105 Dan
    June 12, 2006

    Since you don’t like *sigh*, Dan, how about *yawn* ?

    You know full well that *yawn* is mine! :)

  106. #106 Hank Barnes
    June 12, 2006

    Dale,

    With all due respect, I’ve given you a large free pass on this thread, even though you’ve uttered several falsehoods. But, really, enough is enough. You write:

    That’s what happens when you try to pin your analysis of a scientific hypothesis on a single piece of cherry picked data – you end up getting the wrong end of the stick

    1. Padian is not a “single piece of cherry picked data.” Padian is and remains the largest epidemiological study of heterosexual transmission of HIV in the United States. As you know, it found “NO SEROCONVERSIONS.”

    2. Moreover, Padian is not the ONLY support for the hypothesis that HIV is not a pathogenic virus. There’s hundreds of other papers. Padian, however, is a clear expression on this one relevant issue.

    You wrote earlier:

    Hank, Duesberg is not an appropriate citation for evidence of anything pertaining to HIV or AIDS as Duesberg has published no clinical or laboratory studies that contain original data.

    What a joke.

    1. He’s a member of the National Academy of Science. Are you?

    2. He’s published about AIDS in Science, Cancer Research, Proceedings of National Academy of Science, and 200 other scientific journals. Where are your publications in these journals?

    I will gladly and proudly cite Duesberg, you can cite the fradulent Bob “Scientific Misconduct” Gallo all you want.

    Hank B

  107. #107 Dan
    June 12, 2006

    These “fatal flaws,” as you call them, apply not only to HIV research, but to every type of infectious disease.

    You’re not making much sense here. The very words fatal flaw imply a deal-breaker. If a concept, paradigm or hypothesis is fatally-flawed, then it’s irreparably broken, useless.

  108. #108 Hank Barnes
    June 12, 2006

    Queen of Straw,

    These “fatal flaws,” as you call them, apply not only to HIV research, but to every type of infectious disease. Luckily, most people realize how absurd it would be to throw the whole germ theory of disease out the window, but somehow HIV is the exception.

    You can refute the HIV theory, without refuting the entire germ theory, duh.

    Some viruses do kill — see small pox, see polio, see flu.

    Hank Barnes

  109. #109 Tara C. Smith
    June 12, 2006

    Dan–hence the scare quotes. *You* call them “fatal flaws.” I see them as a normal ingredient in scientific research programs.

    Hank,

    You can refute the HIV theory, without refuting the entire germ theory, duh.

    Indeed. But the objections you–and Duesberg, and others–raise about HIV, if applied universally, would render all infectious disease research null and void. [This is usually where you bring Koch’s postulates into the discussion, Hank.]

    Some viruses do kill — see small pox, see polio, see flu.

    Some of your buddies don’t seem to think influenza kills either–or even exists. (See, for example, the end of this post).

  110. #110 Dale
    June 12, 2006

    Hank,

    Padian IS a single paper. From which you selectively cite a single piece of data, the prospective study. You persist in ignoring the retrospective study that supports the heterosexual transmission of HIV. You also ignore all the other data including cohort studies that I’ve pointed out to you that demonstrate heterosexual transmission of HIV.

    So I stand by my statement.

    What I said about Dr. Duesberg was not meant to slight the man or his scientific accomplishments. He has plenty. But none of them involve original research on HIV or AIDS. What his papers on these subjects are, are opinion pieces; his interpretations of other investigators’ published data.

  111. #111 Hank Barnes
    June 12, 2006

    Dale,

    Padian IS a single paper. From which you selectively cite a single piece of data, the prospective study

    No, it is the longest epidemiological study on the issue of heterosexual transmission of HIV. Either cite a better American study or shut up.

    Hank

  112. #112 cary stanger
    June 12, 2006

    Hi Hank, they’re never going to listen to you, you might as well give up. Who cares, nobody believes them anyway, all they do is shoot the messenger all the time. Nobody believes this shouting anymore about sex killing everybody. Nobody gives a you know what about the A word because it only happens once your old and on the drugs, so who cares? I know who Christne Maggiore is. We read her book in critical thinking class. Aids is over.

  113. #113 Wilhelm Godschalk
    June 12, 2006

    My, my everybody’s out of the woodwork again, now that the weekend is over. And there are some real doozies again:

    Tara
    Of course they had “viral load,” there was virus in the blood.

    And then you have the nerve to say you’re “explaining the evidence to the likes of Hank et al. here, and they keep returning with the same refuted arguments”
    Ye gods! You’re just making a statement about “virus in the blood” without any underlying evidence at all! Right from the pulpit. Well, Dan says somewhere that you’re short on humility. I wonder if he means you’ve got balls…
    We’ve torn the HIV/AIDS theory to shreds, time after time, simply by asking questions. The stopgaps the orthodoxy has come up with to explain the many quirks of “HIV” are getting so wild and unbelievable that pretty soon there will be no more dissidents, because they all died laughing. You “refuted” absolutely nothing. I’m sorry if you’ve heard some of our arguments time and again. We’ve heard some of the orthodoxy’s battlecries time and again too: Such as “virus in the blood” and “HIV, the virus that causes AIDS”.

    Yes, I agree that PCR is sensitive. So sensitive that you could detect DNA in a rock. But don’t try to tell me that whatever you amplify with PCR and grow in a co-culture must be “HIV”. To make that statement, you must have pure HIV for comparison. Isolation anyone?

    The “dissidents” have nothing but old arguments
    Yes. Some of them just won’t go away, because neither you, nor any of the big shots have ever been able to answer them.
    But I’m happy to come up with new ones. Now and then I take a paper apart that is offered by the HIV hustlers as “proof” of something. Invariably, it turns out that they have not done proper control experiments, or they start out by accepting the very things they’re trying to prove as the gospel truth right from the start. Circular reasoning is “in” these days.

    But the objections you–and Duesberg, and others–raise about HIV, if applied universally, would render all infectious disease research null and void.

    Not all infectious diseases. But it would behoove the scaremongers to look into the underpinnings of some of those spooky virus diseases they have been hawking lately: SARS, Ebola, Hep-C, H5N1 Bird Flu, etc.
    And by the way, the post by Liam Scheff you’re referring to doesn’t deny the existence of Influenza virus as a whole, but only that silly bird flu virus that’s supposed to have us shaking in our boots.

    Dale
    But none of them involve original research on HIV or AIDS.

    Well now, that’s understandable. Who wants to work on something that doesn’t exist? I would be so ashamed I couldn’t face anybody and say: “I’m working on HIV”.

    You persist in ignoring the retrospective study that supports the heterosexual transmission of HIV.
    Huh? So why is AIDS in America still restricted to the original high-risk groups, gay men and drug users?
    Tara, help! You’re an epidemiologist. Can you explain this fact with your “stone in the water causing ripples” theory?
    (And while you’re at it, tell us also why in Africa the northern Islamic countries are not affected).

    Cary Stanger
    Aids is over.
    Right on, man! I didn’t know there were schools that have a “critical thinking class”. That makes me a little more optimistic again. I agree that we’re sawing at the roots of the HIV/AIDS paradigm. But… AIDS is not over until Hatchet Day.

  114. #114 Dan
    June 12, 2006

    So why is AIDS in America still restricted to the original high-risk groups, gay men and drug users?
    Tara, help! You’re an epidemiologist. Can you explain this fact with your “stone in the water causing ripples” theory?

    Brilliant, Wilhelm.

    I look forward to that explanation as well. I have a feeling it’s going to be one of the more tortured explanations we’ve heard in recent memory.

  115. #115 Tara C. Smith
    June 12, 2006

    You’re just making a statement about “virus in the blood” without any underlying evidence at all! Right from the pulpit.

    I’ll remind lurkers here that not only does Wilhelm deny that HIV causes AIDS, he aruges that HIV doesn’t even exist–something even Duesberg acknowledges (but he argues that it’s merely a non-pathogenic “passenger” virus). Even the anti-HIV groups can’t get their stories straight.

    And by the way, the post by Liam Scheff you’re referring to doesn’t deny the existence of Influenza virus as a whole, but only that silly bird flu virus that’s supposed to have us shaking in our boots.

    I didn’t say Scheff denied the existence of H5N1. That’s why I pointed to the bottom of my post, where I cited Lanka’s denial of any human virus causing disease, and Crowe’s denial of the existence of H5N1.

    So why is AIDS in America still restricted to the original high-risk groups, gay men and drug users?
    Tara, help! You’re an epidemiologist. Can you explain this fact with your “stone in the water causing ripples” theory?

    First, of course, AIDS isn’t “restricted” to these groups. Heterosexually-transmitted HIV is well documented, though certainly less common than homosexual spread. And is it really that surprising to you that homosexual people generally have sex with other homosexuals, and heterosexuals with other heterosexuals, and that diseases that appear in one group may not be equally distributed in another? Seems rather common-sensical to me.

    Additionally, studies have shown that HIV isn’t all that easily transmitted via sex. Direct injection–such as via re-used needles–is more efficient. (Why is it, I wonder, that needle exchange programs have led to decreased HIV incidence where they’re implemented? Seems to me to fit nicely with a blood-borne pathogen).

    (And while you’re at it, tell us also why in Africa the northern Islamic countries are not affected).

    You have a unique definition of “not affected.” From this site:

    The advance of AIDS in the Middle East and North Africa has continued with latest estimates showing that 67 000 people became infected with HIV in 2005. Approximately 510 000 people are living with HIV in this region. An estimated 58 000 adults and children in 2005 died of AIDS-related conditions.

    Although HIV surveillance remains weak in this region, more comprehensive information is available in some countries (including Algeria, Libya, Morocco, Somalia, and Sudan). Available evidence reveals trends of increasing HIV infections (especially in younger age groups) in such countries as Algeria, Libya, Morocco and Somalia.

    More at the link.

  116. #116 cary stranger
    June 12, 2006

    This is why no one cares, because you don’t read. Youre just talking about estimates in AFrica but you already know that testing isnt accurate and has over 60 false positives, and you also know that the estimates are based on samples taken from pregnant women in poor countries and then spread to the rest of the people in the country. Everybody Already Knows That Tara, that’s why nobody cares and nobody believes it. Youre tired.

    Thanks Wilhelm, it was a math class in logic principles and arguments and the teacher told us we could do a project and recommended me the book because I’m out and loud about it.

  117. #117 Dan
    June 12, 2006

    Additionally, studies have shown that HIV isn’t all that easily transmitted via sex.

    Padian, anyone? Thank you.

  118. #118 Dan
    June 12, 2006

    Wilhelm: So why is AIDS in America still restricted to the original high-risk groups, gay men and drug users? Tara, help! You’re an epidemiologist. Can you explain this fact with your “stone in the water causing ripples” theory?

    Tara: First, of course, AIDS isn’t “restricted” to these groups. Heterosexually-transmitted HIV is well documented, though certainly less common than homosexual spread. And is it really that surprising to you that homosexual people generally have sex with other homosexuals, and heterosexuals with other heterosexuals, and that diseases that appear in one group may not be equally distributed in another? Seems rather common-sensical to me.

    I think it’s time for us to introduce you to a new concept, Tara. It’s called bisexuality. You may want to work this one into your equations.

  119. #119 Tara C. Smith
    June 13, 2006

    cary,

    This is why no one cares, because you don’t read. Youre just talking about estimates in AFrica but you already know that testing isnt accurate and has over 60 false positives, and you also know that the estimates are based on samples taken from pregnant women in poor countries and then spread to the rest of the people in the country. Everybody Already Knows That Tara, that’s why nobody cares and nobody believes it. Youre tired.

    Indeed, many early seroprevalence studies were done in pregnant women, but since then, a large number of population-based studies have been carried out (see one review of them here, for example). Additionally, I challenge you to let me know just which HIV test you’re speaking of, and cite its false-positive rate. Certainly you’re not just parroting what you’ve heard and read from the HIV “dissidents” and have read the literature yourself, right?

    Padian, anyone? Thank you.

    Sure; this is actually an appropriate time to pull that study out. But again, I’ll note that was a study where a high percentage of the participants used condoms and refrained from high-risk sexual behavior, and each couple was only followed for a (relatively) short time period. It showed the virus wasn’t easily transmitted, but not that “no transmissions occurred,” as Hank tries to say.

    I think it’s time for us to introduce you to a new concept, Tara. It’s called bisexuality. You may want to work this one into your equations.

    Thank you, Dan, I’m quite familiar with the term–and MSM but aren’t “gay,” or “straight” but on the down-low, or “bent” but don’t necessarily consider themselves either bisexual or homosexual, or people who refuse to accept any kind of label, etc. etc. I realize there are many permutations and shades of sexuality. Nevertheless, that doesn’t change the fact that generally, homosexuals and heterosexuals don’t have a lot of overlap as far as sexual partners go.

  120. #120 McKiernan
    June 13, 2006

    McK was commenting the other day on another blog :

    The Padian study demonstrated non-seroconversion in 175 discordant heterosexual, monogamous couples. The study started out with infected bi-sexual men and their female partners. They couldn’t find enough so they “expanded recruitment criteria” regardless of risk group or gender. Then, the Padian papers are published and lo and behold, of the 884 people (442 pairs) only 350 (175 pairs) were left to put on the results page 545. The result represents 39.5 % of the study group. And the study found: “Because of deaths as well as the break-up of couples, attrition was severe..”

  121. #121 cary
    June 13, 2006

    Oh Tara so it’s up to me to prove to you that the tests dont have false positives? I’m not mister statistics Tara but I would expect you to know more about it. The tests dont work because they are nonspecific and come up positive for all sorts of things, then they are only accurate for some people in risks groups. Thats why you cant test everybody, because if you did you couldnt use the tests. I know that, so if you want to quote some number from a test its like a number from a commercial to me, its just advertizing. You so stoopit! You even said only 38 percent of everybody in the beginning testing group was positive out of 100 percent that had AIDS, so what’s the test for TARA?

    It’s tired bullshit and if you cant beat a high school junior at this you should retire to the prom queen allstars.

  122. #122 Tara C. Smith
    June 13, 2006

    Oh Tara so it’s up to me to prove to you that the tests dont have false positives?

    You’re making the claim here; I’m asking you to cite where you got the information from. I understand that you can’t, because you’ve not read the literature. You’ve swallowed what the “dissidents” tell you. That’s OK. Especially if you’re a high school junior, I’m pleased you’re looking into this area at all. I’m just asking you to do a bit of research on your own to find out where their claims come from.

    You even said only 38 percent of everybody in the beginning testing group was positive out of 100 percent that had AIDS, so what’s the test for TARA?

    You’re conflating several tests. One can isolate virus; can test for antibodies (using several different tests, I might add), or use RT-PCR to look for viral RNA. Each has different advantages and limitations, and different sensitivity and specificity.

    It’s tired bullshit and if you cant beat a high school junior at this you should retire to the prom queen allstars.

    :) Never was the prom queen type, and I’m not looking to “beat” anyone. I’m merely explaining my views and the science behind them.

  123. #123 Frodo
    June 13, 2006

    Hello Tara and Hank,

    I apologize for not getting back to you. I am about halfway through the reading you sent in the links. It is really a lot to absorb and I will have to unpack it a little to formulate a few appropriate questions. I should have said, I am doing this research as part of a research project for a paper on Right/Left divide in science. I had orginally wanted to focus on stem cells, but too many other people were doing it, so I looked for other options. I want to say thanks in advance for answering questions and providing some research leads.

    I don’t know if this thread will be active in a day or two, if not I’ll try to email you if possible with follow-up, but I’ll try to get my questions posted by tomorrow (tomorrow and Wednesday are crazy for scheduling any free time) and that will most likely be sufficient for what I’m looking for for this part of the research. Maybe I can be in touch at another time?

    Frodo (aka Neil in email)

  124. #124 Darin Brown
    June 13, 2006

    Frodo,

    It’s heartening to know of your interest in this topic. But, really, it has little, or nothing, to do with “Left” or “Right”. Really.

  125. #125 Darin Brown
    June 13, 2006

    Frodo,

    If you really want to understand what’s going here, I suggest you read John Lauritsen and Ian Young’s book “The AIDS Cult”, and most especially Casper Schmidt’s 1984 article “The Group-Fantasy Origins of AIDS” (linked to at the link below). That will cut to the chase for you. And tell you a lot more than these false dichotomies over “Left” and “Right”.

    http://www.reviewingaids.org/awiki/index.php/The_AIDS_Cult

  126. #126 Dale
    June 13, 2006

    Is HIV “restricted” to gay men and drug users? That will come as a big surprise to the CDC who keep and publish the statistics on such things! According to the latest HIV surveillance report available online, heterosexual transmitted cases represent over half of all new cases among female Americans over the past few years and about 20% of new cases among black male Americans.

  127. #127 Frodo
    June 13, 2006

    a couple of quick questions, I’m going to try this early and see if I can wrap it. Sorry if I don’t make much sense, too much caffeine not enough sleep…

    True/False: The “dissidents” are also called the “denialists” but by their critics,
    The convention is the “mainstream” or “orthodoxy” What else am I missing in naming the groups?

    One of hte main conventions of the (I’ll call them the dissidenters) is that HIV tests are either prone to error or are just not accurate?

    One of the second or secondary claims is that HIV has never been “isolated” in a pure sense?

    One of the main claims of the mainstream is that HIV has been isolated in a pure sense and two that HIV tests are accurate?

    Two questions: Does the mainstream claim that the dissenters are totally incorrect? Does the orthodoxy claim that the mainstream is totally incorrect?

    Are there any religious and or political motivations on the part of the mainstream or on the part of the dissenters in arriving at their views?

    For Tara and Hank, I read most of the posts each of you showed me. Tara, I read a couple of your posts but I focused on the blog about Africa. You focused your argument on the writer Tom Bethell, who is a writer for the American Spectator which is a Right wing or center Right journal. Were Bethel’s politics influential in his assessment of AIDS in your opinion? In your blog you debate a number of people but not Bethell. Did he decline to be interviewed? Was there anything in his assessment that you agreed with, because you seem to dismiss him pretty quickly. (that seems to have been the purpose of your blog on his writing). Do you feel that politics played any part in your dismissal of his work?

    Hank I also read the Dean’s World blog on The New York Times’ editorial by Moore (forgetting the first name, sorry). The editorial seems to be about blogs like Dean’s World and to be fair, like this, that are debating AIDS science without mainstream guidance or “peer-review” or approval from them. There seems to be a power issue in this statement in that one side could argue that they do not need permission to discuss an issue from the institutions that are in the habit of managing the issue. Is that the main idea in this fight or is it secondary to the issue of the fight (is it a power issue or is the issue of the tests and isolation primary?)

    I am finding some of the arguments more compelling than I considered, especially those about testing, because my introduction to this was Gerd Gerenheizer’s book “Calculating Risks” which assessed the structure of testing in a variety of fields including HIV, the contention of the book was that testing requires prevalance and without prevalance tests become inaccurate (the book was about testing theory). I always found that to be a fascinating idea ever since I read it, because I had assumed that tests were plus or minus, but it makes sense that they rest on prevalance. The dissenters claim is that the assumption is problematic because it predates the test, so that if the assumption is incorrect, the test results will also be incorrect.

    This reminds me of a number of historical precedents for testing or labeling populations that are now considered irrational or out of favor. I would say that this is the dissenters’ strongest point, but that may be because the technical aspects of the isolation are beyond me. If it is true that HIV has not been isolated and the mainstream knows this, then they are stonewalling the dissenters with power politics. If it is not true than the dissenters are raising questions in public that could destabilize a public health issue, but on the other hand, one has to ask about the right to raise questions, especially because some of the people are researchers themselves, (those who are asking the questions).

    It’s intriguing, more than I thought it would be, and I havent quite found the Right/Left divide which is what I was looking for. Although it seems that the mainstream is using the tactics of the Right more often, claiming authority, and refuting argument by claiming the argument, etc, which is interesting and different than on the stem cell issue and the abortion issue.

    Thank you in advance for your help with answering or correcting these points. Please direct me to a second set of papers to read, anything with the associated politics would be helpful.

    peace,
    Frodo

  128. #128 Frodo
    June 13, 2006

    whoops! error!!

    that should have been “do the dissenters think that the mainstream is totally incorrect” from the heading “two questions”.

    I won’t have time to look back for a couple of days at which point I will collect the answers I receive (thanks to all who participate). I’m a little brain-drained so please forgive the errors. I appreciate your help, thanks Tara and Hank, and Darin for those links which I will definetely read (but next week!)

    peace,
    Neil

  129. #129 Tara C. Smith
    June 13, 2006

    Hi Frodo,

    Regarding the science, you ask:

    One of the main claims of the mainstream is that HIV has been isolated in a pure sense and two that HIV tests are accurate?

    Indeed.

    Two questions: 1) Does the mainstream claim that the dissenters are totally incorrect? 2) do the dissenters claim that the mainstream is totally incorrect?

    For both questions, you have a problem. The “dissenters” are far from unified in their views. One group claims that HIV has never been isolated. Another claims that it has, but it’s just a harmless virus. Still others claim that the “mainstream” has it mostly right, but science is just too much in the hands of Big Pharma and their AIDS drugs are terrible. Since their views pretty much run the spectrum, it’s hard to answer your questions from either POV.

    Are there any religious and or political motivations on the part of the mainstream or on the part of the dissenters in arriving at their views?

    Again, all sides are represented by a variety of religious and political opinions. You have some on the left who are very into “alternative” medicine and hate anything pharmaceutical; others who mistrust the government and anything associated with it. You have some on the right who still view AIDS as a “lifestyle” disease, and therefore the sex and drug use associated with it are punishment for these “sins.” Largely, though, I think political and religious matters don’t play a role for most folks.

    For Tara and Hank, I read most of the posts each of you showed me. Tara, I read a couple of your posts but I focused on the blog about Africa. You focused your argument on the writer Tom Bethell, who is a writer for the American Spectator which is a Right wing or center Right journal. Were Bethel’s politics influential in his assessment of AIDS in your opinion? In your blog you debate a number of people but not Bethell. Did he decline to be interviewed? Was there anything in his assessment that you agreed with, because you seem to dismiss him pretty quickly. (that seems to have been the purpose of your blog on his writing). Do you feel that politics played any part in your dismissal of his work?

    I’ve not interviewed anyone; several of the “dissidents” were alerted to my post and dropped by to give their two cents. Bethell simply wasn’t one of them, despite Bialy’s invitation for him to come by and “spank me” in the initial thread.

    As far as Bethell himself, it’s not his politics that had me disgusted with him; it’s the anti-science point of view he takes throughout the Politically Incorrect Guide to Science. He uses the same tactics throughout–selectively showing the science, using lots of “god of the gaps” type of arguments, relying on newspapers and magazines as sources instead of the scientific literature. His chapters on evolution are even worse than his on HIV. Additionally, because he failed to even mention his belief that HIV doesn’t cause AIDS, I think he’s being rather dishonest throughout that entire chapter.

    Hank I also read the Dean’s World blog on The New York Times’ editorial by Moore (forgetting the first name, sorry). The editorial seems to be about blogs like Dean’s World and to be fair, like this, that are debating AIDS science without mainstream guidance or “peer-review” or approval from them. There seems to be a power issue in this statement in that one side could argue that they do not need permission to discuss an issue from the institutions that are in the habit of managing the issue. Is that the main idea in this fight or is it secondary to the issue of the fight (is it a power issue or is the issue of the tests and isolation primary?)

    It’s not just sites like Dean’s world. While he discusses HIV, it’s not his primary topic. Other sites like Virusmyth and Rethinking AIDS (kind of a virusmyth version 2.0) have collections of the anti-HIV articles. As they note:

    Thanks to the ascendance of the internet, we are now able to reinvigorate our informational campaign.

    Why do you think, Neil, that these people publish on the internet instead of in scientific journals? I’m sure someone will answer that they’re somehow persecuted, and while they hate it when I compare them to creationists, that’s the exact same excuse that group gives when they publish on the internet instead of in journals as well. Food for thought.

    I am finding some of the arguments more compelling than I considered, especially those about testing, because my introduction to this was Gerd Gerenheizer’s book “Calculating Risks” which assessed the structure of testing in a variety of fields including HIV, the contention of the book was that testing requires prevalance and without prevalance tests become inaccurate (the book was about testing theory). I always found that to be a fascinating idea ever since I read it, because I had assumed that tests were plus or minus, but it makes sense that they rest on prevalance. The dissenters claim is that the assumption is problematic because it predates the test, so that if the assumption is incorrect, the test results will also be incorrect.

    I’m not sure what you mean when you say that “testing requires prevalence.” You mean a *knowledge* of the prevalence of an agent?

    As you note, no, tests aren’t simply plus/minus. Even something that has that kind of readout–such as a drugstore pregnancy test–has an error rate. This goes back to the sensitivity and specificity issue I mentioned above. Generally, the first test for HIV antibodies is an enzyme immunoassay of some time (such as the ELISA you’ll often see mentioned). If this is positive, it’s followed up by a Western blot test for confirmation. Newer rapid tests (more akin to a pregnancy test) are also in use that are highly sensitive and specific (see an overview here), but these also need to be followed with a Western for confirmation. You can see for yourself that even for these rapid tests alone, the sensitivity and specificity is very high (Table 1). Coupled with a confirmatory Western, the chances of a false-positive or negative result are very, very low.

    Note also that they do take a person’s risk level into account when counseling them about the results. I assume this is what you’re getting at with the mention of prevalence.

    This reminds me of a number of historical precedents for testing or labeling populations that are now considered irrational or out of favor.I would say that this is the dissenters’ strongest point, but that may be because the technical aspects of the isolation are beyond me. If it is true that HIV has not been isolated and the mainstream knows this, then they are stonewalling the dissenters with power politics.

    It’s not true. Even Peter Duesberg, who’s long been the most prominent scientist to argue against HIV causation of AIDS, acknowledges that it’s been isolated.

    In Conclusion

    HIV has been isolated by the most rigorous method science has to offer. An infectious DNA of 9.15 kilo bases (kb) has been cloned from the cells of HIV-antibody-positive persons, that – upon transfection – induces the synthesis of an unique retrovirus. This DNA “isolates” HIV from all cellular molecules, even from viral proteins and RNA. Having cloned infectious DNA of HIV is as much isolation of HIV as one could possibly get. The retrovirus encoded by this infectious DNA reacts with the same antibodies that cross-react with Montagnier’s global HIV standard, produced by immortal cell lines in many labs and companies around the world for the HIV-test. This confirms the existence of the retrovirus HIV.

    It’s only the fringe element of the anti-HIV groups that makes the claim that HIV’s never been isolated. See micrographs of the virus yourself here.

    If it is not true than the dissenters are raising questions in public that could destabilize a public health issue, but on the other hand, one has to ask about the right to raise questions, especially because some of the people are researchers themselves, (those who are asking the questions).

    None of the “dissenters” are HIV researchers, just to be clear.

    It’s intriguing, more than I thought it would be, and I havent quite found the Right/Left divide which is what I was looking for. Although it seems that the mainstream is using the tactics of the Right more often, claiming authority, and refuting argument by claiming the argument, etc, which is interesting and different than on the stem cell issue and the abortion issue.

    Indeed. Stem cells and abortion focus more on morality. As I mentioned above, I find the HIV “debate” more similar to the ruckus over evolution (and indeed, Moore mentioned that in his editorial). In both cases, the mainstream science is well supported, but argued against by a handful of credentialed scientists who use the internet and trade press (in lieu of the scientific literature) to sell their message.

  130. #130 Hank Barnes
    June 13, 2006

    Typical straw girl:

    I’ll remind lurkers here that not only does Wilhelm deny that HIV causes AIDS, he aruges that HIV doesn’t even exist–something even Duesberg acknowledges (but he argues that it’s merely a non-pathogenic “passenger” virus). Even the anti-HIV groups can’t get their stories straight.

    Why not address the claims that Wilhelm makes? Also, since you regularly trash Duesberg (200 peer reviewed papers to your 3), you are not permitted to use him as a foil to DODGE Wilhelm.

    Both Wilhelm and Duesberg have demonstrated the lack of evidence that HIV causes of AIDS. They have differing reasons for so concluding.

    But, your buddies, Montagnier (co-factor) and Gallo (sole cause) have differing explanations as to causation as well.

    Hank B

  131. #131 Dan
    June 13, 2006

    Even the anti-HIV groups can’t get their stories straight.

    That’s right, Tara. We’re a diverse bunch of people, all asking questions from different points of view. You make it sound like a bad thing.

    I find your choice of language interesting. Instead of the belittling “get their stories straight”, you could be more professional and say something like “they aren’t in agreement with each other”. That would be far too nice though, it seems.

    Also, to use the term “denialist” is about as ugly, unprofessional and low as you can go. As most people know, we get this term from WWII…it’s used to describe people who say the holocaust never happened. Wow. It’s just amazing to me that you could so readily throw that term around. Do we laugh when we see pictures of emaciated children in Africa, Tara?

    Please take note of this tactic, Frodo. That term instantly strips us of our humanity. It’s also a falsehood. None of us deny that people are sick and dying. The only thing we question is the role of the causative agent, HIV.

  132. #132 Tara C. Smith
    June 13, 2006

    That’s right, Tara. We’re a diverse bunch of people, all asking questions from different points of view. You make it sound like a bad thing.

    I don’t think it’s a bad thing. Again, I think it’s like the anti-evolution folks. You tolerate each other under the “big tent” of anti-HIV “dissidents,” just like the Discovery Institute caters to the YECs, OECs, etc., even though the beliefs of many of the groups in the tent are mutually exclusive.

    I find your choice of language interesting. Instead of the belittling “get their stories straight”, you could be more professional and say something like “they aren’t in agreement with each other”. That would be far too nice though, it seems.

    Funny how y’all come on here and insult me a dozen ways from Sunday, then scold me for not being nice enough. That, Alanis, is ironic.

    Also, to use the term “denialist” is about as ugly, unprofessional and low as you can go. As most people know, we get this term from WWII…it’s used to describe people who say the holocaust never happened. Wow. It’s just amazing to me that you could so readily throw that term around. Do we laugh when we see pictures of emaciated children in Africa, Tara?

    Do you laugh about the Holocaust, either? This is an appeal to emotion, pure and simple. I didn’t even use “denialist” in my last response, and I do generally try to avoid it. I’ve asked y’all for a neutral term previously, though, and no one’s provided it. I put “dissident” in the scare quotes because that one’s not neutral either, and IMO not deserved. A denialist is one who denies, period. It’s unfortunate that y’all have to continually conflate it with Holocaust revisionism, because it has a much wider connotation than that, and I feel the term is accurate. You choose to cherry-pick the literature to the extreme, denying the vast majority of the research done in the field. Look at Hank–he continually cites a 1997 study (that doesn’t even support his views!) and little else.

    Please take note of this tactic, Frodo. That term instantly strips us of our humanity. It’s also a falsehood. None of us deny that people are sick and dying. The only thing we question is the role of the causative agent, HIV.

    More appeal to emotion in lieu of a discussion of the science–another tactic to notice.

  133. #133 Hank Barnes
    June 13, 2006

    Hi Frodo,

    You seem like a reasonable fellow. I don’t speak for any group, just myself.

    So, here’s my take:

    Most people believe that HIV: (1) kills a set of white blood cells, leading to opportunistic infections, (2) is sexually transmitted and (3) can be stopped by various prescription drugs.

    All gov’t funding for scientific research follows this paradigm. This is the majority view. The scientists get billions of $$ for research, the drug companies make billions of $$ selling drugs.

    In contrast, my working hypothesis is this:

    1. Initially, the scientific establishment had the right answer on AIDS. Here’s an editorial in 1981 in New England Journal of Medicine:

    Perhaps one or more of these recreational drugs is an immunosuppresive agent. The leading candidates are the nitrites, which are now commonly inhaled to intensify orgasm. Users of amyl nitrates are more likely than non-users to have had hundreds of sexual partners and to contract venereal disease.

    Let us postulate that the combined effects of persistent viral infection plus an adjuvant drug cause immunosuppression in some genetically predisposed men.
    (Durack, NEJM vol 305, 1465-66 (1981).

    2. However, the “virus hunters,” led by Dr. Robert Gallo, at the National Cancer Institute hijacked the theory to convert this drug disease into an infectious disease. The problem, though, left uncorrected from 1984 – 1992, was that Gallo was a fraud.

    3. Thus, the whole AIDS enterprise was steeped in deception, and sent down the wrong tracks by Gallo.

    4. One courageous Professor at Berkeley, Dr. Peter Duesberg, pointed out this fraud in the Proceedings of National Academy of Science in 1989. But, he was vilified and ostracized and then ignored.

    5. This would be only an academic exercise, except for another huge mistake. Gallo et al failed miserably to develop a vaccine, and then resorted to a toxic, cancer chemo drug called AZT. This cancer chemo was given to 300,000 or so, mostly gay men from 1987-1997.

    6. My working hypothesis is that most of these people were killed by AZT, not the underlying virus.

    7. The other AIDS drugs are deadly as well, and cause liver failure, heart attacks, anemia and white blood cell loss. (See Reisler paper in JAIDS.)

    8. So, counterintuitively, I posit that the drugs have made things far worse than the disease.

    If you google “Duesberg” you will get the full story. It is big, sprawling and complex. You can scroll thru and get a lotta info, both pro and con.

    Best,

    Hank B

  134. #134 Dan
    June 13, 2006

    Let me help you out here, Tara. A neutral term you could use is “questioners”, or “HIV questioners”. Quite neutral, and much closer to the truth than the blunt-instrument, overly-simplistic and emotionally-loaded “denialist”.

    If you’re sincere about using a neutral term, then I look forward to you replacing “denialist” with “questioner”. Thanks, Tara.

  135. #135 Darin Brown
    June 13, 2006

    Frodo (Neil),

    Tara said,

    “Why do you think, Neil, that these people publish on the internet instead of in scientific journals? I’m sure someone will answer that they’re somehow persecuted, and while they hate it when I compare them to creationists, that’s the exact same excuse that group gives when they publish on the internet instead of in journals as well. Food for thought.”

    Thanks for the lead-in, Tara. Readers, esp. Frodo, wishing to evaluate the validity of Tara’s comparison with IDers may wish to browse the recently added Serge Lang Memorial HIV/AIDS Archive, with nearly 600 pages of documentation of communication between dissidents, journal editors, mainstream scientists, journalists, etc. This is hard documentation of the journalistic suppression, manipulation, and censorship that takes place every day:

    http://www.reviewingaids.org/awiki/index.php/Document:Lang

  136. #136 Darin Brown
    June 13, 2006

    “You can see for yourself that even for these rapid tests alone, the sensitivity and specificity is very high (Table 1). Coupled with a confirmatory Western, the chances of a false-positive or negative result are very, very low.”

    Huh, Tara. You know, a lurker might be forgiven for coming to the conclusion that you the WB as a “gold standard”.

    “It’s only the fringe element of the anti-HIV groups that makes the claim that HIV’s never been isolated.”

    Delighted to see you implicitly acknowledge that we’re significant enough to have a “fringe”!!

  137. #137 Darin Brown
    June 13, 2006

    “More appeal to emotion in lieu of a discussion of the science–another tactic to notice.”

    No, this is just a reasoned response when labelled with a term associating oneself with Holocaust deniers. The “denialist” label itself is such “an appeal to emotion”.

    Besides, your comment seems more accurately a description of the behavior of John Moore, AIDS researcher, who not only wrote a hysterical, emotional Op-Ed (i.e. you can say almost anything you want) in the NY Times, he then declined a “discussion of the science”, preferring to “expose charlatans” in some as-yet unspecified manner…

    http://www.reviewingaids.org/awiki/index.php/Document:Bialy/Moore_debate

  138. #138 Hank Barnes
    June 13, 2006

    Darin Brown,

    That entry you have for Professor Serge Lang (Yale) has some incredible documentation. Well done.

    I had the pleasure of meeting him once for dinner. Great man, and a sad loss.

    Hank Barnes

  139. #139 Dale
    June 13, 2006

    Given that John Moore is an author on more than two dozen papers containing HIV/AIDS research while Harvey Bialy has only authored opinion pieces on the subject, I can see why Moore might feel it would be a waste of his time to discuss the science with Bialy. Bearing in mind the tone of Bialy’s “invitation”, I can further see why Moore might decline in less than polite terms. Just my opinion of course.

  140. #140 Wilhelm Godschalk
    June 13, 2006

    Tara:
    Why do you think, Neil, that these people publish on the internet instead of in scientific journals?

    I can answer that question for you, Neil. The scientific journals, as well as the daily press are part of the corrupt scheme. Even Peter Duesberg cannot get his papers published anymore. Fortunately, he is a member of the National Academy of Sciences, so he can always publish in the Proc. Natl. Acad. Sci.
    The rest of us dissident scientists don’t have this outlet. Besides, we are still in the stage of questioning the paradigms of the orthodoxy (and they are weird!). Even if it were possible to do our own research on HIV/AIDS (it isn’t; no money), I for one would be too ashamed to show my face on the streets if I had to confess working on “HIV”. And there are plenty others who think the same way. Why waste your profesional life on something that doesn’t exist?
    And please don’t let anybody get away with the lie that Duesberg claims to have isolated HIV. In his paper in Continuum Magazine he mentions “molecular cloning” (!) I suspect that he was joking, because this is exactly the kind of crap the orthodoxy wants to sell us. “Molecular cloning” has to do with transcription of DNA. Now would that qualify as isolation of an RNA-containing virus? Who could take that seriously? So we publish on the internet; that way we can reach people. Meanwhile, the once distinguished journal “Science” has sunk to the level of the “National Enquirer”.

    Frodo
    There seems to be a power issue in this statement in that one side could argue that they do not need permission to discuss an issue from the institutions that are in the habit of managing the issue.
    Well, of course there is a power issue. Have you read John Moore’s answer to Harvey Bialy’s invitation to a debate? I haven’t seen anything that arrogant since Hermann Goering.
    John Moore is a fraud and a bully (and you can tell him I said so). One would think that nobody can claim to be a scientist without his permission. Every time I read about an idiot like that (Mark Wainberg is another one), I’m looking more forward to Hatchet Day.

    Oh, and eh, Neil… watch this spiel by Tara:

    “…and while they hate it when I compare them to creationists,…”

    That’s a typical strawman argument. HIV/AIDS dissidents have absolutely nothing to do with creationists. The issues are totally unrelated. I don’t even know any dissident who is also a creationist. But when you snuffle around on discussion fora and blogs, you’ll find this tactic very often. It’s not just Tara who does this; it’s very common in fairytale-virus land.
    Now if I were to compare the HIV-apologists with the nazis, I would be much closer to the truth. But I’m not going to do that, of course ;-)

    Tara:
    I didn’t say Scheff denied the existence of H5N1.

    Well, I do (deny the existence of H5N1, I mean).

    It’s only the fringe element of the anti-HIV groups that makes the claim that HIV’s never been isolated. See micrographs of the virus yourself here.

    [groann!!] Did everybody take a good look at what Tara pointed to in the Big Virus Picture Book? cartoons, for catsake! In living color! And that’s supposed to convince us? Just one paper on isolation please, Tara. Complete with a “Materials and Methods” section.
    And no hanky panky with PCR, stimulation with PHA, and co-cultures.
    Once more for the lurkers: HIV has never been isolated, so its existence is at least doubtful.

    Dale
    Given that John Moore is an author on more than two dozen papers containing HIV/AIDS research while Harvey Bialy has only authored opinion pieces on the subject, I can see why Moore might feel it would be a waste of his time to discuss the science with Bialy.

    Well, I’ve already given my evaluation of John Moore above. He is a total fraud. Why should a scientist like Bialy waste his time writing papers on a subject that is completely science fiction? (supposing he would get them published at all). I really wonder how the scientific community will react, once they realize 25 years of published work can be thrown away, because it has no bearing on the real world.

    Oh, and before I forget, Tara…
    The problem with the “HIV tests” is not just that they’re not reproducible or inaccurate: they are completely based upon wrong thinking. Antibodies don’t always signal an active infection. They signal a former infection that has been beaten back. It’s like a sign “Kilroy was here”.
    The antibodies that are found in the Western Blot react with proteins from a kit (with a package insert that says the kit should not be used for this purpose) that are assumed to come from HIV. But as nobody has ever even seen an HIV particle, we have to take Gallo’s word for it (because he’s the patent holder and makes money off these kits.
    So we shouldn’t just talk about sensitivity or specificity (or the lack thereof) but about applicability. The whole concept sucks.

  141. #141 funkyfrank
    June 13, 2006

    Dale, you know what’s good about you?

    You’re just soft enough to get really deep in the cracks, but hard enough to stand up to tough stains.

  142. #142 funkyfrank
    June 13, 2006

    You know why Wilhelm doesn’t believe in AIDS?

    He never saw Dale’s behind.

  143. #143 funkyfrank
    June 13, 2006

    You know why John Moore published all those books?

    He was trying to get away from having to spend time with his bastard son Dale.

  144. #144 Chris Noble
    June 13, 2006

    For those people calling for John Moore or others to debate Harvey Bialy.

    Who is going to judge the outcome of such a debate? Scientists that have experience and have worked with HIV or people like Hank Barnes who are proud of their own ignorance?

    If the “dissidents” judge at the end that Harvey Bialy won the debate and at the same time everybody else thinks that John Moore won the debate what would have been achieved?

    The way that any such “debate” proposed by “dissidents” is formulated is such that everybody else has to prove to the “dissidents” that HIV exists and causes AIDS. This is fundamentally assymetric. It allows the “dissidents” to just repeat “that’s not proof” when any evidence is presented. The “dissidents” want to set themselves up as the ultimate arbiters of science. This is not the way that science works. If it was then we would still be sitting in a cold dark cave while the “fire dissident” was holding up progress.

    Science is about competing ideas. Theories are overthrown if somebody can successfully argue that an alternative hypothesis better explains all available data. “AIDS dissidents” on the other hand focus on negative science – on denying. This is similar to the various varieties of creationists/IDers that focus on denying the evidence for evolution.

    A few “AIDS dissidents” have put forward alternative theories for the causation of AIDS. They are mutually exclusive and rely on a selective analysis of the available data. They each claim that the available evidence supports their own theory. They can’t all be right. However, instead of debating each other they form strategic alliances to fight the common “enemy”. In South Africa David Rasnick who apparently believes that HIV exists but does not cause AIDS is working for Matthias Rath who believes that HIV exists and causes AIDS but that his vitamins are better at suppressing HIV than ARVs while Rath’s spokeperson Anthony Brink denies the whole “germ theory of disease”. This is exactly the same as YECs, OECs and IDers joining together to fight against evilution.

    In calling for a public debate the AIDS “dissidents” imply that they are capable of a rational debate. For 20 years the various flavours of AIDS “dissidence” have put forward mutually exclusive theories about the causation of AIDS. In that time they have not been able to convince each other that their ideas are better. If they were capable of rational debate and their hypotheses were based on an honest and complete interpretation of the available evidence then they should have come to a consensus by now. They haven’t.

    If “AIDS dissidents” are serious and honest about debating then they can debate each other. Why don’t they? There is no scientific reason. There are political reasons. Their strategic alliance is purely political

  145. #145 Dale
    June 13, 2006

    I for one would enjoy hearing AIDS dissidents debate each other. Good idea!

  146. #146 Viji
    June 13, 2006

    Just a note, Hank Barnes working hypothesis and his quote referencing of an an editorial in 1981 is misleading

    HANK BARNES WROTE
    “1. Initially, the scientific establishment had the right answer on AIDS. Here’s an editorial in 1981 in New England Journal of Medicine:

    Perhaps one or more of these recreational drugs is an immunosuppresive agent. The leading candidates are the nitrites, which are now commonly inhaled to intensify orgasm. Users of amyl nitrates are more likely than non-users to have had hundreds of sexual partners and to contract venereal disease.

    Let us postulate that the combined effects of persistent viral infection plus an adjuvant drug cause immunosuppression in some genetically predisposed men.
    (Durack, NEJM vol 305, 1465-66 (1981).”

    That was an early hypothesis (they postulate) when there is little or no available data or information. They certainly got the first part right “persistent viral infection” since its been found to be reproducibly true. While the part where they postulate that adjuvant drug may contribute to immunosuppression may be off the mark, since there are many available observations that poor communities across Africa and Asia afflicted with the HIV virus, with no access to the “recreational drugs” or HAART, still progress to AIDS, by that I mean depletion of T-cells and subsequent immunodeficiency.

    Hank, you’ve always try to sidestep this important observation by blaming this to be caused by underlying disease, tropical afflictions, and malnutrition. Its dishonest to say so. As a matter of fact many of these diseases you’ve put your blame on, i.e. like malaria or even malnutrition, does not cause the drastic T-cell depletion and imumunodeficiency reminiscent of AIDS.

    Although I concede that HAART is one of the most toxic regimens available to combat HIV infection, but it is also the only effective measure to delay or halt the progression towards AIDS for some individuals. HAART can reduce HIV load to very low levels, , and every ID physician knows that once you remove HAART, the HIV virus relapse to pre-HAART levels, and progression to AIDS is imminent. So your claims that HAART somehow causes AIDS is plain wrong.

    HAART is linked to significant morbidity like liver failure, and it is a true risk that some individuals who are not at the best of health can succumb to the treatment, but it is also rightly observed that HAART helped prolonged the lives of other individuals, persons who would otherwise progress to AIDS and expire. Its the choice of people afflicted with HIV-AIDS to accept HAART knowing the risk to be able to buy some time, and for some, suffering from the serious side affects, or not take HAART and taking a chance on the time they take to progress to AIDS.

    This is analogous to the treatment of cancer decades ago, when toxic chemotherapy and harsh radiotherapy are used. And even with the availibility of less harsh treatment option we have today, some equally toxic regimens are still retained to kill the most recalcitrant cancer cells. There is also no certainty a cancer patient can avoid a relapse, but it is choice to make whether to take the treament or not, undersatnding the risks. So I hope that we will spend less time and energy bickering while contributing little to the advancement of treatment and spend more time trying to tackle the problem.

  147. #147 Chris Noble
    June 14, 2006

    Dale wrote:

    I for one would enjoy hearing AIDS dissidents debate each other. Good idea!

    I would be willing to pay money to watch Duesberg and the Perth Group argue it out. The probability of the Perth Group convincing Duesberg that HIV doesn’t exist (or in their weasel terminology – has not been proven to exist) or Duesberg convincing the Perth Group that HIV does exist is vanishingly small but the entertainment value would be immense.

    Maybe Al-Bayati could try to convince Duesberg that his theory of recreational drug causation of AIDS is wrong. It’s really all about glucocorticosteroids. Taking too much cocaine, nitrites, and/or alcohol etc causes headaches. People take aspirin for the headaches. Too much aspirin causes thrombocytopenia. They are then prescribed glucocorticosteroids for the thrombocytopenia. The glucocorticosteroids then cause AIDS. Much simpler! Occam’s razor!

    What about undiagnosed syphilis? Too much semen? Benzene in lubricants? HHV-6? They want debate? Why don’t they debate? What are they waiting for?

    Can we start up a collection? I’ll start with $100 (American or Australian I don’t care).

  148. #148 Viji
    June 14, 2006

    Wilhelm Godschalk, I’ll add some comments on parts of your | June 13, 2006 09:33 PM entry, In am not an expert or familair with John Moore or Harvey Bialy, I’m only going to stick to your comments about detection of HIV and your belief that HIV is a fiction of imagination

    You described yourself in previous posts as bioscience researcher and so you also profess to be a person familiar with the operation of many biological, molecular, instrumental techniques under the sun ,

    thus you love to trumpet the “assertion” of being an expert in the current research developments to critique the basic laboratory techniques used in diverse fields ranging from stem cell research, microbiology to HIV research.

    Alas, when I read your comments, you present doubts to such claims, as you seem to have a penchant of bemoaning even the most basic of bioscience techniques. For example, the use of PHA stimulated-PBMCs, co-cultures, or PCR when bioscience scientist know that these are the tried and tested protocols used in all related research fields, such as stem cell culture or basic molecular biology, HIV research not being the exception. You either have only slight experience in cell culture or worse you are just critiqing research on a pretense of being an expert.

    Since PBMCs are not the only cell types capable of allowing HIV replication, I’m going to give you an example of that does not utilise PHA-PMBCs, co-cultures, or penicillin, ingredients that you seems to think are “witches brew”

    For my work previously, I had cultured HIV from sero-positive blood in monocytes and macrophages isolated from sero-negative blood donors. These primary human macrophages cultivated in RPMI medium, with no added penicillin, antibiotics, PHA, or co-cultures you seem to be so particular about,

    The RPMI is only supplemented with human serum – natural in your case.

    The presence of HIV can be determined with mnay methods or a combination of all of them:

    -Reverse Transcriptase activity assay (specificity for detecting only HIV RT enzymes ensured by the stringent magnesium-dependance of this enzyme as opposed to other retrovirus utilising manganese),
    -p24 antigen production, immunoblotting for HIV specific proteins,
    -intracellular flow cytometic analysis for HIV specific proteins (HIV core antigens),
    -and/or detection of HIV DNA using PCR (HIV LTR, gag, LTR-gag sequences found only in HIV).

    These are technically sound, reproducible, and specific methods. Just in case you start trying a ridiculous deriding of RPMI being a witches brew (was it Hank or you who introduce this terminology – Can’t recall), RPMI is the Roswell Park Memorial Institute medium, the basic growth medium tested and optimised for the primary culture of human cells from a human donor, a nutrient rich medium not unlike the ingredients you find in your blood, containing much phosphate and is formulated for 5% CO2 – also optimised to mimic human blood CO2 and energy source conditions)

    I am not sure what is your basis of ridiculing the various standard methods used in almost all of biological research other than as your dishonest attempt to slander and discredit HIV research.

    If you are doubtful of such established and tested techniques, that you might as well call every little thing that bioscience research has provided and contributed to the human health a bluff.

    The aforementioned methods can be referenced from section 12 of the Current Protocols in Immunology, developed by my former mentor Suzanne Crowe and Katherine Kedzierska at the Macfarlane Burnet Institute of Medical Research and Public Health, Australia in 2001.

    And if you want to find out the methods and materials of how to get micrographs and visualisation of HIV, you can try to contact this person mak@burnet.edu.au, Burnet’s a non-profit organisation, although Johnson can be difficult at times, I think he’ll try his best to help if you try not to ask rudely.

    Cheers

  149. #149 Chris Noble
    June 14, 2006

    Viji, Godschalk’s claim to fame is to have published a few papers on Turnip Yellow Mosaic Virus in the 60s and 70s.

    Apparently all viruses can be understood from his limited experience of TYMV.

    Immediately after Godschalk exited academia the whole basis of science deteriorated. Any paper on viruses that doesn’t have a Spinco model E ultracentrifuge in the methods section is obviously wrong. If PCR or other newfangled molecular biology stuff is used it must be bullshit.

    Godschalk has found in recent times that if he pretends to be an expert and attacks anyone that thinks that there is overwhelming evidence that HIV exists and causes AIDS he gets adulation from other “dissidents”.

    For the record I have referred him to papers like this one from 1987 Fine structure of human immunodeficiency virus (HIV) and immunolocalization of structural proteins.

    Not only does this paper show excellent electronmicrographs of HIV showing a conical core and knobs it also uses immunoelectronmicroscopy to identify the proteins in the viral particles. Quite a coincidence that antibodies to viral proteins coded by viral RNA just happen to bind to specific parts of the virus! This answers the normal “dissident” tactic of repeating “that’s not a virus it’s a just a vesicle” with fingers firmly planted in ears.

  150. #150 Chris Noble
    June 14, 2006

    Here’s a brilliant quote from our resident expert in molecular biology:

    There are only 4 bases. That doesn’t allow for all that many variations (compared to the amino acids in proteins).

    Godschalk seems to be unaware that it takes 3 nucleotides to code for 1 amino acid. There are 4^3 = 64 possible combinations that code for only 20 amino acids (and start and stop codons).

    The genetic code is degenerate. The possible variation in the genome is greater than in the proteome.

    Somebody that makes simple mistakes like this has to be extremely arrogant to pretend to be an expert.

  151. #151 Hank Barnes
    June 14, 2006

    Viji,

    Hank, you’ve always try to sidestep this important observation by blaming this to be caused by underlying disease, tropical afflictions, and malnutrition.

    Ummm. Tropical afflictions and malnutrition do cause immune suppression. Many other things do too, including drugs.

    Here’s Robert Gallo from his autobiography:

    “Of course, immune suppression has occurred in the past, and especially the recent past in association with some drugs, radiation, & and pronounced malnutrition.” (Gallo, Virus Hunting: AIDS, Cancer, and the Human Retrovirus – A Story of Scientific Discovery, p.291.)

    Its dishonest to say so.

    It’s dishonest to falsely claim the above.

    As a matter of fact many of these diseases you’ve put your blame on, i.e. like malaria or even malnutrition, does not cause the drastic T-cell depletion and imumunodeficiency reminiscent of AIDS.

    A lie. See Gallo’s quote above. Immune deficiency was recognized well before AIDS was concocted in 1981.

    Although I concede that HAART is one of the most toxic regimens available to combat HIV infection,

    I’ll take it!!

    HAART can reduce HIV load to very low levels,

    It’s already at low levels, dufus. Gallo claims he found it in only 36% of the AIDS patients. So, either the other 64% had it at undetectable levels or didn’t even have it.

    So your claims that HAART somehow causes AIDS is plain wrong.

    I never made this claim. Man, you sure get the simple things wrong. See if you can follow: You admit that HAART is a toxic regimen. Some of its side-effects (like neutropenia, bone marrow-disease) overlap with the some of the symptoms of AIDS. Very simple.

    Also, I note that you entirely side-step of the issue of AZT, and whether it was good to give this dangerous chemotherapy as monotherapy to AIDS patients for 10 years.

    HankB

  152. #152 Frodo
    June 14, 2006

    Tara and Hank (and everyone who responded),

    Thanks for your responses. this will be my last entry, mostly because this is taking up an insane amount of time just to keep up with the reading, but I really appreciate your responses. Again, I am a little overwhelmed by the research. I’ll try to keep this short, here are a couple of things that caught my attention.

    I note that there are more similarities between the groups than I would infer if I were only to read Tara’s blog’s headlines. For example, you both agree that the tests are imperfect, it seems to be a matter of degree. I think an argument can be made that if the assumption of prevalance is falsified, than the test results for that population would be incorrect. (And I should correct this, my bad, it was Gerd Gigerenzer, (not gigenheizer) who wrote the book “Calculated Risks” (not calculating risks),

    http://en.wikipedia.org/wiki/Gerd_Gigerenzer
    http://www.amazon.com/gp/product/0743205561/103-8954556-7311033?v=glance&n=283155

    Also, I think it can be argued that both sides consider many factors to be important in the development of AIDS, but when polarized, each side goes to a corner (the AIDS centrists say it’s HIV only, the dissenters say it’s many things). This is also surprising, because it looks like there is more common ground than is being explored. The method of the centrists is to downgrade the relevance of what the dissenters say, so that probably helps keep this fight going. I think if you wanted to you could create a cooperative quorum to work out more common ground.

    On persuasion,First, Tara, you made some comments in your notes that went to persuasion, and analysis of, essentially, why I should not trust the dissenters, giving the impression that you were trying to persuade me that the dissenters were the bad guys among the two camps. You offered a lot of research too, but the personal slant was or is perhaps damaging from a political point of view to your message (ie negative campaigning). The dissenters tended to offer information accompanied by a plea to give it a fair review. I saw a lot of personal commentary in the remarks from both camps. There was a lot of animosity between the two groups so I’m going to guess that you guys really don’t like each other even if you are trying to be civil.

    Hank gave me reading and said that it was too much to assimilate in a short reading. That was probably the most realistic thing I heard. It is way,way too much to fully ‘get’ in a couple of days. My head is pounding from trying to do half of the reading everybody sent.

    To summarize, I appreciate everybody’s time, I am a little surprised because I can’t find the obvious ‘flat earth’ argument on either side, both seem to be making points. But maybe it should be moderated by an impartial judge, if there is such a thing, because there is a lot of emotion in the comments, from both sides, which also surprised me on a purely medical issue. (abortion comes to mind, but I think that is qualitatively different, and stem cell issues, but that arises from within the abortion issue, though it is a much weaker argument).

    I don’t see any hard Right ethical statements in this, which makes it a very odd fight, I’d say that the centrists would be center or party Left and the dissenters radical Left or Libertarian, so is it Left versus Left?

    Peace,

    Neil (aka Frodo)

  153. #153 Viji
    June 14, 2006

    Hank, you’re misreading my comments and stretching your interpretation

    I said “As a matter of fact many of these diseases you’ve put your blame on, i.e. like malaria or even malnutrition, does not cause the drastic T-cell depletion and imumunodeficiency reminiscent of AIDS.”

    Look carefully I said – MALNUTRITION/MALARIA does not cause (T-CELL DEPLETION REMINESCENT OF AIDS) & (IMMUNODEFICIENCY REMINESCENT OF AIDS)

    Anybody knows that malnutrition can lead to a weakened immune system but MALNUTRITION HAS NEVER BEEN OBSERVED TO LEAD TO MASSIVE T-CELL DEPLETION AS IN AIDS PATIENTS; and ultimately it is the this T-cell depletion that heralds the collapse of the immune system – hence ACQUIRED IMMUNE DEFICIENCY!

    True, there are immunosuppresent drugs available, but these are usually used to treat a varitey of medical conditions from autoimmune diseases and post organ transplantation… for a simple introduction proceed to

    http://en.wikipedia.org/wiki/Immunosupressive_drug

    As far as I know from the literature, NONE CAUSE THE DEPLETION OF T-CELLS, THE HALLMARK OF HIV-AIDS

    “Of course, immune suppression has occurred in the past, and especially the recent past in association with some drugs, radiation, & and pronounced malnutrition.” (Gallo, Virus Hunting: AIDS, Cancer, and the Human Retrovirus – A Story of Scientific Discovery, p.291.)”
    Anyone can see the above statement is a generalisation of immune suppression – to communicate the phenomenon of immune suppression to the masses, while Hank you are amatuerishly taking this statement to be fact

    Hmmm.. I may have gotten this wrong
    “So your claims that HAART somehow causes AIDS is plain wrong”
    I apologise, as you seemed to be touting that HAART causes AIDS in your comments before

    AZT? I am not an expert on AZT. I have only worked on the biology of HIV and isolation/culture of HIV from clinical sources, i.e. patients, and in the field; so I’ll refrain from commenting specifically on AZT. I am just HIGHLIGHTING that there are certain AIDS populations with no access no HAART or AZT who tests HIV sero-positive, shows drastic T-cell depletion, and AIDS .. Just to show you that your working hypothesis must need some re-working

    Cheers

  154. #154 Wilhelm Godschalk
    June 14, 2006

    Chris Noble
    If the “dissidents” judge at the end that Harvey Bialy won the debate and at the same time everybody else thinks that John Moore won the debate what would have been achieved?

    Ah! Its good you are back. Now I don’t have to look for you in every nook and cranny.
    Yes, finally I agree with you on something! This would probably happen. But it wouldn’t be a problem, of course. The main goal of the debate would have been reached. I’m sure Bialy could never convince Moore, and vice versa. But all the lurkers in the background, having heard the arguments from both sides, then could start to think for themselves, and make up their own minds. And that’s all we want; not grey masses being intimidated by pathetic little bullies, as is the case now.

    The way that any such “debate” proposed by “dissidents” is formulated is such that everybody else has to prove to the “dissidents” that HIV exists and causes AIDS. This is fundamentally assymetric.

    Whawazzat? Are you implying that we (the sane people) have to prove that HIV does not exist? Proving a negative, just to be “symmetrical”? After all the ridiculous claims that have been (and will undoubtedly be) made about the mythical “HIV” we would have cut out our work for us for centuries to come. If I claim the planet Pluto is made of cheese, is it upon you to prove that it is not? Ever heard of “burden of proof”?

    It allows the “dissidents” to just repeat “that’s not proof” when any evidence is presented.

    Yeah. Whenever they look at a table, they say “It’s a cow”. When asked for evidence, they proudly announce: “It has 4 legs.” And we shouldn’t even criticize this “evidence”?

    This is not the way that science works. If it was then we would still be sitting in a cold dark cave while the “fire dissident” was holding up progress.

    Aw, it would be easy enough to prove the reality and the power of fire. There will be no “fire dissidents” after I light a fire under your rear end… Or would you agree that this is not such a good example?

    Science is about competing ideas. Theories are overthrown if somebody can successfully argue that an alternative hypothesis better explains all available data.

    No, that’s not the only way to overthrow theories. A theory also gets discarded if it consistently leads to wrong predictions. But if you wish to call that “negative science” or “denial”, you probably would not have thought much of Lavoisier’s work, when he disproved the phlogiston etheory of oxidation. (The orthodoxy of that time tried to explain the weight gain upon oxidation of metals by assigning a negative mass to phlogistone (!) And you would have fitted right in with them).

    This is similar to the various varieties of creationists/IDers that focus on denying the evidence for evolution.

    All you lurkers: See the strawman again? Creationism and evolution have nothing to do with this discussion. Besides, I don’t know any AIDS-dissident who is a creationist.

    A few “AIDS dissidents” have put forward alternative theories for the causation of AIDS. They are mutually exclusive and rely on a selective analysis of the available data.

    Yes indeed. Pity that the “available data” all come from the orthodoxy. Wouldn’t it be nice if they could collect their own data? But who would fund their research?

    However, instead of debating each other they form strategic alliances to fight the common “enemy”.

    Naturally. “The enemy of your enemy is your friend”. I would rather associate with a witch doctor than with the unsavory characters who try to bully us into believing the totally ridiculous HIV-causes-AIDS theory. And the “common enemy” – make no mistake about it – is you (and the people who funded your study).
    Oh… and don’t think dissidents don’t debate each other. There has been a discussion between Duesberg and the Perth Group. And on http://www.AIDSMythExposed.com and numerous fora in a multitude of languages, we do debate each other.
    But first, we have to fight our common enemy, of course. We’ll settle our internal discussions after Hatchet Day.

    For 20 years the various flavours of AIDS “dissidence” have put forward mutually exclusive theories about the causation of AIDS. In that time they have not been able to convince each other that their ideas are better.

    Well, I’ll be… You goons have repressed us for 25 years, and in all those years you have not come up with anything that’s even halfway plausible, let alone backed up by evidence. “HIV Science” reads like it has been written by the brothers Grimm. Time to let go of all that research money, Klutzes United! I have a constructive proposal: Why not put this “AIDS research” in the hands of the toxicologists from now on? I’m sure they will come up with better things that your far-fetched virus theory. And if you behave, maybe the toxicologists can use somebody who has experience with aerosols…

    Don’t go away. I’m not yet finished with you.

    Godschalk seems to be unaware that it takes 3 nucleotides to code for 1 amino acid. There are 4^3 = 64 possible combinations that code for only 20 amino acids (and start and stop codons).

    That’s what I mean. Not a very efficient coding system, is it? Considering that the replacement of just one amino acid can have a profound effect on the activity of a protein, it takes 3 nucleotides to code for the change. In cryptography this would mean that the encrypted text would be 3 times as voluminous as the plain text.

    I’ve seen how it all began, and it wasn’t a pretty sight. A group of my colleagues was working on protein biosynthesis. They had a witches’ brew (yes I coined the phrase), and they claimed they could put in a polynucleotide, and produce a polypeptide chain based on these codons. Well, these guys really blew their horn about it, but their results were dismal. I suggested that, if they would throw an old shoe into the mix, they would also get the same result. (You see, I haven’t changed through the years) This “old shoe theory” did not do anything for my popularity, but it was right on target. Since that time, they had to come up with all kinds of magical but undetermined “elongation factors”, “prime factor” and “factor XYZ489″. And I must say, the model they came up with (ribosomes that come rolling down a molecule of messenger RNA, picking up amino acids in the process) was in every way as laughable as the HIV/AIDS story. But I guess that’s how these molecular geneticists are: A strong preoccupation with the bizarre.

    Although I concede that HAART is one of the most toxic regimens available to combat HIV infection, but it is also the only effective measure to delay or halt the progression towards AIDS for some individuals.

    Oh, sure. It stops them right in their tracks. They die of liver failure, and that’s very effective in keeping them from getting full-blown AIDS.

    What about undiagnosed syphilis? Too much semen? Benzene in lubricants? HHV-6? They want debate? Why don’t they debate? What are they waiting for?

    If you would read the dissident’s boards more often, you would know that these debates are already taking place. So youn kep your money in your pocket. But of course, this attempt at “divide and conquer” won’t keep us from our first task in life: Debunking the apologists.

    Viji, Godschalk’s claim to fame is to have published a few papers on Turnip Yellow Mosaic Virus in the 60s and 70s.

    Is that all you could find?

    Any paper on viruses that doesn’t have a Spinco model E ultracentrifuge in the methods section is obviously wrong. If PCR or other newfangled molecular biology stuff is used it must be bullshit.

    I used every technique I needed for my projects. I didn’t need 20 other guys to help me. I’m sure you wouldn’t recognize a Spinco Model E if it fell on your head, but one run of these famous “HIV-preparations” in this centrifuge would prove beyond a reasonable doubt that all these claims to “HIV isolation” are indeed bullshit.
    Today’s molecular bioklutzes may know ambiguous techniques such as PCR, but the only physical method they know is counting bands on a polyacrylamide gel.

    …and attacks anyone that thinks that there is overwhelming evidence that HIV exists and causes AIDS.

    I’ve been hearing about this “overwhelming evidence” for 22 years now. So where are you hiding it? It’s not in the scientific literature. The only thing I can find there is hundreds of thousands of papers based on the assumption that HIV exists, and that it causes AIDS.

    And then… the Gelderblom paper again. As I explained to you before, the work itself is excellent. They have produced nice pictures of eh… something. My question was: “Nice particles, but what are they?” And it still is.

    Not only does this paper show excellent electronmicrographs of HIV showing a conical core and knobs it also uses immunoelectronmicroscopy to identify the proteins in the viral particles. Quite a coincidence that antibodies to viral proteins coded by viral RNA just happen to bind to specific parts of the virus!

    Not elementary at all, my dear Watson! How do they know it’s HIV? By decree? The conical core should already raise suspicions, but nothing seems to faze these one-track minds.
    How do you know that these are “antibodies to viral proteins coded by viral RNA”? By circular reasoning of the same caliber that brought us those wonderful serological tests for HIV?
    Yes, all this stuff comes from cell cultures. But the connection with a human retrovirus exists only in the mind of the real believer.

  155. #155 Chris Noble
    June 14, 2006

    Pseudoscientists never admit to a mistake.

    HIV sequences are obviously retroviral because they code for proteins Gag, Pol and Env that are homologous with all other retroviruses. It is nonsensical to claim that they could be anything.

    Godschalk attempts to refute this by coming up with a spurious ad hoc argument.

    Homology? There are only 4 bases. That doesn’t allow for all that many variations (compared to the amino acids in proteins).

    Here Godschalk compares the 4 nucleotides with the 20 amino acids. In reality there are 64 possible codons for 20 amino acids. There is more variation in the codons than in the amino acids. Godschalk is just plain wrong. How his “argument” was supposed to be a refutation of the homology of HIV proteins with other retroviruses is a mystery.

    Does Godschalk admit to being wrong?

    That’s what I mean. Not a very efficient coding system, is it? Considering that the replacement of just one amino acid can have a profound effect on the activity of a protein, it takes 3 nucleotides to code for the change. In cryptography this would mean that the encrypted text would be 3 times as voluminous as the plain text.

    No. He just pretends that this is what he meant all along. Read what he wrote first and it doesn’t agree at all. Godschalk is just making this stuff up.

    But more importantly how does this refute the homology of HIV with other retroviruses? It doesn’t.

  156. #156 Dan
    June 15, 2006

    Chris,
    you’ve got your sights trained on Wilhelm at the moment, but could you take a break and answer a couple of questions I’ve had waiting for you?

    Here’s one of the problems I’m having with this 36% issue…maybe Chris can clarify these statments of his on the issue that are at odds with each other.

    First, he says:
    The first tests were relatively crude. The specificity and sensitivity of these early tests were not high. Why expect the first tests to be perfect?

    Simple enough. He’s saying the tests are crude and imperfect.

    Then, he says:
    …why were 36% of AIDS patients infected with a virus that is present in only very low levels in the general population? Coincidence?

    This would imply that the tests AREN’T crude and imperfect.

    Which is it, Chris? Help us out here.

    And after that, I’d like to hear more about this scientific standard where a pathogen need only be found in 36% of people with the disease to be proclaimed as the cause of this disease. That sounds very interesting.

  157. #157 Chris Noble
    June 15, 2006

    Dan, here’s what I wrote before:

    Dissidents” go on and on about the various tests for being completely unreliable. They do this by citing studies that show that false positives do occur and extrapolate this to “totally unreliable”. A false dichotomy.

    Do you understand what a false dichotomy is?

    You are asking me to choose between the tests being %100 reliable and %100 meaningless. This is a false dichotomy.

  158. #158 Chris Noble
    June 15, 2006

    Whawazzat? Are you implying that we (the sane people) have to prove that HIV does not exist?

    No, I am saying that people like Duesberg and the Perth Group who claim that they have valid alternative theories should concentrate on providing evidence for these theories or at least demonstrating that their theories are a) consistent with all available evidence and b) better explain the evidence compared to the theory that HIV causes AIDS.

    The fact that “dissidents” focus on negative science puts them in the same class as creationists/IDers. And no I am not claiming that HIV “dissidents” are all creationists (some like Phillip Johnson are). I am saying they use the same pseudoscientific arguments. They both demand public debates for instance.

    Your argument about Lavoisier is wrong. The “phlogiston theory” was not overthrown by armchair “phlogiston” dissidents. It was overthrown because Lavoisier demonstrated that another theory “oxygen theory” better explained the available evidence.

    If you would read the dissident’s boards more often, you would know that these debates are already taking place.

    No, they are not taking place. Can you provide any evidence that Duesberg and the Perth Group have been having any serious debates since 1996?

    They gave up trying to convince each other. Why?

    Can you provide any valid reason why Duesberg and the Perth Group do not debate each other? Each of them claim to be rational and both say they want to debate the subject.

  159. #159 Darin Brown
    June 15, 2006

    “The fact that ‘dissidents’ focus on negative science puts them in the same class as creationists/IDers. And no I am not claiming that HIV “dissidents” are all creationists (some like Phillip Johnson are). I am saying they use the same pseudoscientific arguments.”

    What is “negative science”? Does this just mean any kind of disagreement with current consensus? Wouldn’t this automatically put anyone who disagrees with anything in the same class as creationists/IDers?

    “Pseudoscientific arguments”. YOU GUYS pseudoscientific tactics are isomorphic to the IDers — distraction, obfuscation, rhetoric, lying, every trick under the sun. (If you even know what the word “isomorphic” means.) The ONLY difference between you guys are IDers are

    1. You have the consensus.

    2. The IDers aren’t killing tons of people.

  160. #160 Scott Kirwin
    June 15, 2006

    http://www.lacitybeat.com/article.php?id=3887&IssueNum=157

    Let’s see…
    Toxic reaction to a drug that kills a thousand people a year OR
    Politically correct diagnosis with no evidence…

    Shame on you, Tara.

  161. #161 Dan
    June 15, 2006

    You are asking me to choose between the tests being %100 reliable and %100 meaningless. This is a false dichotomy.

    Nobody’s asking you to do anything, except to not contradict yourself. You’re trying to have it both ways on these early tests.

  162. #162 Dale
    June 15, 2006

    Did you read the coroner’s report Scott? There was plenty of evidence for EJ’s diagnosis (PCP in her lungs, p24 in her brain and an HIV+ mother) and no evidence of a toxic reaction to an antibiotic.

  163. #163 Dan
    June 15, 2006

    Dale,
    do you mean to say that the coroner’s report included Christine’s “status” in determining the cause of EJ’s death?

  164. #164 Scott Kirwin
    June 15, 2006

    Dale
    Four months after EJ’s death the cause was listed as
    “unknown”. If AIDS is so obvious, why wasn’t it blamed for her death?

    That’s right? The coroner didn’t know Christine was HIV+ and therefore didn’t have the right bias in place to make the decision.

    We’ll also just ignore the lymphocyte count of 10,800. No need to allow pesky counter-evidence to get in the way of our a priori decision.

    Do I sound snide? Yes – because I BELIEVED YOU. EJ’s death convinced me that the Denialists were wrong. Shame on me for being so easily convinced.

    You’ll have to do better next time.

  165. #165 Hank Barnes
    June 15, 2006

    Viji,

    Holy Smokes! Is it Christmas? An AIDS activist actually apologizing?

    I apologise, as you seemed to be touting that HAART causes AIDS in your comments before.

    Well, Sir, that’s rather classy of you. I will try to emulate your fine lead for the remainder of the discussion.

    You wrote:

    AZT? I am not an expert on AZT. I have only worked on the biology of HIV and isolation/culture of HIV from clinical sources, i.e. patients, and in the field; so I’ll refrain from commenting specifically on AZT.

    This is a crucial component of the debate. AZT is highly-toxic. In fact, it kills leukocytes and neutrophils. I quote:

    “Anemia, leukopenia, and neutropenia were the major hematologic abnormalities attributable to AZT, and these were found in a majority of subjects receiving the drug (Table 2). (Richman et al, Toxicity of AZT, NEJM, 317:192-197 (1987).

    Not to mention, that in animal studies it causes cancer. (See Diwan (1999).

    Again I quote: The results confirm that AZT is a moderately effective perinatal carcinogen in mice, targeting several tissue types

    It makes no sense to treat a depletion of subset of white blood cells, with a drug that kills all types of white blood cells.

    It makes no sense to give carcinogenic “medicine” to sick people.

    The administration of AZT in 1500 mg daily doses from 1987-1997 — greatly exacerbated, if not created, the AIDS epidemic of those years — my working hypothesis.

    You have to look at the entire picture with an open mind. If you a priori fervently believe that HIV is a deadly virus and that the drugs save you, you cannot interpret the complex picture.

    Respectfully, Hank Barnes

  166. #166 Zach
    June 15, 2006

    “It makes no sense to treat a depletion of subset of white blood cells, with a drug that kills all types of white blood cells.”

    I’m confused as to how depletion of leukocytes and neutrophils is considedered all types of white blood cells when you still have lymphocytes, monocytes, basophils, and eosinophils.

  167. #167 Hank Barnes
    June 15, 2006

    Zach,

    Leukocytes = white blood cells

    The others (lymphocytes, monocytes et al) are sub-sets of these white blood cells.

    Do you have anything of substance to add?

    HankBarnes

  168. #168 Dan
    June 15, 2006

    It makes no sense to treat a depletion of subset of white blood cells, with a drug that kills all types of white blood cells.

    AIDS is never going to end with that kind of thinking. That’s just crazy talk.

    I’m sure some of our medical/science authorities can show you the errors of your thinking on this one, Hank.

  169. #169 Dale
    June 15, 2006

    Four months after EJ’s death the cause was listed as
    “unknown”. If AIDS is so obvious, why wasn’t it blamed for her death?
    That’s right? The coroner didn’t know Christine was HIV+ and therefore didn’t have the right bias in place to make the decision.
    We’ll also just ignore the lymphocyte count of 10,800. No need to allow pesky counter-evidence to get in the way of our a priori decision.

    It’s all about probability Scott. There are a very large number of causes of death that can present with similar gross symptoms. To find a probable cause of death a coroner will start performing tests looking for a single most likely cause among all possible causes. In EJ’s case, she was a white child of wealthy and presumably non-drug using parents. She was, according to her parents, a healthy child. The prevallence of HIV among such children is almost vanishingly small. So in the absence of evidence to the contrary, a coroner would likely start with the assumption that EJ was HIV negative. The tests that would have been performed looking for causes of death would have been chosen based on that assumption. The fact that 4 months went by with no probable cause of death suggests that those tests were negative.

    But the child of an HIV+ mother has up to a 25% chance of being HIV+ herself and if that child is HIV+ then there are a number of other causes of death that become statistically more probable, including PCP pneumonia which is the most common cause of death among such children.

    So knowing Christine was HIV+ may well have biased the coroner to do a test for PCP. Or not, I’m just guessing. But unless you believe in conspiracies, there is no reason to believe that knowledge in any way influenced the results of the test. Or the results of the test for p24 in the brain which (reading between the lines) appears to have possibly been done because there were lesions in the brain that were typical of HIV induced lesions.

    PCP in the lungs and HIV protein in the brain are strongly indicative of an HIV infection and a suppressed immune system. If Christine was HIV- and there was no evidence of any other means by which EJ might have acquired HIV, then the coroner might have performed additional tests to look for another explanation of the test results. But the combination of an HIV+ mother, PCP in the lungs and p24 in the brain, makes AIDS related pneumonia the most probable cause of death.

    The lymphocyte counts neither support nor call the diagnosis into question. Although CD4+ T cell counts and CD4+: CD8+ Tcell ratios tend to be consistantly lower in AIDS patients then in normal patients, according to the literature that I could find, the same thing isn’t true of total lymphocyte counts.

  170. #170 Dale
    June 15, 2006

    It makes no sense to treat a depletion of subset of white blood cells, with a drug that kills all types of white blood cells.

    Well actually it does in theory, but only if killing all types of white blood cells completely erradicated the virus. Neither AZT nor any other current treatment for HIV does that.

  171. #171 Hank Barnes
    June 15, 2006

    Dan,

    It’s even a worse trade-off, when one considers how few T4-cells are even infected with HIV.

    “A surprisingly low number of T cells are infected with HIV in AIDS(1), and immunosuppression occurs prior to depletion of CD4 cells.” (See Hoffman et al, PNAS, 88:3060-3064 (1991).

    So, to fight a few infected T4-cells, you randmomly kill all leukocytes with AZT. That ‘s like trying to save your house from termite damage, by machine gunning those little critters!

    A bad idea.

    HB

  172. #172 Dan
    June 15, 2006

    So, to fight a few infected T4-cells, you randmomly kill all leukocytes with AZT. That ‘s like trying to save your house from termite damage, by machine gunning those little critters!

    Sounds like something Homer Simpson would do.

  173. #173 Dan
    June 15, 2006

    Hank: It makes no sense to treat a depletion of subset of white blood cells, with a drug that kills all types of white blood cells.

    Dale: Well actually it does in theory, but only if killing all types of white blood cells completely erradicated the virus. Neither AZT nor any other current treatment for HIV does that.

    And that justifies the use of AZT how?…

  174. #174 Hank Barnes
    June 15, 2006

    Homer Simpson could probably provide better care than some of these AIDS experts:)

    HB

  175. #175 Zach
    June 15, 2006

    “Zach,
    Leukocytes = white blood cells
    The others (lymphocytes, monocytes et al) are sub-sets of these white blood cells.
    Do you have anything of substance to add?
    Hank Barnes”

    I made an error; however, I think that it was rude to ask if I had anything of substance to add.

  176. #176 Hank Barnes
    June 15, 2006

    Well, please forgive my rudeness. As Bruce Springsteen used to sing, “It’s Hard to be a Saint in the City.”

    Hank Barnes

  177. #177 Dale
    June 15, 2006

    And that justifies the use of AZT how?…

    What justified AZT was data like this “The Centers for Disease Control (CDC) received reports of 593 cases of acquired immunodeficiency syndrome (AIDS) in the US between June 1, 1981, and September 15, 1982. Death occurred in 243 (41%) of these cases. The incidence of AIDS by date of diagnosis has roughly doubled every 6 months since late-1979, and an average of 1-2 cases are now diagnosed per day. The mortality rate for cases diagnosed over 1 year ago exceeds 60%.” (from MMWR Morb Mortal Wkly Rep 31, 507 (1982).

    The initial short term data on AZT indicated some benefit and people who were given a 60% chance of dying within a year were not particularly interested in waiting 5 years or more for the FDA to complete all the carefully controlled drug trials that might have revealed that AZT monotherapy was not very effective long term.

  178. #178 Wilhelm Godschalk
    June 15, 2006

    Chris Noble:
    Pseudoscientists never admit to a mistake.
    Now we’ve reached the point where it’s implied that I’m a pseudoscientist by a guy who set his first toddling steps in the field of science just a few short years ago, and is now making more noise than anybody else. Oh well, I shouldn’t be surprised. Piglets squeal a lot louder than grown pigs too.

    HIV sequences are obviously retroviral because they code for proteins Gag, Pol and Env that are homologous with all other retroviruses.

    This statement contains a lie at every two or three words.
    1. How do you know they are “HIV sequences” without having isolated the pure virus?
    2. “obviously retroviral”? Why?
    3. “Gag, Pol and Env that are homologous with all other retroviruses” Pray tell me what other retroviruses. Most of our knowledge about retroviruses comes from chickens and mice. All this hogwash about human retroviruses didn’t come into play until the Gallo era. Do they exist at all?
    And by the way, there are many human proteins that are homologous with proteins found in other species. Does that mean past “infections”??? …Or just the efficiency of nature?

    Here Godschalk compares the 4 nucleotides with the 20 amino acids. In reality there are 64 possible codons for 20 amino acids. There is more variation in the codons than in the amino acids. Godschalk is just plain wrong.

    I see it, but I can’t fathom it yet: You’re actually comparing the number of amino acids with the sequences of 3 nucleotides?? (Apples and oranges?) That’s gross! Do you realize how many possible sequences of 3 amino acids there are, compared to those measly 64 for nucleotides? And add to this the various conformations a protein with a certain primary structure can assume, with a profound effect on its biological functioning. Then you may begin to realize the enormous complexity of the protein world. And in addition to proteins, there are polysaccharides, lipoproteins, spingolipids, and RNA. But you and your ilk are doing nothing but putter around in the simple-minded realm of DNA, a dull macromolecule with very limited configurations and functions. All the while pretending that you hold the code to all living processes. But in reality it’s the world view of a goldfish in a round glass bowl. And remember: you heard it here first.

    How his “argument” was supposed to be a refutation of the homology of HIV proteins with other retroviruses is a mystery.
    I wouldn’t be surprised if it will remain a mystery to you forever. I’m getting tired of repeating the questions: How do you know they are “HIV proteins”? And what other retroviruses do you mean? The old familiar ones, in mice and chickens, or Gallo’s creations?

    No, I am saying that people like Duesberg and the Perth Group who claim that they have valid alternative theories should concentrate on providing evidence for these theories

    Oh, I agree… but who will pay for these studies, while all the money goes to the HIV-hustlers?

    The “phlogiston theory” was not overthrown by armchair “phlogiston” dissidents. It was overthrown because Lavoisier demonstrated that another theory “oxygen theory” better explained the available evidence.

    Yes, he did. But not until after it was shown (by “negative” scientists?) that metals gain weight upon rusting or calcification, so that the phlogiston orthodoxy had to come up with a “negative weight” to explain it.
    Well, at least Lavoisier still had a chance to prove his point. He had enough money of his own to pay for his research. And he had the time… before he was executed.

    No, they are not taking place. Can you provide any evidence that Duesberg and the Perth Group have been having any serious debates since 1996?
    They gave up trying to convince each other. Why?

    I have given the reason several times already: No funding. So there’s little sense in keeping up the debate of you don’t have the means to look for evidence to prove your point. I don’t agree on all points with Duesberg (I don’t believe HIV exists). Nor with the Perth Group’s emphasis on oxidative stress (I think mitochondrial damage, leading to a decreased energy production is the cause of the trouble) I could think of a few simple experiments to bear out my view, but it’s not going to happen.

    Dale:
    Damn! I had given you more credit than considering you as someone who dances on the grave of an innocent child. Did you have to bring this up?

    Did you read the coroner’s report Scott? There was plenty of evidence for EJ’s diagnosis (PCP in her lungs, p24 in her brain and an HIV+ mother) and no evidence of a toxic reaction to an antibiotic.

    Well, you may honestly believe that, but it’s a pack of lies. This coroner, James Ribe, is a totally corrupt thug, who has on previous occasions changed his original testimony, just to please the district attorney.
    The first autopsy revealed nothing special, and the body would be released for burial. Until the bloodhounds learned who the mother of this child was. That’s when Ribe got involved, and from that moment on, the cause of death changed from “inconclusive” to “AIDS”
    A later autopsy by Mohammad al-Bayati showed that there was no PCP in the lungs. p24 in the brain? Maybe. So what? I’ve been trying in vain to explain to several pharma phlunkies that the p24 proteins are omnipresent. They are proteins used in the transport of cellular materials through membranes. So finding p24 in the brain is like finding sand on the beach. But they hold on to the silly dogma that this p24 is special, because it has been coded for by HIV-related DNA. Sorry if that makes anybody die laughing, but you know how they are: Never a direct argument, but always playing the ball back to DNA, because that’s the only thing they know.
    Yes, the girl’s mother is “HIV+”. But her husband is not. Neither is her son. (Padian anyone?)

    …lesions in the brain that were typical of HIV induced lesions

    Oh were they, really? Who was it originally, pointing at brain lesions, declaring ex cathedra: “These be HIV-induced!”? How the hell would anybody know that? By just looking at them? Histology must have made great strides since I last looked. Now they can look at a tissue sample and see what caused the injury…
    Tell me, Dale, are you always this gullible? I thought… maybe we could do some business in the near future.

    Tara:
    You’re conflating several tests. One can isolate virus; can test for antibodies (using several different tests, I might add), or use RT-PCR to look for viral RNA.

    Eh… we’ve been trying to tell you this: One cannot isolate virus. What is done is inoculate a co-culture with a sample of the patient’s blood plasma, and then claim that it’s HIV that’s growing there. It works the same as the magician’s trick where he pulls a rabbit out of a hat. Once you kno how that tick works, you also know what co-culturing is all about.
    Yes, you can test for antibodies. But the question remains: Antibodies against what?
    RT-PCR? Great. So you find a “viral load”. But how do we know it’s viral RNA we are finding?

    Viji
    Alas, when I read your comments, you present doubts to such claims, as you seem to have a penchant of bemoaning even the most basic of bioscience techniques.
    Sorry Viji, that I didn’t get around to your comments before.
    I actually bemoan the absence of physical methods in contemporary bioscience. These methods have the advantage that there is solid theoretical knowledge behind them; you know what’s happening. With the biological methods that’s not so. Too many unknowns, too many basic assumptions (that may or may not be true), and too much room for interpretation.

    The presence of HIV can be determined with mnay methods or a combination of all of them:

    -Reverse Transcriptase activity assay (specificity for detecting only HIV RT enzymes ensured by the stringent magnesium-dependance of this enzyme as opposed to other retrovirus utilising manganese),
    -p24 antigen production, immunoblotting for HIV specific proteins,
    -intracellular flow cytometic analysis for HIV specific proteins (HIV core antigens),
    -and/or detection of HIV DNA using PCR (HIV LTR, gag, LTR-gag sequences found only in HIV).

    I came up with the qualification “witches brew” because years ago, colleagues of mine worked on protein biosynthesis where they tried to make specific peptide sequences by coding with synthetic polynucleotides. They also used the most elaborate mixtures (containing puromycin, etc.) They never got the results they expected, so they had to invent all kinds of cofactors to explain those failures.
    But let’s look at the methods you advocate for the determination of HIV. They are all markers, by the way.
    1. Reverse Transcriptase activity assay. Well, you obviously know that reverse transcriptase is a common enzyme, presnt everywhere. But you single one out specifically, as belonging to HIV, on the basis of its Mg++ dependency. Now that’s something you have to be careful with. This, too, reminds me of the bad old days when one group of researchers found a stimulation of protein synthesis, while others found an inhibition. Dependence of biological systems on metals such as magnesium or manganese can vary greatly. Even different versions of the same enzyme may be different in that respect, as you know. But I find it’s going a little too far to assume that one enzyme is viral, just because it has a greater dependence on Mg++.
    2.p24 antigen production. Same story. p24 proteins are common transport proteins that occur in every cell. To single one out and declare it to be of HIV-origin, just because someone has sequenced a piece of DNA that codes for it, is an unwarrented conclusion.
    3. intracellular flow cytometic analysis for HIV specific proteins How come everybody is so sure about “HIV-specific” proteins? They have no standard to compare it to. (Namely the pure virus itself).
    4. and/or detection of HIV DNA using PCR I don’t doubt for a moment that you can find even the tiniest amounts of DNA with PCR. Forensic chemists do it all the time. But how could anybody know if that DNA was put there by HIV? I know they have sequenced lots of material. But in order to know where it came from, you must have a standard of comparison (HIV itself).
    LTR-gag sequences found only in HIV ? How do they know? It was thought originally that Reverse Trascriptase was specific for retroviruses. Now we know that’s not so. A human body is a complicated machine. Lots of things can originate from it. Maybe also all those markers that are considered specific for HIV.

  179. #179 Dale
    June 15, 2006

    Damn! I had given you more credit than considering you as someone who dances on the grave of an innocent child. Did you have to bring this up?

    I didn’t bring it up, I was just responding to Scott’s comment. However, for what it’s worth, I think EJ’s death was a tragedy but that her parents may well have acted in what they believed were her best interests. I don’t understand their actions (particularly not telling the ER staff that EJ ‘might’ be HIV positive) and I think they were terribly wrong but I don’t think they should be prosecuted.

    What I said about the lesions was that it might have been their appearence that was suggestive of HIV and that prompted the immunological testing for p24. That was speculation on my part. In any case it would have been the positive test results that confirmed the presence of HIV.

  180. #180 Dan
    June 15, 2006

    What justified AZT was data like this “The Centers for Disease Control (CDC) received reports of 593 cases of acquired immunodeficiency syndrome (AIDS) in the US between June 1, 1981, and September 15, 1982. Death occurred in 243 (41%) of these cases. The incidence of AIDS by date of diagnosis has roughly doubled every 6 months since late-1979, and an average of 1-2 cases are now diagnosed per day. The mortality rate for cases diagnosed over 1 year ago exceeds 60%.” (from MMWR Morb Mortal Wkly Rep 31, 507 (1982).

    Ok, well all this info is from before “HIV” was deemed the cause of AIDS. So, if we take this information as presented, there would be no reason on earth to take AZT, being that “HIV” (or any other single microbe causative agent) had been found during this time to be the cause of AIDS, unless people just enjoy ingesting poison, that is.

    Second, back to Hank’s point. It makes no sense to treat a depletion of subset of white blood cells, with a drug that kills all types of white blood cells.

  181. #181 Dale
    June 15, 2006

    A later autopsy by Mohammad al-Bayati showed that there was no PCP in the lungs. p24 in the brain?

    al-Bayati never performed an autopsy – he couldn’t have as he’s not a medical doctor and thus no qualified to perform autopsies. What he did was read the coroner’s report and come up with his own interpretation.

    And we know it’s retrovirus because the DNA sequences purified away from all cellular and proteins can be introduced into uninfected cells and will lead to the production of infectious virus. According to Peter Duesberg that’s about the most stringent test for a virus that anyone’s ever come up with.

  182. #182 Dale
    June 15, 2006

    It makes sense Dan because immune cells are constantly being formed and destroyed within the human body. Kill the cells off with drugs and the patient will be very prone to infection for a period of time but the immune system will regenerate within a few weeks. But that only works if the initial treatment kills all the infected cells or enough to allow a reconstituted immune system to clear the virus on its own and apparently neither AZT monotherapy nor HAART are capable of doing that. Still, the early clinical trials showed that on a short term basis AZT helped AIDS patients. And as I recall there was a huge political push from gay activists to make AZT available as soon as possible.

  183. #183 Dan
    June 16, 2006

    Kill the cells off with drugs and the patient will be very prone to infection for a period of time but the immune system will regenerate within a few weeks.

    How does the immune system regenerate if you’re taking AZT indefinitely? The killing of cells becomes a constant. So not only do you have “HIV” killing off cells, but you have AZT doing it as well. At what point is the immune system given a chance to regenerate? As I remember from a couple friends who took AZT back in the early 90’s, they took it until they died.

    Still, the early clinical trials showed that on a short term basis AZT helped AIDS patients.

    In what way exactly?

    And as I recall there was a huge political push from gay activists to make AZT available as soon as possible.

    You recall correctly. As I mentioned to Simon above, I didn’t understand why gay men were so quick to make their bed with the pharmaceutical companies. Your explanations of the whys and hows and AZT only confirm my former (and continuing) apprehension.

  184. #184 Dale
    June 16, 2006

    The immune system won’t regenerate if you’re bombarding it constantly. What I said was if you could treat for a limited period of time and totally eliminate the virus (which was the hope with AZT or HAART), then upon stopping treatment the immune system could regenerate.

    As far as how the early trials showed AZT helped patients, I suggest you go to the National Library of Medicine online and read the papers or at least the abstracts for yourself.

  185. #185 Dan
    June 16, 2006

    As far as how the early trials showed AZT helped patients, I suggest you go to the National Library of Medicine online and read the papers or at least the abstracts for yourself.

    I asked because you said the initial short term data on AZT indicated some benefit and the early trials showed AZT helped patients. For the benefit of all who are following along here, including those quiet “lurkers”, why don’t you just tell us how AZT “helped”?

  186. #186 Dale
    June 16, 2006

    Basically literature says that markers of immune function, various disease symptoms and mortality rates all temporarily improved. But like I said, read it for yourself and decide for yourself.

  187. #187 Viji
    June 16, 2006

    Hank,

    First foremost, I am not an AIDS activist.

    I am just a scientist who happens to be working on projects from the understanding of antimicrobial resistance in infectious agents such as MDR bacteria, worked previously on HIV and Flaviviruses West Nile virus, and most recently on drug development and improvement of regimens for MDR Acinetobacter baumannii and Pseudomonas aeruginosa.

    And importantly, despite your incessant accusations of scientists all over the world being “bought” by multinational drug companies, and can never be trusted, a lot of us at the forefront of infectious diseases research, including us (our lab group) has no financial or commercial links with them. We only hold NHMRC grants that we wholly use for the experiments aiming at the betterment of public health, projects that we devote all out time and effort, on top of having a meagre salary. So do us a favour by trying not to be rude on your rude and unethical smear campaigns.

    Which makes me wonder what drives you/ what is your agenda to take up so much of your time and effort (since you are not a scientist) to debunk HIV?

    You said Holy Smokes! Is it Christmas? An AIDS activist actually apologizing?
    Perhaps your statement reflects that you’ve never took the opportunity to look at the issues with a clear mind, admit to mistakes if you find some, and apologise if you’ve been wrong. Your comments before do show your arrogance that you’re right no matter what, and all instances contrary to your view is wrong and from people none the wiser.

    My profession trains me to critically appraise available information and empirical research using my theoretical understanding of the science and practical experience working the science as the foundation of my arguments. I would not jump to conclusions for mere cherry-picking of a few articles or publications that do not present hard reproducible evidence – rather perspectives or statistical conclusions that can be widely interpreted.

    The fact is, I had looked at Duesberg’s arguments, I respect his right to dissent, and had taken his points into consideration, I too conclude that environmental factors such as drug use or co-infections may have contributions to the morbidity and mortality of AIDS, just as every other infectious diseases and ailments, these environmental and circumstancial factors act in concert with that initial infectious agent to determine the outcome of the disease.

    Yet to tell me to discount HIV as the causative infectious agent of AIDS, because an early error in Gallo’s experiments, and at the same time ignoring the wealth of empirical, reproducible, technically sound “bench” research is just plain wrong and unscientific.

    Moreover, in the face of these hard research, you, Wilhelm Godschalk, and your clique of persons that does not believe in HIV, attempts to undermine the validity of these research by spreading misinformation with bizarre and false accusations like your statement that

    (1) “every study after Gallo is based on the assumption that HIV causes AIDS”

    when you know that the correct statement should be:-

    “Gallo first described HIV as the primary infectious agent that lead to AIDS, his early methods were crude and not always indicative, but with the development of research technologies (technologies not exclusive for HIV research but all scientific research), subsequent research in this areas has unequivocally shown that HIV can be cultured from AIDS and HIV positive persons, but not found in healthy individuals; similarly, definitive HIV markers such as RT activity, p24 antigen, HIV specific sequences has also been unfailingly shown to be present in AIDS HIV positive patients and not found in healthy individuals”

    (2) Wilhelm Godschalk’s reasoning in his attempt to disagree with “all research that does not agree with him” is even more bizarre, starting with his obsession that nothing is true until you can physically visualise or isolate the virus to the finest of details. Sure, I give hime the credit for using the centrifuge to separate the Turnip Yellow Mosaic Virus in the 60s, but did he tell anyone the fact this virus like the closely related TMV are atypically large viruses relative to retroviruses, which are so much harder to even isolate?

    The fact is, you can separate HIV particles in the lab, we us the ultracentrifuge to extract HIV particles in the sample of a AIDS patient, and this fraction can be used to infect cell cultures and grow up more HIV particles.

    In addition, he seems to love propagating the false idea that all viruses can be isolated and viewed physically. Some of the more common viruses that afflict us such as the Human Papillomavirus and Epstein-Barr virus have also never been “physically isolated and visualised” to Wilhelm’s standards and whims.

    When he is shown micrographs of HIV, a few groups in the world that has successfully done so, he laughs it off as cartoons, not not once acknowledging the authenticity and the amount of work put into the mammoth technical difficulties of this achievement. What disrespect towards science.

    (3) His description of molecular methods such as PCR as nothing less than a method based on witches brews, or voodoo black magic, also highlights how far removed he is from current research. Molecular techniques have been around for decades, with the theory behind PCR validated clearly described. PCR is utilised in the most basic processes of manufacturing and human activity, such as in the production steps of insulin, creation of drought resistant crops, to forensic science. Yet Wilhelm has little idea what PCR is except “forensic chemist does it”

    (4) His description of basic cell culture methods is even more bewildering, as he seems to have no idea about the difficulty to grow primary human cells outside the body. Just one decade ago it was near impossible, it is the triumph in overcoming the many technical/biological hurdles in the formulation of the “witches brew” cell culture medium that enables us to mimic human physiological conditions that are able to coax cells to grow and divide in vitro. From personal experience, it is not easy to grow primary cells even with the avaible witches brew. And every other time these primary cells isolated from our body just refuses to grow.

    (5) In fact, Wilhelm should be proud of his friends, they’re the pioneers of in vitro protein synthesis, which is another technically massive hurdle, and the pioneering work was done throughout the 60s and 70s. It is not surprisingly they were unsuccessful, but it was thier unsuccessful attempts plus the work of pioneers like them that contributed to the wonders we see today, of superb productivity of in vitro protein synthesis we have today.

    (6) I am bemused to find Wilhelm’s statement

    and/or detection of HIV DNA using PCR I don’t doubt for a moment that you can find even the tiniest amounts of DNA with PCR. Forensic chemists do it all the time. But how could anybody know if that DNA was put there by HIV? I know they have sequenced lots of material. But in order to know where it came from, you must have a standard of comparison (HIV itself). LTR-gag sequences found only in HIV? How do they know? It was thought originally that Reverse Trascriptase was specific for retroviruses. Now we know that’s not so. A human body is a complicated machine. Lots of things can originate from it. Maybe also all those markers that are considered specific for HIV.

    It’s another indication of his ignorance in molecular biology or HIV research.

    A simple fact that these sequences, LTR, gag, tat, etc. can ONLY be isolated from AIDS HIV positive patients, those on HAART or “illicit drugs” if you may, and also those AIDS HIV positive persons who have no exposure to these drugs in Africa, Asia and the Oceanic island nations, BUT the same sequences that are not isolated from healthy HIV negative persons.

    The same observation can also be said for HIV specific proteins

    I am not going to waste my time explaining p24, if you’re interested seek out this review, suitable for lay persons http://www.theannals.com/cgi/content/abstract/27/4/450?maxtoshow=&HITS=&hits=&RESULTFORMAT=1&andorexacttitle=and&titleabstract=p24+antigen&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT

    Human reverse transcriptase? You must be joking. Even if we speculate that there might be a human reverse transcriptase yet to be described, a thorough look at human physiological processes discounts the need of a reverse transcriptase, so its plausible (science has yet to describe everything) but highly unlikely.

    A combination of all the tests I’ve described earlier that all shows positive for HIV infection is already sufficient correlation to pin HIV as a primary causative agent to AIDS. If you choose to suggest another contributing causative agent, or even a co-acting agent for AIDS, please show me the experimental evidence, or else refrain from speculation and passing it off as fact.

    In analogy, even convicting a person for murder in a court of law does not need as stringent a criteria as suggested by Wilhelm. As if we were to accept Wilhelm’s whims in proving HIV causes AIDS, it would be akin having the jury and the judge to personally witness the murder taking place to be able to reach a verdict, strong evidence such as blood stains, motive, murder weapon, witness account is irrelevant.

    To disregard the obvious relationship between HIV and AIDS is both denial and irresponsible. Irresponsible as you are spreading misinformation that can undermine the public health initiatives designed to curb the spread of the disease.

    I respect your right to dissent, but are totally appalled by you lack of a sense of social responsibility. I refrain from commenting on AZT because I have limited experience in the development and use of AZT to make a critical comment. I am trying to be responsible for my statements, but I do not see Hank nor Wilhelm sharing such sensibilities.

    They come out with half baked statements formulated from their ignorance or inexperience with certain subjects and research areas. They frequently mount dishonest and misleading arguments, on the false pretence of being an expert in these specialised research areas. Such an irresponsible actions serve only to confuse and mislead lay people like Frodo who are not equipped to look at the information with scientific analysis.

    If you disagree with the use of toxic AZT, which the scientific literature also clearly shows, campaign against its use, I will certainly support your cause. But you’re not helping anyone trying to deny HIV’s relationship with AIDS.

    I have spent way too much time away from my work trying to present useful facts and information to counter any misinformation. Obviously individuals like Hank and Wilhelm recalcitrant to evidence (no matter how clearly studied the evidence are) that do not support their beliefs.

    Do not expect me or anyone else who are involved in science to seriously consider your views until you can present me hard evidence contrary to the results I have seen and continue to see in front of me everyday in my lab. It does not take that much to finance a small scale pilot. Do not bemoan the lack of funding, as we know that to be able to secure funding like the NHMRC you need convincing preliminary results, NOT just the regurgitation of a perspective paper written a decade ago.

    I cannot afford to lose any more time trying to explain facts to persons not even willing to listen

    Hank you mentioned in your reply

    You have to look at the entire picture with an open mind. If you a priori fervently believe that HIV is a deadly virus and that the drugs save you, you cannot interpret the complex picture.

    I’ll end my involvement in the comments with this reply to you

    You have to look at the entire picture with an open mind. If you a priori fervently believe that HIV is NOT the deadly virus related to AIDS, and that anything else is the real causal agent, including illicit drugs, HAART, malnutrition, co-infection, government secret weapon, pharmaceutical sponsored drug evil scheme, many poor Africans/Asians who don’t take AZT or HAART but have AIDS and tested HIV positive must have acquired immunodeficiency by some other means BUT IT CANNOT BE HIV, you cannot interpret the complex picture.

  188. #188 Hank Barnes
    June 16, 2006

    Viji,

    I refrain from commenting on AZT because I have limited experience in the development and use of AZT to make a critical comment.

    Which means, despite your excessive verbosity, you are missing the primary element of the dispute.

    So, now who’s half-baked?:)

    Hank B

  189. #189 Gene Semon
    June 16, 2006

    “Human reverse transcriptase? You must be joking. Even if we speculate that there might be a human reverse transcriptase yet to be described, a thorough look at human physiological processes discounts the need of a reverse transcriptase, so its plausible (science has yet to describe everything) but highly unlikely.”

    Hank just directed me here and I found this more or less at random.

    This statement by Viji is astonishing in its ignorance. No less an authority than Stephen Jay Gould has described human reverse transcriptase and its physiological processes.

    “…discounts the need…”?! How about the evolution of the vertebrate immune system?

    Before you make a complete fool of yourself, Viji, look up Line 1.

    It’s way beyond speculation, friend.

    As far as p24, it’s a non-specific stress protein. Recent mainstream HIV research describes how different cellular proteins can associate with HIV genome.

    That’ all for now. I can’t wait to look at this entire thread.

    Gene Semon

  190. #190 Gene Semon
    June 16, 2006

    Hi Tara,

    Nice blog you’ve got going here. A lot of fun for us denialists looking for a life.

    Comments while taking a break from perusing this absolutely fascinating thread:

    Surely reason and science is something we can all hang on to. No argument. As far as some rote responses I’m already detecting as I proceed thru this wondrous thread; are they, strictly speaking, rational?

    Since you know NAR, what about it? The substantive point; did Gallo in fact falsify himself? He certainly DID succeed in the production of reverse transcriptase far beyond Montagnier. (Let’s give credit where credit is due.)

    Oh yeah, the rote responses: misinterpret the paper, poorly preserved samples, contamination etc., etc. to results or conclusions you don’t like.

    But let’s proceed to the substantive points in your response to Hank of June 6. Go to Gallo/fasify thread at NAR and, at the bottom you’ll see my citation of the Gallo et al cDNA HYBRIDIZATION experiments where the hit ratio is even lower. Remember, this has nothing at all to do with viral load; it’s a measure of PRIMARY HIV infection, the GOLD STANDARD, (and I’m not talking about Perth Group).

    Antibodies non-specific.

    I doubt if bad samples or my misinterpreting apply here so we’re looking for your best counter-argument.

    Cheers

  191. #191 Gene Semon
    June 16, 2006

    Hi Tara,

    Nice blog you’ve got going here. A lot of fun for us denialists looking for a life.

    Comments while taking a break from perusing this absolutely fascinating thread:

    Surely reason and science is something we can all hang on to. No argument. As far as some rote responses I’m already detecting as I proceed thru this wondrous thread; are they, strictly speaking, rational?

    Since you know NAR, what about it? The substantive point; did Gallo in fact falsify himself? He certainly DID succeed in the production of reverse transcriptase far beyond Montagnier. (Let’s give credit where credit is due.)

    Oh yeah, the rote responses: misinterpret the paper, poorly preserved samples, contamination etc., etc. to results or conclusions you don’t like.

    But let’s proceed to the substantive points in your response to Hank of June 6. Go to Gallo/fasify thread at NAR and, at the bottom you’ll see my citation of the Gallo et al cDNA HYBRIDIZATION experiments where the hit ratio is even lower. Remember, this has nothing at all to do with viral load; it’s a measure of PRIMARY HIV infection, the GOLD STANDARD, (and I’m not talking about Perth Group).

    Antibodies non-specific.

    I doubt if bad samples or my misinterpreting apply here so we’re looking for your best counter-argument.

    Cheers

  192. #192 Hank Barnes
    June 16, 2006

    Hey Gene,

    Here’s your quote re Gallo’s “follow-up” work.

    Shaw, Hahn, Arya, Groopman, Gallo, Wong-Staal; Science, V226, 1165-1171, 12/7/84

    “HTLV-III (pro)viral DNA can be detected in low levels in fresh (primary) lymhoid tissue of a minority of patients with AIDS or ARC but appears not to be present in Kaposi’s Sarcoma tissue.” (from Abstract)

    “We have described here the molecular cloning and analysis of the full-length HTLV-III proviral genome from the cell line H9/HTLV-III.”

    “In most of the patients in which HTLV-III DNA sequences were detected in fresh tissue, the signal intensities were weak”.

    “In all, HTLV-III sequences were detected in only 9 out of 65 (AIDS) patients evaluated (Table 1). . . None of the five Kaposi’s sarcoma tissue specimens was positive for HTLV-III DNA sequences.”

    Table 1 shows for “clinical diagnosis” of “AIDS (tissue) : 15 (peripheral blood mononuclear cells) samples tested, 1 positive; 19 (lymph node cells) samples tested, 4 positive; 8 (bone marrow mononuclear cells) samples tested, 0 positive; 11 (spleen) samples tested, 2 positive; 5 (Kaposi’s sarcoma) samples tested, 0 positive.” (Note: KS was original “signal” disease)

    ” . . . (A)s shown herein, HTLV-III DNA is usually not detected by standard Southern hybridization of these same tissues (from most patients with AIDS or ARC) and, when it is, the bands are often faint. . . (T)hus, the lymph node enlargement commonly found in ARC or AIDS patients cannot be due directly to the proliferation of HTLV-III infected cells.”

    Three questions, Gene:

    1. Why did Gallo find HIV (HTLV-III) sequences in ONLY 9 of 65 AIDS patients?

    2. What was causing AIDS in the OTHER 56 patients?

    3. Do these paltry findings support or undermine the hypothesis that AIDS is solely caused by HIV?

    HankB

  193. #193 Dale
    June 16, 2006

    1. Why did Gallo find HIV (HTLV-III) sequences in ONLY 9 of 65 AIDS patients?
    2. What was causing AIDS in the OTHER 56 patients?
    3. Do these paltry findings support or undermine the hypothesis that AIDS is solely caused by HIV?

    1. sensitivity of his assay. sequences found in FRESH tissues in only 9 of 65 but cultured cell lines could be derived from most. As the authors note, their data suggests that less than 1 in 10 cells is infected in many of these samples.
    2. HIV. see answer to 1.
    3. these findings, in conjunction with all the other data out there, support the hypothesis that HIV causes AIDS. Doesn’t really address the question of co-factors.

  194. #194 Gene Semon
    June 16, 2006

    A sex and blood pandemic, caused and transmitted by an AIDS virus, has never been demonstrated, any time, anywhere. All epidemiological “data”, and statistics derived therefrom are educated and not so educated guesses. In Africa and India, never validated mathematical models produce computerized hallucinations. In USA, better guesses show flat human retroviral prevalence contrasted with AIDS bell-shaped curves, which falsify HIV=>AIDS epidemiological claims. (3)

    To maintain the model of a pathogenic retrovirus, ad hoc multiple behavioral possibilities have been postulated and attributed to it; then described to laypersons as a wily, insidious virus with 9 heads and a Star Wars shield to boot. These many elaborations to explain ongoing observed subgenomic transcriptions and variations of the HIV genome arise from $150 billion of creative enthusiasm but can hardly be said to represent a scientific theory. In Scientific American, March, 2006, pg 76, Gregory Chaitin describes Leibniz: “(I)f the only law that describes some data is an extremely complicated one, then the data are actually lawless.” (2)

    Measuring 140 or so bp of the gag gene, as in a set of major PCR papers, is certainly sensitive, but for what? (1)

    We need to rethink AIDS in the light of peer-reviewed science that looks at malnutrition, poor infrastructure (e.g. the WHO declared pure water crisis) and chronic environmental diseases caused by pollution. (see chronicillnet.org, Howard Urnovitz, PhD). Retroviral transcription (“HIV”) is a method used by the cell to deal with excess stress – effect not cause. AID is a broad phenomenon, a symptom of environmental disease. S is severe redox imbalance caused by oxidosis (too many free radicals)/dysoxygenation (deranged cellular metabolic machinery) – serious energy deficiency: AED.

    Cheers

  195. #195 Hank Barnes
    June 16, 2006

    Hi Gene,

    Thanks a bunch. Interesting observations. Broad minded, anti-reductionist — I like ‘em:)

    Enjoy the weekend,

    Hank B

  196. #196 Viji
    June 16, 2006

    Interesting indeed, thank you Gene for providing some fresh highlights into some issues

    But I’ll need the references to substantiate the points you draw from in your comments to look further into them

    For example, you’ve commented on epedimiological studies, and labelled Indian and African studies to be weak (your interpretations, or you have a epidemiologist actually commenting and studying the African Indian data?), and presented guesses to interpret the US data (source? Your guesses and interpretations?)

    Certainly the current model of HIV-AIDS is based on a non-endogenous pathogenic retrovirus, an infectious agent that are blood borne. Such a description can change with further insights and inroads into our understanding of the aetiology of AIDS, but current research findings do indicate the presence of a non-endogenous pathogenic retrovirus in which we named HIV

    Similarly you’ve brought up the concept of “Retroviral transcription (“HIV”) is a method used by the cell to deal with excess stress – effect not cause.” and your references to studies pioneered by Howard Urnovitz may point to AIDS as a human physiological response to stress by producing a endogenous retrovirus or something akin to HERV-K, BUT still it shows the existance of a pathogenic infectious agent that can be transmitted, doesn’t it? The only difference is that this endogenous infectious agent is human derived.

    A simple observation that “human physiological stress derived endogenous infectious agent” positive blood when used in blood transfusion to a person who is other wise healthy or “human physiological stress derived endogenous infectious agent” negative, would soon become “human physiological stress derived endogenous infectious agent” positive, and go on to develop “human physiological stress derived endogenous infectious agent” “associated” AIDS

    It doesn’t seem to me very different from the aetiology of AIDS with HIV. Perhaps if that line of research shows promising results, we could rename HIV as “human physiological stress derived endogenous infectious agent” HPSDEIA

    And what we are certain is that current HAART treatment regimen, although not a cure for AIDS, and can often be associated with morbidity, suffering, and mortality not associated with AIDS, can reduce drastically the “human physiological stress derived endogenous infectious agent” loads (even when administered when the loads are high pre-treament), and prevent or delay a progression to AIDS.

    You were right to identify that AIDS is a chronic disease, chronic in the sense that HIV can evade clearance from the body. HAART can be sufficient to reduce HIV loads to near undetectable levels, but once HAART is removed, we see a rebound to pre-treatment levels as observed clinically. One possible reason for this “chronic” or “persistent” HIV infection is that HIV can remain dormant in the human genome (part of tis life cycle) very much like endogenous retrosequences, and the other is that HIV evades HAART in HAART inaccessible body sites, such as tissue macrophages, and beyond the blood brain barrier. I was part of the group pioneering this line of research, studying the human cellular splicing factors that is hijacked by HIV to be able to undergo chronic low level of replication in macrophages.

    Although HAART is just a band aid measure when what we need is an effective vaccine and total clearance of HIV, alot of the HIV research groups are pioneering work in these areas trying to improve the situation. If you insist on the HIV-AIDS phenomenon being stress derived, you may also embark on this line of research, it will certainly help to alleviate the problem, and contribute to our understanding of AIDS aetiology, BUT do not chide the efforts of others trying to solve the problem with available the available infromation at hand

  197. #197 Viji
    June 16, 2006

    Hey Gene, you are surely a cynical person. You wrote

    This statement by Viji is astonishing in its ignorance. No less an authority than Stephen Jay Gould has described human reverse transcriptase and its physiological processes.

    Hahaha, you are even as rude as refering me to “it”

    Anyway, that aside, have I made a fool of myself? Maybe I had, I could have missed a few recent developments or two, if so I do apologise for the misinterpretation based on my current understanding BUT

    a “human reverse transcriptase” would be interesting indeed! But its your bad for not even providing references or links so that I can chase on this

    But nonetheless, I’ve done a bit literature search on this “Stephen Jay Gould” via Google Scholar and Stanford University’s Highwire Press (Pubmed included),

    And I found only this
    “On “Genomenclature”: A Comprehensive (and Respectful) Taxonomy for Pseudogenes and Other “Junk DNA”
    Certainly not any hands on work that describes a human reverse transcriptase. I’ll need references if I should be able to read up human RTs

    Most of Stephen Jay Gould have been focused a lot on Paleobiology, Evolution theory, Science History-Politics-Religion, less little in the way of cell biology experiments etc. But that is based on the 90 articles I find using Highwire Press.

    Direct me to some hard references if you may, so that I can read about it

    Mayhaps, you have confused retrogenes for reverse transcriptase?

    Cheers

  198. #198 Wilhelm Godschalk
    June 16, 2006

    Dale:
    al-Bayati never performed an autopsy – he couldn’t have as he’s not a medical doctor and thus no qualified to perform autopsies.

    You’re mostly right about that. Although I would replace “not qualified” by “not authorized”. After all, he’s a pathologist. But that happens when a professional group appropriates the sole right to certain activities.

    And we know it’s retrovirus because the DNA sequences purified away from all cellular and proteins can be introduced into uninfected cells and will lead to the production of infectious virus. According to Peter Duesberg that’s about the most stringent test for a virus that anyone’s ever come up with.

    That’s exactly the part I can’t possibly agree with. How can you determine the presence an RNA-containing virus if you start out with DNA that is supposedly produced by this virus, and let this DNA replicate in a cell culture that contains who knows how many kinds of DNA on its own? Besides, there is no production of infectious virus, because from the supernatant of the cell culture nobody has isolated complete virus particles. “Virus-like particles” at best. vesicles probably). Sure, there may be something infectious, but that’s not unusual with DNA. Even when insects sting a plant, bacterial DNA may cause tumors at that spot.
    This whole “molecular cloning” business has never appealed to me. There are too many holes in that theory. I don’t know why Duesberg said that. Maybe he was joking; maybe it wasn’t his day.

    As far as how the early trials showed AZT helped patients…

    Well, of course it did. The early patients were also seriously ill. AZT has a strong cytotoxic action. It kills cells indiscriminately, including bacteria and fungi. So the short-term effect looks beneficial, because humans are more durable than bacteria. But in the long run, the patient succumbs, and the undertaker takes over.
    AZT is a remarkable drug: The less you take of it, the better it works.

    Viji:
    OK mate, you asked for it. Lucky for you, your present work has to do with bacterial systems. Your virus work on “HIV” was probably a youthful delinquency. I’ll forgive you for that; you’re safe now for the outraged mob, carrying axes and torches, when they come knocking at doors on Hatchet Day.
    They’ll probably pass your door now. Nevertheless, your last post was totally off the wall:

    Moreover, in the face of these hard research, you, Wilhelm Godschalk, and your clique of persons that does not believe in HIV, attempts to undermine the validity of these research by spreading misinformation with bizarre and false accusations like your statement that
    (1) “every study after Gallo is based on the assumption that HIV causes AIDS”

    It’s just too pathetic for words that scientists are working so hard on a line of inquiry that is so obviously wrong.
    Just take a paper at random, written jointly by 7 or more of these hard-working people. Read the Introduction, Materials and Methods, and Results. Stop there. At that point, remove all the references to “HIV”. Try not to even think about it. Then write your own Discussion section, based on what you have read. You’ll see that there is no need for “HIV” or any virus to explain the data. After you’ve done this, read the conclusions of the 7 dwarfs. You’ll laugh your ass off, guaranteed!

    HIV can be cultured from AIDS and HIV positive persons, but not found in healthy individuals

    No, it cannot! That’s what I’m trying to tell you all this time, but you’re so dense. Isolating HIV from AIDS patients or HIV+ persons has never been done. Sure, you can commit PCR on blood plasma, and amplify any genetic material in there, but calling this “viral load” is about as scientific as collecting signals from outer space, amplifying them, and claiming that it’s rock music from the Andromeda galaxy.
    You can only culture “HIV” (or whatever) in your witches’ brew (on which you’re probbly an expert). And who knows what’s in those cells to begin with?
    If you would take a few drops of the supernatant of the culture and put it in an analytical ultracentrifuge, it would become immediately obvious what kind of heterogenious crap you have there. Virus particles would produce one sharp peak. But I predict you would see a broad bell-shaped gaussian curve. But I’m dreaming. There probably isn’t even one analytical ultracentrifuge at the institute where you work. Not even anybody who knows what it is. Physical methods are not “in” anymore.

    similarly, definitive HIV markers such as RT activity, p24 antigen, HIV specific sequences has also been unfailingly shown to be present in AIDS HIV positive patients

    That’s what worries me. Lots of markers, no virus. In order to know for sure that these markers ar specific for HIV, you have to show at least once that they originate with the virus and nothing else. But if you don’t even have the pure virus…

    Wilhelm Godschalk’s reasoning in his attempt to disagree with “all research that does not agree with him” is even more bizarre, starting with his obsession that nothing is true until you can physically visualise or isolate the virus to the finest of details.

    Well, I would feel very uneasy (actually, I would feel like a fool) working on a “virus” I cannot isolate, and only exists in the tales I’ve heard from others. That’s plain old scientific skepsis. What’s bizarre about it?

    but did he tell anyone the fact this virus like the closely related TMV are atypically large viruses relative to retroviruses, which are so much harder to even isolate?

    I don’t think any plant virologist would call TYMV and TMV “closely related”. TMV is tubular, TYMV is icosahedral in shape. The hosts are different too. But maybe I’m nitpicking. But the second statement just plain wrong. TYMV is not “atypically large” There was at one time a discussion about its particle weight, but our group at Jesse Beams’lab at UVa. published the definitive paper on it: It’s 5.45 million Daltons. A typical retrovirus has a particle weight of about twice that. True, retroviruses are enveloped, and that doesn’t make isolation any easier. But if they could do it with mouse viruses. they should be able to do it for a human retrovirus, if such a beast exists. Good grief, they’ve had 22 years to do it!

    …we use the ultracentrifuge to extract HIV particles in the sample of a AIDS patient, and this fraction can be used to infect cell cultures and grow up more HIV particles.

    Yes, of course. But if you examine this fraction by electron microscopy before infecting your cell culture with it, you don’t find any virus particles! Neither did Montagnier or Gallo, but now, 22 years later you should be able to do better. And if you’re stubbornly insisting that there are virus particles in that 1.16 fraction, show me. No culturing, please, or other hanky panky.
    We really don’t base our criticism on faults in Gallo’s work only, but mainly on the failure of the other klojo’s that came after him, and not only were unable to do the isolation experiment right, but were even too pigheaded to recognize that the most plausible reason for not finding virus particles is simply that there are no virus particles.

    In addition, he seems to love propagating the false idea that all viruses can be isolated and viewed physically. Some of the more common viruses that afflict us such as the Human Papillomavirus and Epstein-Barr virus have also never been “physically isolated and visualised” to Wilhelm’s standards and whims.

    Whims? If I can’t see the Emperor’s clothes, then he’s naked. If they can’t isolate a virus, then it doesn’t exist. And you can take your Human Papillomavirus and… Well, sorry about that. But it wouldn’t even hurt, if it doesn’t exist anyway.

    When he is shown micrographs of HIV, a few groups in the world that has successfully done so, he laughs it off as cartoons

    Only when they are cartoons, in living color. There are a few real EM’s around. Most of them show more crappola than “viruslike particles”. I have seen a few picture that looked real. In the famous Gelderblom paper, for example. Hans Gelderlom knows his stuff, and he delivers fine work. But my suspicions are aroused when I look in the Materials and Methods section. Somehow the guys who handed him the sample don’t impress me. They don’t seem either too bright or too honest to me. So I look at the pictures and say: “Nice particles. What are they?”

    Yet Wilhelm has little idea what PCR is except “forensic chemist does it”

    [groann!!] Let me try to explain this one more time, slowly:
    When forensic chemists find a minuscule amount of DNA, too small to be analyzed, they use PCR to amplify stretches of it. When they have turned enough PCR cycles to get a quantity that can be analyzed, they compare it with a bank of known DNA profiles. If the perpetrator is in this collection, his goose is cooked. If he is not, the investigators have a problem.
    Now compare this to an HIV-hack, searching for proviral DNA in a vict… I mean patient. PCR does the job, and the resulting DNA is analyzed. And then… eh… well… harrumph!… The results have to be compared to “known proviral DNA originating from HIV” Do you see the problem appearing on the horizon already?

    In fact, Wilhelm should be proud of his friends, they’re the pioneers of in vitro protein synthesis, which is another technically massive hurdle,

    Our biochemistry lab was meeting place of chemists and biologists. Both groups had totally different methods, but they learned from each other. I would have been more proud of them if they had believed my “old shoe theory”, rather than that ridiculous script of ribosomes “rolling” along a molecule of messenger-RNA.

    A simple fact that these sequences, LTR, gag, tat, etc. can ONLY be isolated from AIDS HIV positive patients, those on HAART or “illicit drugs” if you may, and also those AIDS HIV positive persons who have no exposure to these drugs in Africa, Asia and the Oceanic island nations

    Summarizing: ONLY from sick people. Not so surprising.
    And please don’t compare the undernourished and malaria-ridden people of the third-world countries with the drug users of the developed nations. AIDS in Africa is something entirely different from AIDS in San Francisco.
    But now that we’re on the subject: When did they prove that LTR, gag, tat, etc are viral? Or is it just folklore, being carried down from generation to generation?

    I am not going to waste my time explaining p24, if you’re interested seek out this review, suitable for lay persons

    Holy shit! You’re so far off on p24 that I’m breaking out in hives. You’re quoting an abstract that only looks at p24 through tunnel vision, as a diagnostic for HIV. And their conclusion is even that they’re not sure if it’s any good.
    It’s hardly possible,but… don’t you REALLY know that the p24 protein family has a function in cargo selection for vesicle transport across membranes? I know people in “HIV science” wold rather not hear about vesicles. But jut in case you want to be a real scientist, read all about it:
    This is a paper from MIT.

    Thinking about p24 proteins

    Human reverse transcriptase? You must be joking. Even if we speculate that there might be a human reverse transcriptase yet to be described, a thorough look at human physiological processes discounts the need of a reverse transcriptase

    Well, Gene Semon already washed your ears on this booboo. You couldn’t have put your foot in your mouth any further.
    Reverse transcriptase is omnipresent in human cells. Not needed? Well, perhaps as a repair mechanism for DNA strands?

    In conclusion:
    Gallo’s work was lousy, that’s true. But it has been downhill from there ever since.
    Face it Viji, when you worked on HIV, maybe you were still young and foolish. Not anymore now… ;-)
    You were instructed by charlatans who made you believe you were doing useful work. In reality you were unwittingly contributing to their scheme of genocide.

  199. #199 Viji
    June 16, 2006

    Oops…. Gene,

    Hahaha, you are even as rude as refering me to “it”

    I misread the sentence. My bad, apologies.

    Hank, I’ve read enough publications about AZT to know about its toxic side effects, and know that the toxic side affects are significant enough to suggests a reappraisal of its use in HIV therapy, or maybe relegate or limit its use to extreme cases of infection.

    I refrain from commenting anything about AZTs, as I do not work on AZT’s mechanics, or its properties, or mode of action, PKs, PDs, therefore I refrain from speculating if (in Hank’s word) AZT can create the symptoms of AIDS, A good example is the dramatic loss of T-lymphocytes. Certainly I do not know of any studies that indicate AZT is the reason behind the dramatic loss of T-cells. Therefore I do not wish to post any misleading comments. Unlike you.

    Sure, AZT is a primary of the dispute, but I also know enough about AZT to know it would not cause the T-cell loss phenomenon reminiscent of AIDS. Coupled with my hands-on experience working with HIV samples that definitely provide a strong correlation between HIV and the loss of T-cells reminiscent of AIDS. I do not believe that HIV has no contributions to the development of AIDS.

    And they are plenty of studies out there that support my views and observations. A simple search on Highwire Press of PubMed would also give you too many studies that its ardous to read it all.

    Be reasonable when you come up with half-baked nonsensical rebuttals

    I am even giving you the benefit of doubt by not questioning the fact that you are not a fellow science researcher of any kind, but I think you may be intelligent enough and read widely enough to put forth sound interpretations of your readings. So do not do yourself this misfavour by presenting half baked and skewed ideas, and ironically questioning the intelligence of other people.

    Cheers

  200. #200 Wi;helm Godschalk
    June 16, 2006

    Viji:

    You asked Gene for a reference on human reverse transcriptase.
    Here is one:

    Telomerase

  201. #201 Viji
    June 17, 2006

    Again Wilhelm has outdone himself once more, posting ad-hoc arguments against any experimental results that are contrary to his ideas (never facts)

    Summise to say, he is like a judge or jury that needs to see the murder taking place in his own eyes to prove a murderer, anything else is conspiracy or fallacy.

    True, HIV has never been isolated straight from the body (in Wilhelm’s world), put on the microscope, and scrutinised with Wilhelm’s eyes. That’s Wilhelm whims. He seems to be very knowledgable but fails to tell people it is already immensely difficult to culture environmental viruses and view them according to Wilhelm’s standards, what can we say when its an obligate blood borne, human immune cell dependant retrovirus like HIV, that goes “poof” literally if exposed to the open environment without a protective medium like blood

    THAT is precisely why, predecessors in the study of HIV has formulated a method to “capture” these blood borne viruses in primary cell lines, by tricking the HIV to replicate in the very cells they can infect (harvested from healthy human blood on the day of the experiment – perfectly natural), concentrate these cells tio concentrate the virus, and store them in medium that mimics the protective effect of blood. And what does Wilhelm do? He mocks and ridicules such a breakthrough by looping/replaying his contentions that everything is witches brew, when I’ve already clearly summarised before that everything in the special “cell culture mediums” are found in us humans, nothing dodgy. Clear Wilhelm has little or no idea of cell culture, just his obsession with his work on centrifuge physical methods thats applicable to some plant viruses like TYMV, which in actual fact is totally different with the characteristics of blood borne viruses like HIV

    I should add that I could have isolated HIV from AIDS or HIV postitive individuals, from their blood, separating the virus particles using low temperature ultracentrifugation, and using the fraction to infect primary cells harvested from healthy individuals (I STRESS HEALTHY, NOT AIDS patients), end result, I get lots and lots of viruses, test them using HIV markers and for the presence of HIV specific sequences, and identify them as HIV. A CONTROL cell culture WITHOUT the added HIV fractions, BUT USING the same “withches brew” shows negative for all the HIV testing methods. I think that is enough to tell be the strong correlation between HIV and AIDS in the patients.

    I do not why Wilhelm wishes to press ahead with isolating a live virus by spinning it down in a centrifuge and visualising it under the microscope. Perhaps it can be done, but I postulate that the first step is that we would have to drain the blood from a AIDS patient, to be able to get enough starting material, to increase the chances of capturing the virus that grows in specific cells in human blood, and totally hates the enternal environment. Wilhelm could embark on such a mission if he so wishes, but it would be waste of time AND money, since a less complicated and successcul method via cell cultures are already available

    And I should also stress that the HIV specific proteins and sequences so forth mentioned is painstakingly tested and retested from samples taken from people afflicted with AIDS and determined to be specific to HIV. IF Wilhelm’s wishes to be impossible top the fact that HIV has to do with AIDS, the very least we could definitely say is that these sequences and proteins have a strong correlation with AIDs

    And I do not know where Wilhelm gets the bizarre idea that African HIV and their US cousins are different. Another ad-hoc misdirection. Yeah, AGAIN TRYING to use malnutrition and malaria as excuses. Fine if you’re being so recalcitrant, how about the case of a healthy sportsman or a child who contracted HIV from HIV-tainted blood?

    So what if p24 protein family has a function in cargo selection for vesicle transport across membranes? HIV utilises/hijacks this human physiological function to meet its own life cycle ends. That is why p24 is used as a HIV marker, SO what if p24 can be found in healthy non AIDS humans, during HIV infection it is elevated, thats how we detemine the presence of HIV, silly Wilhelm. and I STRESS that tests in the labs base determination of HIV not on p24 tests only, but complementary-double confirm tests like the ones I’ve mentioned.

    Gene have yet to show me his reference on his human reverse transciptase statement. AND even so, healthy individuals and CONTROL CELL CULTURES (NO ADDED HIV but with witches brew) show no positievs for the HIV RT tests.

    At least the scientist studying HIV is working their asses off, with little renumeration I may add, to pursue a solution to the HIV problem, using the available empirical research results at hand, we may someday be proven to be working on the wrong line of inquiry, but at least we are trying our best with the available data,

    In contrast, I only little contribution from Wilhelm, other than mocking scientific breakthroughs, arguing for the sake of arguing, unreasonably belittling peers, spreading misinformation, and worse wasting my time. If HIV denialists hope to contribute, they have better avenues to advance public health by supporting research contrary to the mainstream views and coming up with workable preliminary experimental data that can be build upon, not muddling everything by spreading misinformation, complaining, using smear campaigns to discredit sound experimental data, deliberately cherry picking information and disregarding anything else, and a lot of times profiteering from books and publicity rather tahn putting the money and effort into hard research.

    I am already regretting having followed this blog piece, as it has taken way too much time away from the work I am doing to help in every little way I can to advance research against infectious diseases. I started commenting when I see all the misinformation and its underlying consequences to public health. Clearly these people are just recalcitrant. Worse, if I stop commenting, I run the risk of misinformation being taken as facts by people not equipped to read the science.

    Wilhelm, stop complaining, if you are interested with proving us wrong, I know you have the expertise to pursue this line of research, like Chris Noble highlighted proove that HIV has nothing to do with AIDS, and come out with results that can reconcile with observations thus far. Don;t waste time complaining. If you think of yourself as my senior, use hard scientific evidence to direct me if you think I am following the wrong path, if not tone down your rude arguments until you do so.
    Sign

  202. #202 Viji
    June 17, 2006

    O dear…. Wilhelm has just shown me that he thinks telomerase are reverse transciptase!!!!

    All along I was thought you were mentioning viral reverse transcriptase or a human equivalent of the viral form

    The two, telomerase and viral reverse transcriptase may share a similar kind of end function generating a DNA strand from an RNA template

    BUT they are totally different both in crystallographic structure and function mechanism

    In anyway you try you won;t be able to even make a “HIV” DNA strand from a “HIV” RNA template using telomerases

    I am putting “HIV” in brackets as I am refering to LTR-gag sequences that you don’t believe to be from HIV per se but are of human origin (still telomerase can;t do anything on LTR-gag)

    And Certainly the RT-assay for HIV shows no positives if you throw in telomerases, it may only detect HIV derived reverse transciptases.

    Silly

  203. #203 Darin Brown
    June 17, 2006

    “Bearing in mind the tone of Bialy’s “invitation”, I can further see why Moore might decline in less than polite terms. Just my opinion of course.”

    Actually, Bialy’s tone apparently had nothing to do with Moore’s declining to debate…it would appear to be more related to Moore’s steadily declining mental state, as can be read at

    http://www.reviewingaids.org/awiki/index.php/Document:The_Professor%27s_Post-TKO_Press_Conference

  204. #204 Darin Brown
    June 17, 2006

    Bialy rocks LIBRadio:

    http://bialystocker.net/files/keidi.mp3

    Check it out; you might learn something.

  205. #205 Dale
    June 17, 2006

    Actually, Bialy’s tone apparently had nothing to do with Moore’s declining to debate…it would appear to be more related to Moore’s steadily declining mental state, as can be read at

    I would agree that correspondance would seem to indicate a declining mental state but would disagree about whose mental state appears questionable.

    Wilhelm wrote As far as how the early trials showed AZT helped patients…
    Well, of course it did.
    So we agree, Wilhelm, that monotherapy AZT was beneficial to AIDS patients in the short term.

    Wilhelm further wrote Sure, there may be something infectious in response to my comment about how the HIV sequences identified in HIV seropositive patients are shown to be viral in nature. Seems we agree on the basic point here as well; namely that the sequences identified as HIV represent an infectious agent.

  206. #206 Gene Semon
    June 17, 2006

    Fine, Viji, but you were the one who said “…a thorough look at human physiological processes…” which presumably includes the human genome – (haha).

    Here’s one I’ve entitled: The Plot Thickens; Adam Pavlíek,1,2 Jan Paes,1,3 Daniel Elleder,1 and Jií Hejnar1,4. Processed Pseudogenes of Human Endogenous Retroviruses Generated by LINEs: Their Integration, Stability, and Distribution. Genome Research, Vol. 12, Issue 3, 391-399, March 2002 (www.genome.org)

    Abstract:We report here the presence of numerous processed pseudogenes derived from the W family of endogenous retroviruses in the human genome. These pseudogenes are structurally colinear with the retroviral mRNA followed by a poly(A) tail. Our analysis of insertion sites of HERV-W processed pseudogenes shows a strong preference for the insertion motif of long interspersed nuclear element (LINE) retrotransposons. The genomic distribution, stability during evolution, and frequent truncations at the 5′ end resemble those of the pseudogenes generated by LINEs. We therefore suggest that HERV-W processed pseudogenes arose by multiple and independent LINE-mediated retrotransposition of retroviral mRNA. These data document that the majority of HERV-W copies are actually nontranscribed promoterless pseudogenes. The current search for HERV-Ws associated with several human diseases should concentrate on a small subset of transcriptionally competent elements.

    Excerpts:

    LINEs, retrotransposons lacking LTRs and containing poly(A) tails, are the most active autonomous transposable elements in the human genome (Kazazian and Moran 1998; Prak and Kazazian 2000). They are estimated to be present in >500,000 copies, comprising 17% of the genome (Smit 1996a, 1999; International Human Genome Sequencing Consortium 2001). However, due to 5′ truncations and deleterious mutations, only 30-60 LINEs per haploid genome are ACTIVE* and transpose along the genome (Sassaman et al 1997; Kazazian 1999; The database of Retrotransposon Insertion into the Human Genome (*Emphasis Added)

    Later, this endogenous reverse transcriptase activity was shown to generate processed pseudogenes also from nonviral (non-LTR) constructs in somatic HeLa cells (Maestre et al. 1995).

    LINEs are the master mobile elements in the human genome.

    END EXCERPTS

    (This last the idea that Gould signed onto in collaboration with a specialist in this field, Jurgen Brosius)

    BTW, pursue the Brosius line: Retroposition – A Persistent and Pervasive Force in Genome Evolution, (http://www.ornl.gov/sci/techresources/meetings/bits2000/abstracts/brosius.shtml)

    As far as telomerase, it equals reverse transcriptase (RNA=>DNA transcription function) + RNA template. It has been phylogenetically traced by Eikbush et al from LTR retrotransposons.

    Sorry about the “fool” comment. It kind of burst out of me when I first landed here, before I had a chance to read your post. No doubt, you would eat me alive in discussion of infectious bacteria.

    Best regards,
    Gene

  207. #207 Gene Semon
    June 17, 2006

    On p24

    I can’t improve on the Perth Group:

    “…to date nobody has proven that p24 is an “HIV” protein. To the contrary, there is ample data that p24 is a
    cellular protein.(11,63-66) Two of the best known experts of HIV and HIV testing, Jörg Schupbach, the principle author of one of Gallo’s 1984 Science papers where isolation of HIV was claimed, and Philip Mortimer, the Director of the UK Public Health Laboratory Service, do not consider the reaction between the p24 antibody and antigens in cell cultures as HIV specific. Using cultures of unfractionated blood and defining detection of p24 as virus isolation, HIV has been “isolated” from 49/60 (82%) of “presumably uninfected, but serologically indeterminate” individuals and in 5/5 ‘seronegative blood donors’. (67) According to Mortimer, ‘Experience has shown that neither HIV culture nor tests for p24 antigen are of much value in diagnostic testing. They may be insensitive and/or non-specific’. (40) Significantly, using monoclonal antibody to p24, the p24 protein (as well as the p120 and p18 HIV proteins), has been identified in normal, non-HIVinfected placentas, especially “in [chorionic] villi with immunopathological evidence of villitis”. (66)

    11. Papadopulos-Eleopulos E, Turner VF. (1994). Deconstructing AIDS in Africa. The Independent Monthly 50-
    51.
    63. Schupbach J, Popovic M, Gilden RV, Gonda MA, Sarngadharan MG, Gallo RC. (1984). Serological analysis
    of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science 224:503-
    505.
    64. Maddox J. (1992). More on Gallo and Popovic. Nature 357:107-109.
    65. Culliton BJ. (1990). Inside the Gallo Probe. Science 248:1494-1498.
    66. Francis DP. The search for the cause. (1983). p. 137-150 In: The AIDS epidemic Cahill KM, ed 1st ed
    Hutchinson Publishing Group, Melbourne.
    67. Gallo RC, Sarin PS, Kramarsky B, Salahuddin Z, Markham P, Popovic M. (1986). First isolation of HTLVIII.
    Nature 321:119.
    40.Mortimer P, Codd A, Connolly J et al (1992). Towards error free HIV diagnosis: notes on laboratory practice. Public Health Service Microbiology Digest 9: 61-64

    Stay tuned for more on telomerase, LTR retrotransposons and DNA repair! Are the blasphemers and scoffers actually going to dare to bring up such verboten subjects as oxidative stress and telomeres? Does the cell have an emergency repair system involving reverse transcription? We mere mortals tremble and shake at the very thoughts.

  208. #208 Dan
    June 17, 2006

    Stay tuned for more on telomerase, LTR retrotransposons and DNA repair! Are the blasphemers and scoffers actually going to dare to bring up such verboten subjects as oxidative stress and telomeres? Does the cell have an emergency repair system involving reverse transcription? We mere mortals tremble and shake at the very thoughts.

    While you nerds duke it out, the rest of us will attempt to simply live.

    Although, if the “HIV”-protagonists continue with their medical eugenics campaign, less and less of us are not allowed the luxury of simply living.

  209. #209 Dan
    June 17, 2006

    Although, if the “HIV”-protagonists continue with their medical eugenics campaign, less and less of us are allowed the luxury of simply living.

    Whoops. You know this is what I meant to say.

  210. #210 viji
    June 17, 2006

    Hello Gene, Thanks for providing the informative links, and indeed this is the most constructive way to communicate ideas and perspectives as opposed to the ruffian ways of using accusations and false stereotyping as evident in Dans latests post June 17, 2006 01:49 PM AND June 17, 2006 02:00 PM; useless mutterings at the only people trying to help. Eugenics Dan says, what does it have to do with Eugenics, he clearly have no idea that what Gene highlighted above is only about what we are beginning to understand about complex cell biology. Pls. refrain from commenting unless you’ve made an effort to understand the science. You’re making a fool of yourself.

    Anyway Gene, I am aware of the presence of retrotransposons*, i.e. LINES and SINES, in the human genome, and have read about how some of these active autonomous transposable elements* can show endogenous* reverse transcriptase activity* to activate some of the pseudogenes* I am a Molecular Biology and Biotechnology major during my university days, these were in the dreaded exams.

    Anyway, I am certainly new to the HERV-W processed pseudogenes showing strong preference for the insertion motif of LINEs, and thanks for the reference.

    In any case, I was originally implying that we currently DO NOT KNOW OF any human reverse transcriptase (in that I mean the viral RT enzyme not retrotransposons) EQUIVALENT to viral reverse transciptase. Certainly you know the distinct structural and mechanical difference between the viral RT and retrotransoposons such as LINE, although the functional end point is reverse transcription.

    (certainly not HIV reverse transcriptase enzyme that has a magnesium preference for its activity, unique from the usual manganese preference for other “free-living” retroviruses, which are not retrotransposons or retroelements found in genomes, indeed retroviruses insert their DNA into the human genome during their life cycle, very much akin retrotransposons (hence the namesake of retrotransposons), HIV does this in order to hijack human physiological processes for its own replication, this insertion is transient, and at the end of the life cycle there is a free-standing virus particle, as opposed to retrotransposons being inserted in the genome)

    In fact you have correctly pointed out that, I QUOTE

    LINEs, retrotransposons lacking LTRs and containing poly(A) tails, are the most active autonomous transposable elements in the human genome (Kazazian and Moran 1998; Prak and Kazazian 2000).

    Later, this endogenous reverse transcriptase activity was shown to generate processed pseudogenes also from nonviral (non-LTR) constructs in somatic HeLa cells (Maestre et al. 1995).

    These pseudogenes are structurally colinear with the retroviral mRNA followed by a poly(A) tail.

    Some fundamental differences between viral RT and retrotransposons, for example,

    Retroviral RT enzyme recognises the LTR (Long Tandem Repeat) sequence as the marker or starting point to begin reverse transcription activity. HIV for example hijacks human splicing factors to splice out a subset of different viral DNA to give a subset of different viral products.

    While I think retrotranposons recognises the poly-A tail of the HERV-W pseudogene family, or the nonviral (non-LTR) constructs in somatic HeLa cells, to initiate reverse transciption activity, very much like the telomerase recognises the poly-A tail and initiate reverse transcription activity (as Wilhelm has kindly referenced us to earlier)

    I am sorry for not clearly pointing out what I meant when there are no human equivalents of viral reverse transcriptase enzyme.

    Lay man terms**
    Reverse transcriptase activity: Able to read RNA and translate into DNA; usual gene expression processes read DNA to mRNA to proteins to expressed phenotype
    Endogenous: Naturally occuring in the human body
    Retrotranposons-active autonomous transposable elements: bits of sequences that are part of the human genome that has the ability to move around autonomously and insert itself in positions of its choice along the near vicinity of the genome it was originally located
    Pseudogenes: Silent or not expressed genes, genes that are usually not part of the human physiological processes programs, some speculate that these pseudogenes are ancient genes inactivated sometime along our climb in evolution, error expression of some pseudogenes have been suggested to cause some forms of cancer

  211. #211 viji
    June 17, 2006

    Gene,

    As for p24, they’ve correctly described the p24 as I QUOTE

    “…to date nobody has proven that p24 is an “HIV” protein. To the contrary, there is ample data that p24 is a
    cellular protein.(11,63-66) Two of the best known experts of HIV and HIV testing, Jörg

    As I mentioned earlier

    p24 protein family has a function in cargo selection for vesicle transport across membranes

    HIV hijacks the normal human physiological “vesicle transport across membrane” towards its own life cycle ends, when newly replicated virus particles need to escape the host cell, they hijacks this normal cell function to “bud” out of the host cell in a vesicle.

    I know that p24 antigen marker were used in the early days of HIV tests used because investigators observed a significant difference in p24 antigen levels between HIV seropositive and HIV seronegative. Presumably our understanding of p24 protein family in humans were little and far in between during the heydays of cell biology and HIV research.

    And understandably, the early tests can be indeterminate and inaccurate at times, because the tests are based upon one part of the HIV life cycle

    Now that we’ve identified p24 homologies in humans too, perhaps that is why the Perth Group found “positive” p24 antigen tests in from 49/60 (82%) of “presumably uninfected, but serologically indeterminate” individuals and in 5/5 ‘seronegative blood donors'”.

    I would refrain from commenting too much. I did not develop the p24 antigen tests and I do not know the threshold value (how high the p24 antigen level shall be before we are confident that the high value is attributable to HIV infection) to differentiate between a definite postitive or negative outcome.

    What I do know is that from what we have learned in cell biology and HIV biology so far, p24 antigen tests are no longer used solely to test for HIV in labs, but a combined diagnostic approach using p24 antigen test, RT activity tests, Western blot for HIV proteins, and PCR amplification and identification of HIV DNA, is used in tandem to determine the diagnostic outcome in labs. I am not sure if the p24 antigen tests are still being used solely to tests for HIV infection in routine health checks.

  212. #212 Dan
    June 17, 2006

    refrain from commenting unless you’ve made an effort to understand the science. You’re making a fool of yourself

    I’ll comment as I please, Viji…especially around HIV protagonists such as yourself. I’ve had to fight for my right to simply live against the likes of “scientists” like you. I’ll continue to fight you bastards. Go to hell, fuckwad.

  213. #213 *Sigh*bomb
    June 18, 2006

    Dan!

    You know that f-wads cause AIDS! You can isolate f-wads in duck urine, then you test negros for antibodies to duck urine and you see, F-wads cause AIDS!

    *Sigh*

    *Yawn*

    *Sigh*

    Dan!

    What do you mean, fighting for your right to live? Everybody knows little fairies have to die because scientists looooooove them soooo much.

    Like they loooooooove n-word people too, that’s why they like to save their lives with fun prizes like Glaxo Charms and Abbot-berry cereal!

    Yay!

  214. #214 viji
    June 18, 2006

    What is f-wads?

  215. #215 viji
    June 18, 2006

    n-word?

  216. #216 viji
    June 18, 2006

    I give up, if Dan intends to act like a bad-mouth ruffian, an impossible child, a fool, a rabble, and a paranoid conspiracy theorist, its Dan’s right to be slanderous too. it’s Dan’s choice.

    Completely no appreciation of science, manners, goodwill, or reason. Just rabble and babble. That’s Dan’s choice. Not mine.

    Have a good one, live in your own Dan’s world, you’ve earned it
    viji

  217. #217 Dan
    June 18, 2006

    Viji,
    unless Tara deletes my posts or closes this thread, I’ll continue to be part of the “conversation”.

    You can call me whatever you like, it’s your right. I think you’re just a wee bit miffed, because unlike other gay men, I don’t see haloes floating over the heads of people involved in “HIV” research. If more gay men took away those haloes, this “AIDS” sham would soon be over with. Unfortunately, for gay men to rid you folks of your haloes, they have to first realize that they’ve placed them atop your pointed heads. I’m working on that one…

  218. #218 Sigh-bomb
    June 18, 2006

    Ruffians? Rabble? Oh Veejeee, you so gay.

    Tuffin up little muffin. Dan the “ruffian” won’t stop you from killing gay men, just from killing him? Get it? F-wad?

    *SIGH* *YAWN* Pointy-head “Rabble!”

  219. #219 *Sigh*bomb
    June 18, 2006

    * AIDS Science – Sex-death Religion
    * AIDSTheory – Viral Dogma
    * Conference Hall – Church of the Inquisition
    * HIV – The MacGuffin
    * David Ho – who?
    * AZT, ddI, Protease Inhibitors, Nevirapine – Nastyass shit
    * David Baltimore – Asshole
    * Anthony Fauci – Ceo of Aids inc
    * Robert Gallo – court jester
    * NIH Granting Process – ballsuck olympics
    * Activists – moonies
    * Patients – Penitents
    * Taxpayer support – Vatican holdings and collections
    * Paradigm critics – Heretics
    * Canceled funding – “We don’t want to look at these possiblities”
    * Evidence overwhelmingly against – See Thomas Kuhn
    * All objections converted to supporting evidence – You have sand in your vagina.

  220. #220 Wilhelm Godschalk
    June 18, 2006

    Viji:
    Summise to say, he is like a judge or jury that needs to see the murder taking place in his own eyes to prove a murderer, anything else is conspiracy or fallacy.

    It may seem strange to you, but things are (or at last should be) like that in science. After a researcher has passed peer review and published a paper about something that may be hard to believe by others, soon there are letters and phone calls arriving with requests for more information. The original researcher then sends out instructions to colleagues as to how they can do the same experiments themselves. And those who are not equipped for it, get an invitation to come to the researcher’s lab. to see the experiments carried out right before their eyes. That’s how you build up credibility.

    what can we say when its an obligate blood borne, human immune cell dependant retrovirus like HIV, that goes “poof” literally if exposed to the open environment without a protective medium like blood

    OK, I grant you that it’s difficult. But that leads us to the question: How can a virus that goes “poof” when exposed to an open environment possibly be an exogenous infectious agent? HIV is supposed to be a contagion leading to a real epidemic, remember?

    He mocks and ridicules such a breakthrough by looping/replaying his contentions that everything is witches brew, when I’ve already clearly summarised before that everything in the special “cell culture mediums” are found in us humans, nothing dodgy.

    Yes, they can culture in cancerous T4 cells called Jurkats (I’ve never used them, but Nick Bennett told me about them). According to what I was told, these Jurkats don’t need stimulation with PHA; that’s old hat. Nevertheless, I just read some very recent papers, and they were still using PHA for stimulation. Now everyone who reads this will ask: Why doesn’t HIV destroy these cell cultures, as T4 cells are said to be the natural point of attack by the virus? Doesn’t that raise any doubts in your mind? (Oh well, it doesn’t of course. You have been told by your sponsors never to have any doubts).
    Let’s not forget that in cell cultures you are working with live cells. They have their own metabolism and reproduction machinery. So they can spring some surprises on you. With an isolated virus preparation it’s possible to have far more control over your experiments.

    Clear Wilhelm has little or no idea of cell culture, just his obsession with his work on centrifuge physical methods thats applicable to some plant viruses like TYMV, which in actual fact is totally different with the characteristics of blood borne viruses like HIV

    Not only Ultracentrifugation. I also used Polarography, Potentiometric titrations, UV Spectrophotometry, Fluorimetry, and other physical methods.
    It doesn’t make any difference in the centrifuge if you have TYMV or a virus like HIV. Ultracentrifugation only sees particles that have a certain sedimentation coefficient and partial specific volume.

    And I do not know where Wilhelm gets the bizarre idea that African HIV and their US cousins are different.

    Bizarre? I think it’s a very logical conclusion. The first AIDS cases were clustered in the gay community. And after 25 years, the syndrome is still mainly concentrated in the “high risk groups”. At first, the “HIV-test” was not even used in Africa. All they needed was sick people. Well, they are easy to find, because there are many endemic diseases among the poor people of Africa. You only have to get diarrhea and/or fever for several days (very common), and you’re already branded as an AIDS patient.
    Sure, the toxic meds seem to help at first. They kill off all the bacterial and fungal infections. And… When these people are treated, they also feed them. Now is it so surprising that the patients react positively to that?
    But in the long run, these poor sould are simply bumped off by the toxic drugs. Why? Because they’re black, maybe?

    I should add that I could have isolated HIV from AIDS or HIV postitive individuals,

    Why didn’t you? It would have made you world-famous.
    But you used only markers. They may occur in sick people, but they are not specific for “HIV”.

    Fine if you’re being so recalcitrant, how about the case of a healthy sportsman or a child who contracted HIV from HIV-tainted blood?

    Are you referring to Magic Johnson? He announced many years ago with much drum-beating that he was seropositive. Nothing bad has happened to him since. If he had used the antiretrovirals, he would be dead by now. He probably never used them, but gets paid to say he does. He’s not a very reliable character.
    And a child? Never heard of such a case. Only about children in Africa being murdered with Nevirapine.

    That is why p24 is used as a HIV marker, SO what if p24 can be found in healthy non AIDS humans, during HIV infection it is elevated, thats how we detemine the presence of HIV, silly Wilhelm.

    I’m flabbergasted. This is meant to be a scientific argument? I invite everybody to read this statement closely, and judge for him/herself who’s being silly here.

    At least the scientist studying HIV is working their asses off, with little renumeration I may add, to pursue a solution to the HIV problem, using the available empirical research results at hand, we may someday be proven to be working on the wrong line of inquiry, but at least we are trying our best with the available data,

    Yes. To the tune of… how many billions of dollars? Oh, I know you’re not getting any of the big money, but the funding for “AIDS” is an outrage, compared to what’s spent on real diseases. Even if “AIDS” existed as a separate disease,it would be still completely insignificant compared to Heart Disease and Cancer.
    I don’t mind scientists working on the wrong line of enquiry, but I bemoan the fact that other directions are not funded at all.

    If HIV denialists hope to contribute, they have better avenues to advance public health by supporting research contrary to the mainstream views and coming up with workable preliminary experimental data that can be build upon,

    No, they don’t. I pointed out already that there is absolutely no funding for No-HIV AIDS research. Even Peter Duesberg, a member of the National Academy, cannot get any research money for AIDS. But the people who should definitely get funded to come up with fresh and unadulterated ideas are the toxicologists and the pharmacologists.

    …and a lot of times profiteering from books and publicity rather tahn putting the money and effort into hard research.

    Again: Who will pay for it? Even the janitor who sweeps up the lab, won’t work for nothing.
    Until the day the whole HIV/AIDS paradigm collapses, or I win 100 million euros in the lottery (whichever comes first), there won’t be a chance to do serious research
    So until that day, all I can do is complaining. I’m sorry if you find my arguments rude. But, you know, sometimes people run out of patience and blow up. That obviously happened to Dan. He was there when it all started to happen. And he is not joking when he is saying he’s fighting for his right to live. On the basis of those wacky “HIV tests” some of his friends were talked into taking the medicines. They’re dead now. Dan is not a scientist, but we shouldn’t blame him for getting fed up with scientists once in a while. He just senses they’re bullshitting. I, on the other hand, know it. And I also know why.

  221. #221 Chris Noble
    June 18, 2006

    Dan wrote:

    Nobody’s asking you to do anything, except to not contradict yourself. You’re trying to have it both ways on these early tests.

    Obviously you do not understand what a false dichotomy is.

    Why do you think the assertion that Gallo’s initial tests were imperfect contradicts the assertion that the observation that 36% of the samples from AIDS patients tested positive with this test is something that has to be explained by “dissidents”?

    All tests are imperfect. They have sensitivities and specificities somewhere between 0-100%. Only in the rhetorical pseudoscience of “dissidents” is it either 0% or 100%.

    Early tests had poorer sensitivity than modern tests. So what?

    Even with the first tests and with poor samples they still found 36% of people with AIDS had detectable antibodies (within the detection limits of the test) to HIV. Controls from the general population do not. Why is this so?

  222. #222 viji
    June 18, 2006

    Wilhelm, another person living in his own narrow defined world

    (1) All scientific findings are peer reviewed, HIV research inclusive, you are the subset of persons who remains recalcitrant even when most of the recent HIV research has been tested, appraised, and validated. When I described you as the impossible judge and jury, I am implying that in your stubborn mind, only methods that you understand are valid, others that you have not make an effort to understand are fairy tales and witches brew, you are living in your own “molecular techniques is wizardry” world when the same techniques have been applied and accepted in almost all science disciplines. You can aptly be described as the anti-molecular biology dinosaur

    (2) What part of obligate blood borne virus do you not understand? “poof” when exposed to an open environment possibly be an exogenous infectious agent Obligate: A must, Blood-borne: Must only be in blood, or bodily fluid containing blood origin immune cells. Exogenous infectious agent? Your TYMV is one of the easy ones, its a plant virus, which usually has to spread via open environment; therefore when subjected to the harsh preparation procedures of centrifugation isolation and even harsher preparation procedures of electron microscopy, you were lucky enough to find some, and the fact TYMV is many times larger than any retrovirus, does that ring a bell in your ancient head? IF you want to try, go ahead, I’m pretty confident with the current HIV identification methods that utilises the whole range of HIV-specific protein, DNA, enzyme, protein, and antigen-detecting methods. Of course dinosaurs like you beg to differ. I for one won’t waste too much time and money being bogged down by “physical methods are obligatory in describing everything – akin persons have AIDS, its because of AZT, lets physically spin down AZT, AZT is the cause of AIDS

    (3) As I mentioned earlier, HIV containing fractions can be spin down using ultracentrifugation, we already know its approximate size, and such fractions can be invaribly used to infect cells or people. If you can;t believe it is HIV, then its still an infectious agent related to AIDS, but it is definitely tested not to be AZT or HAART, as it can replicate. And understandably, if we subject these fractions to harsh microscopy procedures, most of time we would not be successful, people have tried and gotten micrographs of HIV, but Wilheim just laugh off these breakthroughs as cartoons. Wilheim is living in his world of denial

    (4) Sure, we culture HIV in cancerous Jurkat T4 cells, PHA is added to stimulate the presentation of CCR5 and C4 sirface receptors, the very entry point of HIV, can you understand that. And its plain false that you mention Jurkat T4 cells won;t get affected by HIV, they die too, not as drastically, because Jurkat cells double their numbers quickly, enough to replenish tthe ones killed off, its cancerous, understand? We use them because they are fast growing, hardy models to work with. Granted, its very obvious you have never worked with Jurket cells.

    Moreover, I’ve already described to you HIV infection of human macrophages harvested from human blood donors, that does not need PHA stimulation – they already express CCR5 and CD4, perfectly natural – Wilheim’s deviously sidestep this example I gave in order to promote his propaganda/misconception that cell cultures are wizardry

    (5) Isee, your justification that African HIV is not USA HIV is because “the first AIDS cases were clustered in the gay community” and later “African AIDS cases were described” Horseshit-misdirection. Obviously, people already know that the earliest ever sample that is HIV positive originates from Africa. And whole genome sequencing has clearly identified as the same HIV-1 or HIV-2. Second, do you knwo why “the first AIDS cases were clustered in the gay community”, because American institutions are selfish, they won;t study anything unless it afflicts them as well, so the gay cluster acquired AIDS, they begin to study HIV-AIDS, and tracked it back to its origin in Africa. Undertsand? If gay AIDS clusters never occured in the USA, the USA instituions would probably still be attributing sick-drop-dead-AIDS victims in Africa to endemic diseases or malnutrition, as arrogantly as you, Wilheim, just did.

    (6) There are already well documented clinical case reports of otherwise healthy athletes or babies or trauma patients becoming HIV-positive after receiving HIV tainted blood. Enough said, don’t you resort to sad speculations about Magic Johnson, Wilheim, that will just let us look at you with disdain

    (7) I’ve addressed my opinions about p24 antigen tests in the immediate post before to Gene Sermon, I think Wilheim didn’t even care to read it properly, Its a good guess that his intent is just to create trouble and misinformation

    (8)Yeah, no one cared to look at malaria before, because the USA deemed it not their problem. Now with global temperatures rising, and mosquito malaria vectors venturing further north into pristine USA, and malaria developing resistance to the only available treetments, they are seriously starting to give the “Third World Tropical Disease” a look. Good observaton Wilheim. HIV is just another that the USA has put on its priority list, simple as that. Heart diseases and the problem of obesity too.

    (9)Ironically, any funding we receive goes all out into the research to solve diseases such as HIV, we get peanuts and of course a lot of us will develop disease from the noxious reagents and radiation we risk in our experiments. SO therein lies our dedication and sometimes sacrifice.

    But certainly the likes or Wilheim and Dan likes to stereotype us as devils profiteering. They can think what they like, at least we’re spending our lives working on the problem, they don;t appreciate trying to solve a problem, they just sit around idly on their misconceptions, resisting knowledge contrary to thier perceptions, embracing and spreading misinformation, spit profanities, complaining, shrieking, yet spending and doing little to work on the science, some individuals even profit from the selling of misinformative/dissentive bestsellers books, alternative “vitamins” therapy and by the hour $ charge personal apperances (and yet to accuse us of profiteering)

    wasting my time in the process

    I do not think you want to do research, you prob wish to profit from the whole denial issue, or at least try to get your name out after decades of scientific drought

    We all know that to start a meaningful preliminary experiment, you need less than 500,000 dollars, I’m sure you can get the authors of bestsellers to finance you if the official fundings are not forthcoming. These authors seem genuine enough to to cause against AIDS. Don;t complain to us of not having the cash to do research, we all know that research starts cheap and small, its promising preliminary experiments that wins us more funding.

    Yeah I only work for AUD2K per month thats only USD1472, and I’m not complaining about backbreaking 24/7 in the lab. So, is your back aching, Wilheim, from sitting to long in front of the computer?

  223. #223 Chris Noble
    June 18, 2006

    Godschalk wrote:

    Are you referring to Magic Johnson? He announced many years ago with much drum-beating that he was seropositive. Nothing bad has happened to him since. If he had used the antiretrovirals, he would be dead by now. He probably never used them, but gets paid to say he does. He’s not a very reliable character.
    And a child? Never heard of such a case. Only about children in Africa being murdered with Nevirapine.

    This can only be described as Denialism. So-called dissidents claim that antiretrovirals are so toxic that they will kill you within a few years. What about Magic Johnson? Well Magic Johnson is lying. How do you know he is lying? Because if he were taking antiretrovirals he’d be dead by now. Circular logic.

    Never heard of children being infected with HIV from blood products? This is because the source of your information is Denialist web-sites.

  224. #224 Chris Noble
    June 18, 2006

    Godschalk and other “dissidents” are deliberately conflating HIV p24 with other proteins also having a molecular weight of approximately 24 kDaltons.

    The fact that two proteins may have the same approxiamte molecular weight does not make them identical or even necessarily related. Oranges and apples can have the same weight. That does not make them identical.

    HIV has been sequenced. The part of the genome coding for HIV p24 has been identified. It is not endogenous.

    Recombinant HIV p24 is availble from AIDS reagent programs. Monoclonal antibodies directed towards conserved epitopes of the HIV-p24 protein. Tests using these monoclonal antibodies have been tested against recombinant HIV p24.

    The fact that “dissidents” continue to conflate HIV p24 with other unrelated proteins with approximately the same molecular weight only demonstrates their intention to deceive.

  225. #225 Chris Noble
    June 19, 2006

    Godschalks asks:

    Why doesn’t HIV destroy these cell cultures, as T4 cells are said to be the natural point of attack by the virus?

    “Dissidents” go on and on about Gallo stealing HIV from Montagnier. (At other time they claim that HIV does not exist in which case it is very hard to steal). What the “Dissidents” do not mention is the reason that Gallo continues to be credited as the co-discoverer of HIV is that his group managed to find an immortal cell line that would sustain HIV whereas Montagnier could only keep his going by topping it up with fresh donor PBMCs. Gallo’s contribution was essential.

    The cell lines that can sustain HIV culture are the exception not the rule. Most are indeed killed by HIV. The ones that are killed by HIV are not used for culturing HIV for that very reason.

  226. #226 Chris Noble
    June 19, 2006

    The Perth Group have recently written:

    Item 40, Does HIV Fulfil Koch’s Postulates for AIDS? If one accepts that “HIV” and “HIV” antibodies exist, then one has no choice but to also accept that Koch’s postulates have been fulfilled which means that HIV is the cause of AIDS.

    On the other hand Duesberg is adamant that HIV exists and is a normal retrovirus that cannot cause AIDS.

    The two views are diammetrically opposed.

    Why don’t these two opposing groups hold a debate?

    They both express their willingness to publicly debate the issue. Why not debate each other? It’s not lack of funds.

    I’ve even offered to donate money for the cause.

  227. #227 viji
    June 19, 2006

    I wasn’t familiar with the work on endogenous proteins having a molecular weight of approximately 24 kDaltons, or the work on the genetic description of HIV p24

    Was given the impression and probably misread the p24 question, from Gene Semon and (or was it Hank Barnes), who referenced the Perth Group assertions that p24 is a cellular protein, and Gene’s indication that “p24 protein family has a function in cargo selection for vesicle transport across membranes”

    So p24 has nothing to do with the 24 kDalton proteins involved in cargo selection transport across membranes? Is there a p24 protein family?

    I should have double checked the references Gene provided, it seems now that the only relevant paper pertaining to the statement of p24 protein family involved in cargo selection for vesicle transport across membranes” came from

    66. Francis DP. The search for the cause. (1983). p. 137-150 In: The AIDS epidemic Cahill KM, ed 1st ed

    Odd. An old paper, that certainly did not include the latest genetic studies on HIV p24 (?)

    Chris, thanks for highlighting the difference between endogenous proteins and HIV p24, references please.

    Cheers

  228. #228 Piss Knowsbull
    June 19, 2006

    Piss,

    why is it that a dude who got mostly everything right, like Peepee Duesberg, is a ‘denialist’ –

    mostly everything – AZT croaks folks, to know infection is no infection, dormant DNA don’t infectious pathogenesis make…

    And F-bombs like Gallo, Ho and yoself, who get almost everything wrong, are not?

    Everything wrong – the tests, the drugs, the attitude of ungratitude? The devil eats details like you for breakfast, and sh*ts them out at midnight, and you feel born-again, doncha?

    And here you are, everyday, ready to poop on ‘denialism’, like Dan’s, Dan who lives despite your good wishes that he, like other ungrateful Gay men, would just get the message and die (I mean, go get his death sentence through official channels, so you can pretend to wrench your back stuffing the bone-marrow evacuating pills into his gut)?

    And you war-ry that the ‘denialists’ don’t debate each other? Hey f-wad, go read a little about yo project and see what yous find in terms of general agreement among the death-cultists. Apoptosis, Absentee infection, non-pathogenic naked DNA kills people? HIV is truck, HIV needs co-drivers, HIV needs a break?

    Hey s-head, here’s a hypo-thesis: Go find the toilet where your mother conceived you and say a little prayer that you get to look at sunsets without the gay police rounding you up for testing.

    Good work, Piss. You’re beloved to us all. Piss, you really are a hero to millions (of uninformed, terrified people). What I wouldn’t give to see the future history of this religion of yo’s.

    F-y’all! Happy f-mas!

    *Sigh*

  229. #229 Chris Noble
    June 19, 2006

    Protein sequences are available at http://www.ncbi.nlm.nih.gov/entrez

    This is a protein sequence for a HIV p24.
    nawvkvveek gfnpevipmf salsegatpq dlnmmlnivg ghqaamqmlk etineeaaew drvhpvhagp ippgqmrepr gsdiagttsn lqeqigwmts nppipvgdiy krwiilglnk ivrmyspvgi ldirqgpkep frdyvdrfyk tlraeqasqe vknwmtetlx vqnanpdcrs ilk

    This is a protein sequence for a protein belonging to the emp24/gp25L/p24 family.
    msglsgppar rgpfplalll lfllgprlvl aisfhlpins rkclreeihk dllvtgayei sdqsggaggl rshlkitdsa ghilyskeda tkgkfaftte dydmfevcfe skgtgripdq lvildmkhgv eaknyeeiak veklkpleve lrrledlses ivndfaymkk reeemrdtne stntrvlyfs ifsmfcligl atwqvfylrr ffkakklie

    Most people will easily recognise that these two proteins are different.

    “Rethinkers” will try to convince you that because these proteins have approximately the same molecular weight they must be indistinguishable. It’s identical to arguing that two books must be indistinguishable if they have the same weight. Stupid.

    They have been shown the stupidity of this argument time and time again and yet they keep on repeating the same stupid argument.

    They like to call themselves “rethinkers” but they keep on rethunking the same thunk.

  230. #230 Chris Noble
    June 19, 2006

    Piss Knowsbull wrote:

    And you war-ry that the ‘denialists’ don’t debate each other? Hey f-wad, go read a little about yo project and see what yous find in terms of general agreement among the death-cultists. Apoptosis, Absentee infection, non-pathogenic naked DNA kills people? HIV is truck, HIV needs co-drivers, HIV needs a break?

    “Rethinkers” love to point to differences between different “orthodox” AIDS researchers. This is supposedly a weakness whereas the vast differences between various “alternative” AIDS theories are somehow a sign of strength. The “big tent” approach.

    The has been and still is strong debate within AIDS researchers about various aspects of this disease. This occurs through peer-reviewed journals and at scientific conferences. This debate is a fundamental part of science.

    The difference between this and “rethinkers” such as Duesberg and the Perth Group is that progress is made. AIDS researchers do more experiments, present new evidence and manage to convince their colleagues that their ideas are better. Eventually a consensus develops. There still remain many contentious issues but progress is being made.

    In contrast Duesberg and the Perth Group are still stuck in their own pet theories. They can’t manage to convince each other about anything. There is no progress in “rethinker” AIDS science because they aren’t rethinking. They just keep on repeating the same stuff over and over again.

    Duesberg will never agree with the Perth Group that if, as he claims, HIV exists it also fulfils Koch’s postulates and causes AIDS.

    The Perth Group will never agree with Duesberg that HIV exists.

    They are stuck eternally in their own dogma.

  231. #231 viji
    June 19, 2006

    Chris, Thanks for the references

    I was giving Gene the benefit of doubt earlier, not minding to check his references, and took in his staement that there exist p24 gene family similar to that of HIV p24.

    He seems the reasonable lad of the lot, apparently either Gene may have misread the old publications, missed the recent findings on HIV p24 or it was deliberate to mislead me. I wouldn’t know for sure.

    Anyway thanks for the revelation and correction

    Cheers

  232. #232 Dale
    June 19, 2006

    The Perth Group have recently written: If one accepts that “HIV” and “HIV” antibodies exist, then one has no choice but to also accept that Koch’s postulates have been fulfilled which means that HIV is the cause of AIDS.

    In other words it would appear that the Perth Group is saying that Peter Duesberg must either recant his belief in the existence of HIV or accept that HIV is the cause of AIDS.

    Love it!!

  233. #233 Dan
    June 19, 2006

    But certainly the likes or Wilheim and Dan likes to stereotype us as devils profiteering.

    Your words, not mine. Interesting that you should use those words.

  234. #234 Dan
    June 19, 2006

    Even with the first tests and with poor samples they still found 36% of people with AIDS had detectable antibodies (within the detection limits of the test) to HIV. Controls from the general population do not. Why is this so?

    Ok, it looks like you’re attempting to answer my question, Chris, which was: I’d like to hear more about this scientific standard where a pathogen need only be found in 36% of people with the disease to be proclaimed as the cause of this disease. That sounds very interesting

    You seem to be saying that 36% is good enough. My next question is how low can it go? 20%? 10%?

    Poor samples, crude tests, the dog ate the samples, that’s why I found “HIV” in only 36%. I swear all those fags have “HIV”, there’s just a lot of factors (excuses) beyond my control, ok? Please…just let me have this one, OK? When the hell do I get my Nobel prize?

  235. #235 Dan
    June 19, 2006

    at least we’re spending our lives working on the problem, they don;t appreciate trying to solve a problem

    Whoops. It looks like I didn’t have the full picture on the halo issue. I thought it was gay men putting the haloes over the scientists/researchers’ heads. It looks like they place them over their own heads as well.

    Well, Viji-bud, we just see things differently. I’m most definitely working on the “HIV” problem, just not quite the same way you “are”.

  236. #236 Gene Semon
    June 19, 2006

    How about this , Viji?

    Let A = “unrooted HIV star phylogeny”, recombinants of recombinants, a “continuum of genetic variants”. Let SBHIVs = starburst HI virions “with different biological functions” and “no single virion structure”. Let RT = reverse transcriptases with different isoforms. Then A => SBHIVs => RT deductive chain presents a frame for previous points and reconciles Wilhelm and Duesberg. And, since we’re playing symbolic logic, factor the chain into the African and Indian models. Consider also the lower bound heterosexual transmission rate from the PROSPECTIVE part of the Padian study, i.e. zero, and it comes to a great doubt that we need an epidemiologist to tell us that GIGO still holds. (BTW, do you know who and where I’m quoting? I guarantee, not denialist propaganda.)

    “A simple observation that ‘human physiological stress derived endogenous infectious agent’ positive blood when used in blood transfusion to a person who is other wise healthy or ‘human physiological stress derived endogenous infectious agent’ negative, would soon become ‘human physiological stress derived endogenous infectious agent’ positive, and go on to develop ‘human physiological stress derived endogenous infectious agent’ ‘associated’ AIDS

    It doesn’t seem to me very different from the aetiology of AIDS with HIV. Perhaps if that line of research shows promising results, we could rename HIV as ‘human physiological stress derived endogenous infectious agent’ HPSDEIA”

    Nice try, Viji, but I stand by EFFECT, not cause. I think you’re trapped in circular reasoning, boxed into a positivist corner, so to speak, by the inventors of the AIDS virus. Wilhelm, Hank and I are trying to free you from this prison of their making. Let’s recapitulate the theoretical points scattered all over the table.

    Which model better meets Leibniz’ test – a theory has to be simpler than the data it explains, otherwise it does not explain anything – your or ours? Incremental inductivism is also a belief system; your facts are theory laden. Example: HIV hijacks cellular proteins. Really, Viji, you actually said that! (Presumably using its 9 heads and Star Wars shield?) Nor does DNA “direct” anything; very important for our form of life, but a template nonetheless. Nor am I saying that we can “socially construct” any old theory we want or that inductivism isn’t the appropriate move in the right situation. Clearly Kuhn’s historical assessment is valid in describing what constitutes scientific progress.

    Given your concession on HIV associated proteins, you now have to seriously confront Wilhelm’s challenge. These are not “whims” he’s conveying but a distillation of classical theorizing in virology (another one of those damned competing heresies). One of the “old salts” has republished his 40 yr old purification proof where his retroviruses didn’t go “poof” and using 20 ml, far from bleeding anyone dry.

    I would say, given cDNA clones as proof of isolation (HIVs as “living fossils”), the “moving principle”, hence the way forward is in the polymerases, RNPs and regulatory/enzymatic mRNAs. Then it starts to make sense that the cell, although it may be out of sync with the rest of the organism, is still in charge. This is the point of Urnovitz’ informational focus on the dynamic genome and chronic disease. He defines HIV as a set of cellular signals. He’s also said to NIH types: stop putting square pegs in round holes.

    Like dogs chasing their tails, your gang throws around words like “pathogenic transmission”, “replication”, “infectious”, “epidemiological data”, etc. which you hurl like lightning bolts at opponents. But it all adds up to assuming your own conclusions.

    It’s over, Viji. HIV cytopathism is dead, dead, dead! Duesberg killed it a long time ago and the rest of you have to catch up. Your “disciplinary matrix’ is heading off a cliff, so please stop smearing US as a threat to the public health. The body count, as you conceded re AZT, is on your side.

    Speaking of denialism, dishing out advice and threats to the public health, why not focus your talents on the iatrogenic problem?

    POP QUIZ

    a) Which kills more in the good old USA per year, iatrogenic medicine or AIDS?

    b) How many dogs can waste taxpayer money while chasing their tails on the head of a pin?

  237. #237 Gene Semon
    June 19, 2006

    The fact that “dissidents” continue to conflate HIV p24 with other unrelated proteins with approximately the same molecular weight only demonstrates their intention to deceive.
    Posted by: Chris Noble | June 18, 2006 11:55 PM

    Chris Not So noble,

    See above deductive chain. Substitute P24 = gagp24s with different isoforms for RT. Use brain.

  238. #238 Gene Semon
    June 19, 2006

    “I should have double checked the references Gene provided, it seems now that the only relevant paper pertaining to the statement of p24 protein family involved in cargo selection for vesicle transport across membranes” came from
    66. Francis DP. The search for the cause. (1983). p. 137-150 In: The AIDS epidemic Cahill KM, ed 1st ed
    Odd. An old paper, that certainly did not include the latest genetic studies on HIV p24 (?)”

    Here are the corrected Perth p24 references; an original error in transcription!

    63. Vincent F, Belec L, Glotz D, Menoyo-Calonge V, Dubost A, Bariety J (1993). False-positive neutralizable HIV antigens detected in organ transplant recipients. AIDS 7: 741-742

    64. Agbalika F, Ferchal F, Garnier JP, Eugene M, Bedrossian J, Lagrange PH. (1992). False-positive HIV antigens related to emergence of 25-30kD proteins detected in organ recipients. AIDS 6: 959-962

    65. Stricker RB, Abrams D, Corash L. (1985). Target platelet antigen in homosexual men with immune thrombocytopenia. New England Journal of Medicine 313: 1375-1380.

    66. Faulk WP, Labarrere CA. (1991). HIV proteins in normal human placenta. American Journal of Reproductive Immunology 25: 99-104

    67. Schupbach J, Jendis JB, Bron C, Boni J, Tomasik Z. (1992). False-positive HIV-1 virus cultures using whole blood. AIDS 6: 1545-6

  239. #239 Shakesy William
    June 19, 2006

    “Rethinkers” love to point to differences between different “orthodox” AIDS researchers.

    And in the next Piss:

    Duesberg will never agree with the Perth Group that if, as he claims, HIV exists it also fulfils Koch’s postulates and causes AIDS. The Perth Group will never agree with Duesberg that HIV exists. They are stuck eternally in their own dogma.

    Stuck in the middle with Piss…Piss knows Dogzma.

    Reminds me of a joke I wince herd:

    To be, or not to be–that is the question:

    Whether ’tis nobler in the mind to suffer

    The slings and arrows of outrageous fortune

    Or to take arms against a sea of troubles

    And by opposing end them. To die, to sleep–

    No more–and by a sleep to say we end

    The heartache, and the thousand natural shocks

    That flesh is heir to.

    ….

    To grunt and sweat under a weary life,

    But that the dread of something after death,

    The undiscovered country, from whose bourn

    No traveller returns, puzzles the will,

    And makes us rather bear those ills we have

    Than fly to others that we know not of?

    Thus conscience does make cowards of us all,

    And thus the native hue of resolution

    Is sicklied o’er with the pale cast of thought,

    And enterprise of great pitch and moment

    With this regard their currents turn awry

    And lose the name of action.

  240. #240 Gene Semon
    June 19, 2006

    Viji,

    Here’s another qote from the notorious Perth Group, (who like to make trouble for all sides), which connects to the HeLa statement I excerpted from the LINE 1 paper, (Both this and p24 quotes are from their MTCT Monograph),(Before everyone gets all excited, notice its mostly the authors of ref 71, NOT more of that denialist blasphemy):

    In 1989, discussing their studies on human retroviruses, researchers from the University of New York wrote, “Irrespective of the origin of human retroviruses, their presence leads to both practical and theoretical concerns. Presently, the major practical concern is that effective use of PCR as a screening procedure for HTLV-I, HTLV-II and HIV infections must always include appropriate controls to ensure that no endogenous sequences contribute to positive signals. As previously noted, HIV unique primers corresponding to the highly conserved reverse transcriptase region…function well in the PCR amplification of HeLa DNA [a non-HIV-infected neoplastic laboratory cell line] even at annealing temperatures around 60ºC. Another practical concern is that the use of PCR for determining the possible retroviral etiology of a variety of human diseases may be complicated by endogenous retroviruses. Even if cDNAs are used for PCR templates,
    the transcriptional activities of endogenous sequences must be considered” (71)(Interesting, wrong one here too!)

    71.Shih A, Misra R, Rush MG (1989) Detection of multiple novel reverse transcriptase coding sequences in human nucleic acids: relation to primate retroviruses. Journal of Virology 63: 64-75 (correct ref)

  241. #241 Dale
    June 19, 2006

    Of course the potential problem described by Shih and colleagues is only a problem in practice if (1) appropriate positive and negative controls aren’t used in PCR reactions and (2) the primer sequences used in detecting HIV suffer from the same lack of specificity ascribed to the primers described in this paper.

    Also, if p24 shows up as a “false positive” in placenta and/or organ transplant recipients, this isn’t a practical problem in diagnosing HIV infection as such diagnoses are neither carried out on placental tissue nor made in the absence of a medical history that would reveal whether someone was a transplant recipient.

  242. #242 viji
    June 19, 2006

    Gene you said,

    (1) Let A = “unrooted HIV star phylogeny”, recombinants of recombinants, a “continuum of genetic variants”. Let SBHIVs = starburst HI virions “with different biological functions” and “no single virion structure”. Let RT = reverse transcriptases with different isoforms. Then A => SBHIVs => RT deductive chain presents a frame for previous points and reconciles Wilhelm and Duesberg. And, since we’re playing symbolic logic, factor the chain into the African and Indian models. Consider also the lower bound heterosexual transmission rate from the PROSPECTIVE part of the Padian study, i.e. zero, and it comes to a great doubt that we need an epidemiologist to tell us that GIGO still holds. (BTW, do you know who and where I’m quoting? I guarantee, not denialist propaganda.)

    You’re being incomprehensive to yourself and other people. Keep it simple, my understanding from what you;re saying is that (A) a “viral infectious agent” (in your case you would never agree it to be HIV, and which we’ve in the 2000s onwards clearly identified as two major variants HIV-1 and HIV-2, what are you trying to say with “recombinants of recombinants””continuum of genetic variants”?), (B) and the infectious agent have been observed and linked with a host of biological functions in “infected” persons i.e. AIDS, dramatic T-cell depletion, specific viral proteins, DNA etc.(phenomenons only exclusive to persons in whom this infectious agent is detected), and (C) this “viral infectious agent” uses non-endogenous (not found in uninfected persons) reverse transcriptase enzyme in its replicative life cycle. (i) How does this reconcile with Wilhelm and Duesberg? you mentioned “no single virion structure”, I’ve explained before its not as easy as you think to resolve the structure of everything, especially no blood-borne retroviruses, BUT a few things we have to date that pin points an infectious agent (which we call HIV, and you not HIV), we have the crystal structure of HIV-RT which shows that it is not endogenous retrotransposons, and definitely not telomerases. We also have micrographs which Wilhelm ignore. We also have identified proteins specific and DNA sequences specific to HIV, what more do you need? you want us to create the HIV from scratch and show you the “9 heads and Star Wars shield”? (ii) Everytime we put forth the most recent by the year observation of HIV aetiology of AIDS in Africa and South Asia, you run and hide under you almost two decades old Pandian, which the above posts have already discussed the prospective studies’ inherent weaknesses and low coverage. The study was done when out understanding of HIV is still slight, and when the tools to detect HIV was crude and flawed, and when there was social stigma of AIDS that may skew the study, and when a clear picture of HIV genetic and molecular studies were still absent, (iii) What is GIGO? I thought Tara is the epidemiologist, I am not, as her, or some other epidemiologist, don;t push funny questions to me when you know I can;t critically appraise it, I only know what I see from my hands on approach in the lab. And what about you? are you an epidemiologist yourself to peddle your own interpretations? And it does not seem you are actively involved in any research yourself, from the previous post where you mix and mince and mislead, even the statement above from you since to point that you are one of those mathematicians that what to model everything, when you know that the quality of a model depends on the information input, your’s is solely based a certain 2 decade old prospective study

    (2) Like dogs chasing their tails, your gang throws around words like “pathogenic transmission”, “replication”, “infectious”, “epidemiological data”, etc. which you hurl like lightning bolts at opponents. But it all adds up to assuming your own conclusions.

    reflect this statement on yourself and your friends. I was wrong, you’re just as incoherent and rude as your friends, the statement can equally read “Like dogs chasing their tails, your gang throws around words like “Gallo’s a fraud, don;t trust anything else after Gallo”, “molecular biology is wizardry, we need a witch-hunt, burn em all”, “scientist are bad bad people, they exploit us poor souls”, “what HIV-specific? lies, everything wrong with our body with is endogenous”, “Pandian paper is truth, everything contrary to it is false conspiracy”, which you hurl like lightning bolts at opponents, coupled with the most hideous profanities, and evil slanders. But it all adds up to assuming your own denials and conclusions.

    (3)Nice try, Viji, but I stand by EFFECT, not cause. I think you’re trapped in circular reasoning, boxed into a positivist corner, so to speak, by the inventors of the AIDS virus. Wilhelm, Hank and I are trying to free you from this prison of their making. Let’s recapitulate the theoretical points scattered all over the table.

    Am I? the effect is AIDS, many times reproduced and validated studies have provided strong correlations with HIV, or HIV markers. If you don’t agree with a HIV virus, you can still see that its an infectious agent. And in which the most recent HAART regimens that targets the life cycle of this infectious agent that prolong the lifespan and halt the progression to AIDS in most cases. Wilhelm, Hank and you are just spreading your own gospel, with little hard data, apart from the monotonous Pandian and Gallo’s a fraud party line. What you fail to realise is the notority and irresponsible impact of your misleading statements on AIDS prevention. And of course your’re robbing away my time in the lab, Each of your cryptic comment takes at least an hour to understand and reply.

    (4) It’s over, Viji. HIV cytopathism is dead, dead, dead! Duesberg killed it a long time ago and the rest of you have to catch up. Your “disciplinary matrix’ is heading off a cliff, so please stop smearing US as a threat to the public health. The body count, as you conceded re AZT, is on your side.(/i>

    HIV cytopathism is still being observed in the lab and in the human body. Duesberg has his opinions, but he has yet to show a stich of clinical or laboratory data that points to his opinion. And his collegues have found him as stubborn as you, one-mindedly promoting his view and disregarding anything else contrary to that dead set view. I can say that Duesberg might just be having the same faults that all great intellects have, i.e. Stephen Hawking, doggedly holding on to his conceptions, whent he rest fo the world of intellects have moved forward on recent developments

    (5) Given your concession on HIV associated proteins, you now have to seriously confront Wilhelm’s challenge. These are not “whims” he’s conveying but a distillation of classical theorizing in virology (another one of those damned competing heresies). One of the “old salts” has republished his 40 yr old purification proof where his retroviruses didn’t go “poof” and using 20 ml, far from bleeding anyone dry.

    I have adequately explained to Wilhelm about the differences between techniques that can be applied to different organisms. His is the classical theorizing in virology, he is still doggedly holding on to his “golden years”. And a simple look at his comments will tell you how far removed from current research he is by his incessant chide of cell culture and molecualr biology. He has never worked on retrovirus Gene, he worked on a distinctly different and hardier plant virus. He failed to appreciate and comprehend the technical difficulties in studying animal viruses, more so blood borne retroviruses. To conform to Wilhelm’s “classical” views in virology, is analogous to putting 18th century coal fired electric generation to 21st century nuclear power. Gene, if you wish to buy into what Wilheim professes, its your right, but I’m sure you don;t agree to his contentions of molecular biology being wizardry

    (6)Which model better meets Leibniz’ test – a theory has to be simpler than the data it explains, otherwise it does not explain anything – your or ours? Incremental inductivism is also a belief system; your facts are theory laden.

    How much better is your working hypothesis, referenced only on Pandian and a motley of unaccredited and unvalidated “I don’t believe in HIV-AIDS” websites. At least mine theories and real observations are still being challenged by the scientific process and reproduced in countless experiments and clinical observations. You don;t even have a conform working hypothesis, much less any preliminary data or experimental observation to back it up.

    Stop goofing yourself. You’re distracting me from my work. If you choose to buy in to Wilheim, who have done nothing in part of research in 40 years, and not even bothering to look at recent findings, just keep on arguing with yourself.

  243. #243 Wilhelm Godschalk
    June 19, 2006

    Chris Noble
    So-called dissidents claim that antiretrovirals are so toxic that they will kill you within a few years. What about Magic Johnson? Well Magic Johnson is lying. How do you know he is lying? Because if he were taking antiretrovirals he’d be dead by now. Circular logic.

    By George, it is! Here’s another one: So-called AIDS scientists claim that antiretrovirals are beneficial, and will lengthen the lives of seropositive individuals. What about Magic Johnson? Well, he must be taking his ARV’s faithfully. How do you know? Because if he didn’t, he would be dead by now.

    Never heard of children being infected with HIV from blood products?

    No.

    The fact that two proteins may have the same approxiamte molecular weight does not make them identical or even necessarily related.

    Oh come now, Chris. You’ve tried this ploy with me before. You know very well that I wasn’t referring to just any proteins with a molecular weight of 24K. I was pointing at a specific group of “cargo handling” proteins that operate right at the very location where “HIV” is supposed to perform its magic, namely at the cell membrane. The so-called “p24 from HIV” is just one member of that family. Only, by sequencing it, the HIV people have gotten the strange idea that it’s OK to appropriate it as “their” p24. There is not a shred of evidence that it is viral. Of course they may have found some piece of RNA or DNA that may have coded for the protein. But does that prove that an (unisolated) virus has anything to do with it? But maybe, if you keep on repeating it over and over again, most people will start to believe it.

    HIV has been sequenced. The part of the genome coding for HIV p24 has been identified.

    No sleight of hand will help you through this: Something has been sequenced. If the coding for that particular p24 protein has been found, then it must be endemic. There is no indication that it is viral, because no virus can be isolated from these cells.
    If you find something in a human body that you have not seen before, do you always postulate that it must have come from outside?
    I’ve addressed this to Viji already, but let me repeat it:
    Just sequencing something doesn’t mean it’s part of a virus. (Just sitting at the sewing machine doesn’t mean you’re stitching the Emperor’s clothes)

    Recombinant HIV p24 is availble from AIDS reagent programs. Monoclonal antibodies directed towards conserved epitopes of the HIV-p24 protein. Tests using these monoclonal antibodies have been tested against recombinant HIV p24.

    Geneticist’s jargon, to keep you gaffers from understanding how you’re really being bamboozled. They call themselves Molecular geneticists now, to get more respect. They find that a certain protein reacts with antibodies from a seropositive individual. So this protein (p24) must be from HIV (do you get the logic?). Now if you believe this, the rest is easy. And this is the guy who was complaining about circular logic…

    the reason that Gallo continues to be credited as the co-discoverer of HIV is that his group managed to find an immortal cell line that would sustain HIV

    Well, that alone would make anybody suspicious about “a virus that destroys T4 cells.” But, of course we know that, in Gallo’s lab, anything is possible.

    Rethinkers” will try to convince you that because these proteins have approximately the same molecular weight they must be indistinguishable. It’s identical to arguing that two books must be indistinguishable if they have the same weight. Stupid.
    They have been shown the stupidity of this argument time and time again and yet they keep on repeating the same stupid argument.

    This is where it gets hard to stomach you, even for me. But you have been trying to do this time and again: Claiming that any of us has ever suggested that two proteins with the same molecular weight must be identical. Nobody, but nobody is that stupid.
    What I’m really saying is that from a whole family of proteins with an approximate mol. wt. of 24K, all with a function in vesicle transport, the HIV-hustlers just appropriated one, sequenced it, and put it into their data bank.
    Well, if the police look for a fingerprint or a DNA pattern in the data banks, they can be sure that the entries are all genuine, and connected with the persons from which they were taken. Part of the gene bank and the protein bank is just bogus. If it says: “From HIV”, it’s just because somebody uploaded that information. And whoever did that is a criminal.

    The has been and still is strong debate within AIDS researchers about various aspects of this disease. This occurs through peer-reviewed journals and at scientific conferences. This debate is a fundamental part of science.

    I feel the tears coming already. Some people would really start believing that scientists are angels, debating their honest results in a sphere of congeniality. In reality, the chief perpetrators stay out of reach, and wouldn’t think of debating the infidels who don’t believe in their scam. They leave the debating to the Pharma phlunkies (such as Chris Noble), who are beholden to them, and obligated to do their dirty work.

  244. #244 Dan
    June 20, 2006

    Everytime we put forth the most recent by the year observation of HIV aetiology of AIDS in Africa and South Asia, you run and hide under you almost two decades old Pandian, which the above posts have already discussed the prospective studies’ (1)inherent weaknesses and (2)low coverage. (3)The study was done when out understanding of HIV is still slight, and when the tools to detect HIV was (4)crude and (5)flawed, and when there was (6)social stigma of AIDS that may skew the study, and when a (7)clear picture of HIV genetic and molecular studies were still absent

    I’m seeing a pattern here. It’s called the litany of excuses. I numbered them for you. In bold, is the newest addition to the family, I’m betting you’re going to try and get some mileage out of that one.

  245. #245 viji
    June 20, 2006

    Dan,

    Everytime we put forth the most recent by the year observation of HIV aetiology of AIDS in Africa and South Asia, you run and hide under you almost two decades old Pandian, which the above posts have already discussed the prospective studies’ (1)inherent weaknesses and (2)low coverage. (3)The study was done when out understanding of HIV is still slight, and when the tools to detect HIV was (4)crude and (5)flawed, and when there was (6)social stigma of AIDS that may skew the study, and when a (7)clear picture of HIV genetic and molecular studies were still absent

    Good to see that we’re in agreement that with the findings of the Pandian study, and subsequent studies on HIV. Humanity knowledge is still at its infancy, and we have yet to fully describe everything under the sun, that is why there are gaps or flaws in understanding of science, infectious diseases included, and that is also the reason scientist today and generations to come will pioneer work on what is still unknown.

    The only difference between people who are genuinely trying to study the HIV-AIDS phenomenon, and those that refuse to accept HIV exists or is associated with AIDS, is that people that are studying HIV-AIDS have moved further ahead from the days of crude HIV tests pioneered by Gallo, to develop and improve the various methods used to detect HIV, dissect HIV biology, and try to seek a way to circumvent HIV-AIDS

    While people that perceive that HIV does not cause AIDS, are just sitting on top of two decades old Pandian paper, a paper with inherent weaknesses akin the old Gallo paper, taking everything said in the Pandian paper as fact and absolute truth, ignoring any new studies that are contrary to Pandian views, no matter how technically sound the new study is.

    Yet they have the nerve tp shriek at us that have already outlived the Gallo finding to develop ever more accurate and testable findings on HIV-AIDS

    Never once pausing to look at the available information, and reflecting on their own bogged down views.

    Your struggle will just confuse the masses, if you want to show that your views are correct, and redirect research efforts to the right path, then come up with preliminary experiments that can be looked upon and a working hypothesis that can be worked upon

    Don;t waste everyone’s time by arguing for the sake of arguing, for example Wilheim’s incessant prespective that there is no HIV p24, but some endogenous p24 family when there is no studies that indicate so, Wilheims just so boldly state his misconceptions without even a reference.

    Worse, Wilheim just attributes techniques that he clearly does not understand as heresy or wizardry. Where does he base his misconception that sequencing cannot differentiate between endogenous and exogenous sources?
    Simple things like viral LTR is unique enough not to be found in humans, at least not infected ones.

    And the fact that current HIV testing regimens don;t only look at p24 antigen levels, or HIV specific sequences, but take into account a whole range of tests including p24 antigen, HIV specific proteins, HIV specific sequences, viral reverse transcriptase activity, cytopthatic assays, CD4 T-cell counts, etc.

    All of these techniques which have been separately developed by different groups and involved almost all disciplines known to science. So how can a case where all these are tested positive in a sample gathered from a AIDS patient be confounding. What else do you want?

    If you want to believe and tell us that AZT is the primary cause of AIDS, then show us the evidence, show us the AZT markers, tests that can be clearly associated with AIDS. Such preliminary studies don’t even need 10,000 dollars to run. You can;t just convince us by basing your “facts” from a Pandian paper that did not even mention any reproducible technical methods to detect anything, or shrieking at people that don;t hold your views, without scientific evidence, scientist will just regard this as fairy tales.

    What your lot is doing here is just going round and round and round arguing for the sake of arguing, providing just ad-hoc “evidence” and misleading statements. And when people tried to be reasonble to show you finding that disprove your arguments you begin to resort to profanities and name calling, worse, disgrace knowledge by twisting scientific facts to your own interpretations, and disregarding facts that don;t match your views.

    Think before you speak.

  246. #246 viji
    June 20, 2006

    If you want to find out about viral LTRs, the difference between entities that show reverse transcription activity, i.e. telomerases, retrotransposons, retrovirus reverse transcriptase.

    seek out this good, concise review, with references

    Science 15 August 1997:
    Vol. 277. no. 5328, pp. 911 – 912
    DOI: 10.1126/science.277.5328.911
    Perspectives
    MOLECULAR BIOLOGY:
    Telomerase and Retrotransposons: Which Came First?

  247. #247 viji
    June 20, 2006

    For an understanding of the current use of PCR, molecular techniques in clinical microbiology, i.e. identification of infectious agents

    Seek out this recent review
    Clinical Microbiology Reviews, January 2006, p. 165-256, Vol. 19, No. 1
    0893-8512/06/$08.00+0 doi:10.1128/CMR.19.1.165-256.2006

    Real-Time PCR in Clinical Microbiology: Applications for Routine Laboratory Testing

  248. #248 viji
    June 20, 2006

    More on differences in LTRs found exclusively in retroviruses and LTRs found in some endogenous retrotransposons like HERV

    Seek out.
    Science 12 March 2004:
    Vol. 303. no. 5664, pp. 1626 – 1632
    DOI: 10.1126/science.1089670

    Review
    Mobile Elements: Drivers of Genome Evolution
    Haig H. Kazazian, Jr.*

  249. #249 Wilhelm Godschalk
    June 20, 2006

    Dear Tara,

    I wrote two posts yesterday: One to Viji, and one to Chris Noble. Why are you withholding the one in which I answered Viji? It was quite inocuous and scientific. There are no threats or obscenities in it (except maybe the word “bullshit”), and not even a reference to Hatchet Day.
    I got a message back saying something like: “Wait until your post has been checked”, or words to that effect.
    Of course you can do that on your own blog. But do you really want to practice censorship?

  250. #250 Dale
    June 20, 2006

    They find that a certain protein reacts with antibodies from a seropositive individual. So this protein (p24) must be from HIV (do you get the logic?)

    Wilhelm, you make it sound as though the HIV p24 sequence was just plucked randomly out of the human genome, which I know you know is not the case. HIV p24 sequences aren’t found in healthy seronegative individuals nor even in all cells of seropositive individuals as any human gene or endogenous retroviral derived sequence would be. You also forgot to mention that seropositive individuals don’t only make antibodies against p24 but make p24 itself. You further ignore that HIV p24 sequences are found in cells as part of a viral genome and that if the entire viral genome is amplified and purified away from other cellular DNA and proteins, that DNA can be put into uninfected cells which will then go on to make more infectious virus.

  251. #251 Gene Semon
    June 20, 2006

    “How much better is your working hypothesis, referenced only on Pandian and a motley of unaccredited and unvalidated “I don’t believe in HIV-AIDS” websites. At least mine theories and real observations are still being challenged by the scientific process and reproduced in countless experiments and clinical observations. You don;t even have a conform working hypothesis, much less any preliminary data or experimental observation to back it up.

    “Stop goofing yourself. You’re distracting me from my work. If you choose to buy in to Wilheim, who have done nothing in part of research in 40 years, and not even bothering to look at recent findings, just keep on arguing with yourself.”

    Really, Viji, your distracting me from my responses to the few substantive points that you make. If you don’t like my theorizing, fine. If now you don’t like me anymore, I don’t care. But as you descend into johnmoorism with endless repetition of the same argument as a smokescreen to backpedal away from and cover up your HUGE error on human reverse transcriptase and you think my symbolic deductive chain is goofing beacuse you can’t comprehend the essential point of this disagreement, then I can only pity you and your ilk posing as great scientists. You’re all living in your very own Bizarro World. Because you’re at least clever enough to dupe the professionalized incompetents who pose as science journalists, you stiil think you’re really on to progress. I find it particularly hysterical that you don’t get what Duesberg has done, never mind Howard Urnovitz. (BTW, I would love to see one of your clowns, whoops I mean great scientists, take HIM on.) And how did you miss my referencing mainstream HIV research? Are you illiterate? Or perhaps because you don’t really know what’s going on at the cutting edge of your very own specialty, “not even bothering to look at recent findings”? And what the hell is a conform working hypothesis? You guys don’t know how funny you really are.

    Anyway, for now, I won’t waste any more of MY time responding to your evasions and repetitions. All kidding aside, Viji, it’s all of a piece. Wilhem, Duesberg, Perth Group, Bialy, etc., all of us trying to get thru to Church Officials on what constitutes scientific progress.

  252. #252 Hank Barnes
    June 20, 2006

    Buried in the mounds of random thoughts and concepts, Viji wrote:

    Hank, I’ve read enough publications about AZT to know about its toxic side effects, and know that the toxic side affects are significant enough to suggests a reappraisal of its use in HIV therapy

    Reappraise, Baby!

    HB

  253. #253 Gene Semon
    June 20, 2006

    Here’s more of that blasphemous heretical classical virology which, of course, all current practicing scientists KNOW isn’t worth a damn. (See, we have this new technology and we don’t have to reason anymore. Just listen to the bishops. What a relief!)

    Robert J Huebner, The Murine Leukemia Virus Complex. Proceedings of the National Academy of Sciences, (1967) 58, 840 (EXCERPT)

    One of the more obvious yet frequently overlooked facts in considering causes of disease is that very few etiological agents behave exclusively in highly specific fashion. Studies of the whole “icebergs” including the hidden (subclinical) activities of most infectious agents show that the clinical manifestations regarded as most characteristic nearly always represent relatively unusual events in the natural history of such agents. More often than not, therefore, epidemiological studies based exclusively on highly specific clinical manifestations of widespread agents are likely to result in incorrect conclusions which hinder rational control efforts.

    Like many other viruses, leukemia virus (now called retrovirus)* infection appears to be widespread, yet in most natural circumstances it rarely results in clinical disease during the normal lifetime of the infected animal. (PARENS ADDED)

    END EXCERPT

    And now a more current reference:

    Alex D. Greenwood, Fred Lee, Cristian Capelli, Robert DeSalle, Alexei Tikhonov, Preston A. Marx and Ross D. E. MacPhee. Molecular Biology and Evolution 18:840-847 (2001)(EXCERPT)

    More beneficially, endogenous retroviruses (ERVs) have gained novel regulatory functions in the mammalian genome that are now indispensable (Mi et al. 2000). Human immunodeficiency virus (HIV) shares specific functionally homologous sequences with ancient endogenous retroviruses, raising the possibility that recombination with ERVs may change the properties of exogenous retroviruses (Yang et al. 1999). ERVs may also serve as a sequence pool from which exogenous viruses rapidly diversify and could even be the progenitors of exogenous retroviruses (Temin 1980).

    Mi, S., X. Lee, X. Li et al. (12 co-authors). 2000. Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis. Nature 403:785-789.

    Yang, H., E. M. Golenberg, and J. Shoshani. 1996. Phylogenetic resolution within the Elephantidae using fossil DNA sequences from the American mastodon (Mammut americanum). Proc. Natl. Acad. Sci. USA 93:1190-1194.

    Temin, H. M. 1980. Origin of retroviruses from cellular moveable genetic elements. Cell 21:599-600.

    END EXCERPT

    Sound familiar? Could we now have a “conform working hypothesis” with above considered as part of previous denialist posts? (Note especially reference to Nobel Laureate Howard Temin.)

  254. #254 Gene Semon
    June 20, 2006

    The Pope speaks!

    Just found this over at NAR. I think it speaks for itself:

    For Dr Fauci has remarkably suggested that the best antidote to AIDS may be HIV itself.

    But this great man deserves to speak in his own words, as found in his review paper in 2003 in the textbook “Fundamental Immunology” which was edited by William E. and published by Paul Lippincott Williams and Wilkins:

    “Several investigators have demonstrated that there is an increase in CD4+ T cell proliferation in both HIV and SIV infection. In certain studies, the enhanced T cell proliferation that was observed during active disease was significantly decreased following the initiation of anti-retroviral therapy, and proliferation increased again in parallel with plasma viremia following the cessation of treatment in these individuals.”

    In other words, adding HIV to the bloodstream increases T cell count, ARV drug therapy decreases it, and the withdrawal of ARVs increases it again.

    At one stroke, this kind of intervention – Fauci’s brilliant implied suggestion here to replace antiretroviral drugs with a dose of HIV – will restore 61% of AIDS patients in this country to health overnight.

  255. #255 Dale
    June 20, 2006

    Gene,
    Huebner’s statement is not relevant to HIV for which there are several very specific tests for subclinical infections. Were there ELISA or Western blots back in 1967? I know there was no PCR! In any case, while it is true that many viruses rarely cause clinical disease, HIV is an exception. In the 25 years that scientists and doctors have known about HIV studies continue to indicate that about 90% of infected untreated individuals eventually suffer progressive immune suppression.

    Temin’s statement about ERVs and the possibility of HIV recombining with an ERV is just a theoretical possibility as far as I know. There is certainly no evidence that HIV arose from an ERV in the human genome. If it had, there would be one or more ERVs that would be more similar in sequence to HIV than SIV is. No such ERV has been identified so the best available evidence says HIV arose from SIV.

    In other words, adding HIV to the bloodstream increases T cell count, ARV drug therapy decreases it, and the withdrawal of ARVs increases it again.

    Very funny. But increasing proliferation of T cells doesn’t necessarily increase T cell count. T cell count is a measure of the difference between cell proliferation and cell death.

  256. #256 Richard Jefferys
    June 20, 2006

    Gene, and Anthony Liversidge who he is quoting, clearly do not understand the difference between antigen-driven T cell proliferation and homeostastic T cell proliferation. Which is remarkably ignorant given that we’re supposed to believe that their wisdom on this particular subject trumps that of the world’s working immunologists.

  257. #257 RichardJeffrey's Soiled Gloves
    June 20, 2006

    Richard, and Robert Gallo’s used diapers, who he is quoting, clearly does not understand when he is on the wrong side of an issue.

  258. #258 Wilhelm Godschalk
    June 20, 2006

    Viji:
    My previous (elaborate) answer to you was censured away, so I don’t know how this one will fare. Strange, because there was nothing objectionable in it. Just a few snide remarks, that’s all. But let’s move on:

    Don;t waste everyone’s time by arguing for the sake of arguing, for example Wilheim’s incessant prespective that there is no HIV p24, but some endogenous p24 family when there is no studies that indicate so, Wilheims just so boldly state his misconceptions without even a reference.

    You know that’s pretty shabby, dont-cha? because it was I who quoted that MIT paper on the p24 family, in my post of Jun 16, 10:47 It’s still there, so you can check it out.
    And in case nobody has hammered it through your thick skull yet: There is no HIV p24, just a fraudulent entry in the protein bank.
    And indeed, if you would sequence all the p24 proteins involved in cargo loading of membrane vesicles, they are all different. But none belong to a virus.

    ignoring any new studies that are contrary to Pandian views

    What? You mean there are new long-term studies on discordant couples living together, without the negative partner getting “infected”? Show me quick; I must have missed something important. Actually I personally know several discordant couples (one pos., one neg.) They are too smart to let antiretrovirals come between them, and they’re in the process of living happily ever after.

    Am I? the effect is AIDS, many times reproduced and validated studies have provided strong correlations with HIV, or HIV markers.

    Oh, that’s it, right? Correlations. Well, there’s a strong positive correlation between the number of traffic accidents and the price of beans in Boston. Does that mean that one is the cause of the other? I dont think so, and if you don’t believe me, ask Tara; that’s within her field.

    His is the classical theorizing in virology, he is still doggedly holding on to his “golden years”. And a simple look at his comments will tell you how far removed from current research he is by his incessant chide of cell culture and molecualr biology

    Theorizing? In my “golden years” we studied objects that we could isolate and perform measurements on. Molecular Biology was fine until you guys made a mess of it.
    Look, I have nothing against cell or tissue culture. I’ve used it myself. But it’s only useful for culturing viruses. Over-ambitious young investigators tend to forget they are dealing with live cells, where still a lot goes on that we don’t even know yet. If you actually try to perform measurements in a cell culture, it’s like looking at a specimen under a microscope in the middle of a cesspool.
    For valid mesurements, you have to take a virus out of its growth medium; in other word: Isolation.

    What is GIGO?
    That’s an easy one, fortunately. It’s a computer term meaning “Garbage In – Garbage Out”. And it applies prefectly to most of “HIV science”.

    Your struggle will just confuse the masses, if you want to show that your views are correct, and redirect research efforts to the right path, then come up with preliminary experiments that can be looked upon and a working hypothesis that can be worked upon

    Eh… In case you’ve heard of Marie Antoinette (European history), this is a “Let them eat cake” argument.
    You know that’s not a valid option, so why be hypocritical about it. So if we confuse the masses, it’s because we want to. It’s our only chance to break the corrupt system wide open.

    Worse, Wilheim just attributes techniques that he clearly does not understand as heresy or wizardry. Where does he base his misconception that sequencing cannot differentiate between endogenous and exogenous sources?

    Well now, then this is your perfect opportunity to enlighten me (and the other bedazzled souls) about the subject.
    So let’s say, I give somebody who does sequencing for a living a sample. I’m pretty sure he will come up with a sequence. But how does he determine whether the sample was from endogenous or exogenous origin? For all he knows, I scraped the sample out of the cat’s litterbox.

    All of these techniques which have been separately developed by different groups and involved almost all disciplines known to science. So how can a case where all these are tested positive in a sample gathered from a AIDS patient be confounding. What else do you want?

    We just want to be shown the link to a retrovirus they call HIV. Nothing more, nothing less.

    Yet they have the nerve tp shriek at us that have already outlived the Gallo finding to develop ever more accurate and testable findings on HIV-AIDS

    I think we agree that Gallo’s work was sloppy. So why don’t you show us who, in the next generation, has done the work that Gallo claimed he had done: Discovering HIV. (or inventing it, or whatever).

    He has never worked on retrovirus Gene, he worked on a distinctly different and hardier plant virus. He failed to appreciate and comprehend the technical difficulties in studying animal viruses, more so blood borne retroviruses.

    Virology owes a big debt to the plant virologists. The advantage of plant viruses is that they can be obtained in a higher yield, when cultured in living green plants. They are not necessarily hardier. TYMV, for example is very similar to Polio virus. If an animal virus is so unstable that it says “poof” when you try to isolate it, I get very suspicious of the research. A virus that can’t even keep itself together outside the host, has no basis to exist as an exogenous infectious agent. So it may only exist in the minds of callous money grabbers and gullible young scientists.
    And don’t you dare calling “HIV” a “blood borne retrovirus”. They’ve never found it in blood, for catsake! All they’ve got is “Viral Load”. And that can be any nucleic acid crap the human body can produce.

    No, I don’t believe you and your colleagues are devils, Viji. But… Do you know who that guy was, with the black hat, and the goat’s feet sticking out from under his long coat, Viji? I mean the guy who offered you that scholarship.

  259. #259 Wilhelm Godschalk
    June 20, 2006

    Dale:
    Good to hear a serious argument again, for a change.
    But you know, I’m the guy who asks the right questions, not the guy who has all the answers.

    HIV p24 sequences aren’t found in healthy seronegative individuals nor even in all cells of seropositive individuals as any human gene or endogenous retroviral derived sequence would be.

    If we discount the possibility that they didn’t look hard enough (after all, most of the HIV snufflers look at the problem through tunnel vision), then the only conclusion we may draw from this fact is that there is something special going on in seropositive individuals. Looking in the list of sixty-some conditions (including pregnancy) that can cause a positive test, I get a little discouraged. It will take a major effort to find out why this sequence suddenly shows up. One explanation could be, that it’s easier to find something if you’re seriously looking for it.
    The molecular geneticists are generally too big for their britches. They tend to explain every cellular phenomenon in terms of “switched on” or “switched off” genes. Even when a
    simple explanation, based on the laws of physical chemistry would suffice. The original Watson & Crick model is certainly too simplistic; there is far more going on.

    You also forgot to mention that seropositive individuals don’t only make antibodies against p24 but make p24 itself.

    Of course they do. And I honestly think that seronegative individuals also make p24 (in fact, the whole p24 family).
    What about the antibodies against p24? Well, a living organism is not just a bag of genes and enzymes. Our body, and its individual cells, are compartmentalized, so that the separate sections can each perform their functions. Now if our p24 protein (the one the HIV-hustlers claim as their own) is sitting at a cell membrane, doing its job of loading up lipid vesicles with the right cargo, it normally stays there, and never takes an excursion into the blood stream or the lymph system. So the immune system has never encountered it, and there are no antibodies against it. But an illness or a pathological condition may result in p24 being leaked into the bloodstream. And then the immune system will strike against it. It is seen as “foreign”, although it is an endogenous protein.
    This is not a far-fetched fantasy of mine: There are known examples: A diseased heart or liver will leak enzymes (such as Lactic Dehydrogenase) into the bloodstream. And these enzymes are used for diagnostic purposes.
    The LDH enzymes from the heart and the liver are different, by the way. What does this mean for the genome inside heart- or liver cells? Is the human genome really as uniform throughout the whole body as they say?

    Lots of open questions. But nobody is working on them, because the conclusion has been fixed beforehand: This particular p24 must come from an outside virus (HIV), and anybody who doesn’t believe that gets no more money, and his ass is grass. But it’s just this point that is lacking proof. DNA has a way of reproducing, if you put it in a cell (just like rabbits). But just because it is separated from human proteins and other DNA does not convince me that it is viral. They never show real viral particles, just like the poker player who never shows his hole card, after all the other players fold.

    Very funny. But increasing proliferation of T cells doesn’t necessarily increase T cell count. T cell count is a measure of the difference between cell proliferation and cell death.

    Very funny indeed. But, eh… You’re not going to feed us the faucet/drain theory of Ho again, are you Dale? Please!
    Maybe we should go into the T-cell counting technique itself. Maybe that would tell us something. If there are T-cells, and they are not counted… Does that mean they’re not there? Very much like the famous question aboutthe falling tree in the woods. don’t you think?

  260. #260 Wilhelm Godschalk
    June 20, 2006

    Dale:
    Good to hear a serious argument again, for a change.
    But you know, I’m the guy who asks the right questions, not the guy who has all the answers.

    HIV p24 sequences aren’t found in healthy seronegative individuals nor even in all cells of seropositive individuals as any human gene or endogenous retroviral derived sequence would be.

    If we discount the possibility that they didn’t look hard enough (after all, most of the HIV snufflers look at the problem through tunnel vision), then the only conclusion we may draw from this fact is that there is something special going on in seropositive individuals. Looking in the list of sixty-some conditions (including pregnancy) that can cause a positive test, I get a little discouraged. It will take a major effort to find out why this sequence suddenly shows up. One explanation could be, that it’s easier to find something if you’re seriously looking for it.
    The molecular geneticists are generally too big for their britches. They tend to explain every cellular phenomenon in terms of “switched on” or “switched off” genes. Even when a
    simple explanation, based on the laws of physical chemistry would suffice. The original Watson & Crick model is certainly too simplistic; there is far more going on.

    You also forgot to mention that seropositive individuals don’t only make antibodies against p24 but make p24 itself.

    Of course they do. And I honestly think that seronegative individuals also make p24 (in fact, the whole p24 family).
    What about the antibodies against p24? Well, a living organism is not just a bag of genes and enzymes. Our body, and its individual cells, are compartmentalized, so that the separate sections can each perform their functions. Now if our p24 protein (the one the HIV-hustlers claim as their own) is sitting at a cell membrane, doing its job of loading up lipid vesicles with the right cargo, it normally stays there, and never takes an excursion into the blood stream or the lymph system. So the immune system has never encountered it, and there are no antibodies against it. But an illness or a pathological condition may result in p24 being leaked into the bloodstream. And then the immune system will strike against it. It is seen as “foreign”, although it is an endogenous protein.
    This is not a far-fetched fantasy of mine: There are known examples: A diseased heart or liver will leak enzymes (such as Lactic Dehydrogenase) into the bloodstream. And these enzymes are used for diagnostic purposes.
    The LDH enzymes from the heart and the liver are different, by the way. What does this mean for the genome inside heart- or liver cells? Is the human genome really as uniform throughout the whole body as they say?

    Lots of open questions. But nobody is working on them, because the conclusion has been fixed beforehand: This particular p24 must come from an outside virus (HIV), and anybody who doesn’t believe that gets no more money, and his ass is grass. But it’s just this point that is lacking proof. DNA has a way of reproducing, if you put it in a cell (just like rabbits). But just because it is separated from human proteins and other DNA does not convince me that it is viral. They never show real viral particles, just like the poker player who never shows his hole card, after all the other players fold.

    Very funny. But increasing proliferation of T cells doesn’t necessarily increase T cell count. T cell count is a measure of the difference between cell proliferation and cell death.

    Very funny indeed. But, eh… You’re not going to feed us the faucet/drain theory of Ho again, are you Dale? Please!
    Maybe we should go into the T-cell counting technique itself. Maybe that would tell us something. If there are T-cells, and they are not counted… Does that mean they’re not there? Very much like the famous question aboutthe falling tree in the woods. don’t you think?

  261. #261 McKiernan
    June 20, 2006

    And don’t you dare calling “HIV” a “blood borne retrovirus”. They’ve never found it in blood, for catsake!

    Wilhelm, seems Peter Duesberg has a different opinion:


    Continuum

    and

    Human immunodeficiency virus type 1 detected in all seropositive symptomatic and asymptomatic individuals.

    What say you, Wilhelm ?

  262. #262 Chris Noble
    June 20, 2006

    Gene Semon and other “rethinkers” keep on attempting to conflate HIV p24 with totally unrelated proteins with the only justification that they have the same molecular weight.

    HIV p24 shares homology with nucleocapsid proteins from other retroviruses such as equine infectious anemia virus, HTLV-I, mouse mammary tumor virus, feline immunodeficiency virus.

    It is unrelated to the emp24/gp25L/p24 family

    The only thing in common is that they have approximately the same molecular weight.

    Also immunoelectronmicroscopy shows that antibodies directed to HIV GAGp24 bind to the nucleocapsid in HIV.

    Fine structure of human immunodeficiency virus (HIV) and immunolocalization of structural proteins.

  263. #263 Shalini
    June 21, 2006

    HIV deniers? I recently met a SARS-cum-HIV denier who claimed that more people die each year of a ‘sore throat’.

    No amount of persuasion could make him understand that ‘sore throat’ is a symptom, not a disease.

    Sigh.

  264. #264 viji
    June 21, 2006

    Gene, you haven’t yet looked at the most recent reviews I posted above on the differences between entities that has reverse transcription activity, namely endogenous retrotransposons, endogenous telomerases, and exogenous viral reverse transcriptase (the enzyme associated with exogenous retrovirus) have you? or are you ignoring these latest 2004-2006 reviews, in favour of the earlier pioneering observations you reference? The studies you reference were the early landmark studies in those respective areas of research, i.e. first time look at the comparisons between endogenous ERVs and exogenous HIVs

    More research have been done in these respective study areas, we have discovered so much more so much since those early studies, and much more observations were gathered since that time to give us a better picture of it. Read the reviews I’ve posted before and understand the differences between endogenous retrotransposons, telomerases, and viral reverse transcriptase before you start barking the same old arguments

    This whole line of discussion started with the HIV tests involving the use of HIV RT activity levels as an indicator. As I have clearly explained in posts before, we already know sufficiently that HIV RT works in very different ways and is structurally different than endogenous retrotransposons, and although both does reverse transcription, each reverse transcribes only their exclusive targets, i.e. retrotransposons recognises poly A sequences, while HIV RT recognises viral LTR. Read the reviews and you will understand their ultimate function and function mechanism is mutually exclusive.

    And again i stress, we do not only look at one particular HIV test or marker to determine HIV infections, but a multitude of techniques involving totally distinct disciplines of science, so the chances of a false determination of infection is very low. Don;t get yourself deluded by the early studies which utilises only the one available methods, those methods were crude and sometimes inaccurate, but other much stringent methods have already been developed and routinely used

    Harking on the pittfalls of crude tests developed and used 2 decades ago is analogous to trying to run your latest RPG with extreme graphics on a DOS run PC.

    And your accusations are just equally annoying, to my knowledge I have yet in any case avoided any of your arguments, trying my best to post your latests and relevant developments in the areas, while you have been avoiding all the same questions I have on your working hypotheses. Refelct this on yourself, and stop barking accusations.

    the HIV RT activity test issue : already given you adequate references to let you scrutinise the difference between HERVs and HIV RTs

    the p24 tests, I was mislead by you before on you and Wilhiems branding of a certain “human p24 protein family” which I recently found is a fantasy spun by Wilheim with no references, or I’ve missed it, in any case, I believe Chris has already clarify the p24 antigen issue, with the lates references posted to validate his comments.

    Wilheim, in the MIT paper you referenced, there is no mention of the p24 family of vesicle proteins as equivalent to the HIV p24. Chris has earlier posted links that let you see the distictive difference in between HIV p24 and emp24/gp25L/p24 family of vesicle proteins. Look it up first before you start replaying your misconceptions like a broken old recrod. Look for his comments June 19, 2006 02:19 AM

    Comments on the weaknesses of the old Pandain paper has been highlighted in very early comments of this blog post. Read them. If you don’t appreciate the inaccuracy of early tests to detemine HIV infection and the difficulties in such a study, i.e. social stigmata on AIDS, unclear concepts on AIDS, then go on hiding behind your old Pandian paper and ignoring laboratory observations that can are reproducible.

    Wilhiem, despite you touting your “missing and now republished” comments as scientific, anyone can look carefully and find that there is not even a stich of science in his post of June 20, 2006 07:23 PM, like I said arguing for the sake of arguing, analogous to:

    There was a time when people thought the Earth was flat, there were no space ships to take us to the heavens (space) above to see our great blur green globe, or landmark voyages to circumvent oir globe. Thus people settled to the misconception that the Earth was flat, because that seems most logic
    As the science of astrology and geometry developed, some people began to question this explanations, the cutting edge astrological and geometrical calculations seems to point of a spherical globe. But people who did not understand these new techniques cried heresy! A lad who clearly lacks the trainign and understanding of such new techniques, Wilheim the ancient, argued vehemently that the Earth can’t be round, because he contends that everyone who tries standing on a round surface upside down will surely fall flat on his face. There goes his logic, arguing for the sake of arguing, despite so many reproducible astrological observations and accurate geometric calculations. But the intellectuals knew better, they worked on top of this preliminary observations, they stake and took risks, and finally people successfully circumvent the globe…. and what does Ancient Wilhiem do? he was quite a showman, he gathered the uninfarmed masses in the city square, tried to stand upside down on a sphere and fell falt on his face…. He shrieked to the masses,.. YOU SEE!!! THE EARTH CAN’T BE ROUND, ELSE WE WILL BE FALLING OFF, I DON’T KNOW WHAT THOSE ASTRONOMY, GEOMETRY, VOYAGES ARE, THEY MUST BE WIZARDS AND WITCHES ART!

    Until Wilhiem studies the techniques and perform the experiments, or read the recent findings, he’ll just be another dinosaur shrieking his ill informed judegements! Arguing for the sake of arguing.

    Sums it up

  265. #265 Chris Noble
    June 21, 2006

    Wilhelm asks:

    But how does he determine whether the sample was from endogenous or exogenous origin?

    If the sequence is endogenous and part of the human genome then it will be present in every single cell of every single person. It isn’t.

    HIV DNA can only be found in the cells of a relatively small percentage of the population of which the majority suffer from progressive CD4 cell depletion.

  266. #266 Chris Noble
    June 21, 2006

    For anyone that cites “mainstream” papers as evidence for “alternative” theories: write to the authors and ask them whether they agree with your theories.

    If they don’t agree with your interpretation – why?

    It is a common “rethinker” tactic to cite authors like Howard Temin and pretend that his work supports “rethinker” views. Write to Temin and ask him.

    The title of this paper should provide some clues – HIV causes AIDS

  267. #267 Chris Noble
    June 21, 2006

    Godschalk writes:

    Virology owes a big debt to the plant virologists. The advantage of plant viruses is that they can be obtained in a higher yield, when cultured in living green plants.

    This is the reason why early virology revolves around viruses such as TMV – because they can be obtained at much higher yields than other viruses.

    They also readily form crystals even in vivo. They were studied because they were easy.

    The first planets and moons to be studied were those that could be seen with the naked eye. There were also people that refused to look through a telescope at Jupiter’s moons.

  268. #268 Chris Noble
    June 21, 2006

    PS. Viji:

    The paper that people like Hank Barnes keep on misrepresenting is by Nancy Padian not Pandian.

    TYMV is smaller than HIV.

    That isn’t the point.

    TYMV was one of the workhorses of early virology precisely because it was extremely easy to obtain ver high yields of virus. It even forms crystalline arrays in infected cells.

    It is nonsense to insist that all other viruses that have been found subsequently must behave like TYMV.

  269. #269 viji
    June 21, 2006

    Chris,

    Thanks for pointing out my error on my brief statement on the size difference between animal and plant viruses. from Isn;t in this world long enought to have a crack on plant viruses or TYMV. We were lectured during my varsity years about the pioneering work in virology using plant viruses such as the TMV Tobacco mosaic virus, and know about the different approaches used to study animal viruses and plant viruses. Most of my experience working with viruses involve HIV and to a lesser extent West Nile virus. Never need to compare the sizes of viruses before.

    Appreciate the correction
    Cheers

  270. #270 Richard Jefferys
    June 21, 2006

    To follow up on Chris’s point about cites, the attempt by the “Rethinking AIDS” group to defend Celia Farber’s article cites excellent immunology papers by Zvi Grossman, Guido Silvestri, Guy Gorochov, Mario Roederer, Marc Hellestein etc. But these researchers all understand that HIV causes AIDS because their work – which details the pathogenic effects of HIV on the T cell immune system – tells them as much. So, in fact, the denialists are not arguing with the science (since they’re citing it!), they’re arguing with their own ignorant obsession with the ideas of Robert Gallo and David Ho, which are irrelevant for immunologists working on HIV pathogenesis.

    It really just highlights the fact that this is not an issue that has “sides” – this notion is a false construct used for rhetorical purposes by denialists. And it works well for some people, since it creates a nice “us and them,” anti-establishment kind of thing. But in the terms of this construct, researchers like Zvi Grossman are on the other “side” from Rethinking AIDS – so why are they citing his work? They also cite Marc Hellerstein’s excellent research, which exquisitely details the immunological perturbations caused by HIV, and documents how those peturbations resolve as a result of effective antiretroviral therapy. I cannot imagine the cognitive contortions that are involved in this kind of thinking (or should that be “rethinking”).

    Hellerstein’s most recent paper is in the Journal of Clinical Investigation, one of the few remaining journals that offer completely free online access, so it can be read in full here:

    http://www.jci.org/cgi/content/full/112/6/956

    Can the denialists here share their interpretation of these data? Perhaps they can explain why they think the depletion of long-lived naive and central memory CD4 and CD8 T cells occurs in HIV infection if HIV is benign? Or maybe they think such a loss is clinically unimportant? I’d be interested in finding out.

  271. #271 Gene Semon
    June 21, 2006

    More from a denialist obsessed with Bob Gallo (a genius at project engineering,BTW) and helping the acolytes to get Peter Duesberg.

    “Although no one knows why the death of the T4 (CD4) cell should depend on the molecule that defines it, some suggestive findings make it possible to formulate a hypothesis. The killing depends not only on the T4 molecule but also on the viral envelope. (Envelope glycoprotein has an important role in HTLV-III’s entry to its host and also in the death of the host cell.) . . .(L)ike entry to the cell, its death may depend on an interaction between the viral envelope (glycoprotein) and the cell membrane. Perhaps that interaction (which takes place as the virus particle buds from the cell) punches a hole in the membrane. Because the virus buds in a mass of particles, the cell cannot repair the holes as fast as they are made; its contents leak out and it dies.” (Robert Gallo, The AIDS Virus, Scientific American, [Jan 1987] V256, No. 1, 46,)

    “Included in (Peter Duesberg’s) criticism back in 1987 were the following crucial points that stand against the hypothesis and that remain completely unanswered by the scientific orthodoxy in charge of AIDS research:

    ….5. HIV is not directly cytocidal; it does not kill T cells.

    “The last point is of special interest since, in 1995, eight years later, we find in Nature, arguably the leading science weekly journal in the world, the commentary that, at the same time (a) confirms Peter Duesbereg’s contention (point number 5, above) that the evidence could never have supported direct viral killing; and (b) shifts the standard hypothesis around 180 degrees. The Nature commentary, in an article dealing with HIV, said that: ‘… an intrinsic cytopathic effect of the virus is no longer credible.’ (Wain-Hobson, S. Nature, 373: 102, 1995).

    “What very few people realize, including most professors of molecular biology that I know, is that this shift has occurred: that the orthodox view of HIV as a direct killer of human immune cells has been thrown out.” Richard C. Strohman UC Berkeley May 1995 ‘Infectious AIDS; Have we been misled’ (preface book) (1995)

    http://www.virusmyth.net/aids/data/rsforword.htm

    That’s Professor EMERITUS RC Strohman. And SW Hobson, of course, a leading AIDS researcher.

  272. #272 Hank Barnes
    June 21, 2006

    Noble writes:

    It is a common “rethinker” tactic to cite authors like Howard Temin and pretend that his work supports “rethinker” views. Write to Temin and ask him.

    Umm, Temin is dead.

    Good cite to the Blatter, Gallo, Temin debate though.

    But, is there a reason you omitted Duesberg’s initial piece and his response thereto? The entire exchange is here.

    Another debate is festering at Lew Rockwell’s site.

    HankB

  273. #273 Wilhelm Godschalk
    June 21, 2006

    Dale:
    Good to hear a serious argument again, for a change.
    But you know, I’m the guy who asks the right questions, not the guy who has all the answers.

    HIV p24 sequences aren’t found in healthy seronegative individuals nor even in all cells of seropositive individuals as any human gene or endogenous retroviral derived sequence would be.

    If we discount the possibility that they didn’t look hard enough (after all, most of the HIV snufflers look at the problem through tunnel vision), then the only conclusion we may draw from this fact is that there is something special going on in seropositive individuals. Looking in the list of sixty-some conditions (including pregnancy) that can cause a positive test, I get a little discouraged. It will take a major effort to find out why this sequence suddenly shows up. One explanation could be, that it’s easier to find something if you’re seriously looking for it.
    The molecular geneticists are generally too big for their britches. They tend to explain every cellular phenomenon in terms of “switched on” or “switched off” genes. Even when a
    simple explanation, based on the laws of physical chemistry would suffice. The original Watson & Crick model is certainly too simplistic; there is far more going on.

    You also forgot to mention that seropositive individuals don’t only make antibodies against p24 but make p24 itself.

    Of course they do. And I honestly think that seronegative individuals also make p24 (in fact, the whole p24 family).
    What about the antibodies against p24? Well, a living organism is not just a bag of genes and enzymes. Our body, and its individual cells, are compartmentalized, so that the separate sections can each perform their functions. Now if our p24 protein (the one the HIV-hustlers claim as their own) is sitting at a cell membrane, doing its job of loading up lipid vesicles with the right cargo, it normally stays there, and never takes an excursion into the blood stream or the lymph system. So the immune system has never encountered it, and there are no antibodies against it. But an illness or a pathological condition may result in p24 being leaked into the bloodstream. And then the immune system will strike against it. It is seen as “foreign”, although it is an endogenous protein.
    This is not a far-fetched fantasy of mine: There are known examples: A diseased heart or liver will leak enzymes (such as Lactic Dehydrogenase) into the bloodstream. And these enzymes are used for diagnostic purposes.
    The LDH enzymes from the heart and the liver are different, by the way. What does this mean for the genome inside heart- or liver cells? Is the human genome really as uniform throughout the whole body as they say?

    Lots of open questions. But nobody is working on them, because the conclusion has been fixed beforehand: This particular p24 must come from an outside virus (HIV), and anybody who doesn’t believe that gets no more money, and his ass is grass. But it’s just this point that is lacking proof. DNA has a way of reproducing, if you put it in a cell (just like rabbits). But just because it is separated from human proteins and other DNA does not convince me that it is viral. They never show real viral particles, just like the poker player who never shows his hole card, after all the other players fold.

    Very funny. But increasing proliferation of T cells doesn’t necessarily increase T cell count. T cell count is a measure of the difference between cell proliferation and cell death.

    Very funny indeed. But, eh… You’re not going to feed us the faucet/drain theory of Ho again, are you Dale? Please!
    Maybe we should go into the T-cell counting technique itself. Maybe that would tell us something. If there are T-cells, and they are not counted… Does that mean they’re not there? Very much like the famous question aboutthe falling tree in the woods. don’t you think?

  274. #274 Wilhelm Godschalk
    June 21, 2006

    Thank you for commenting.

    Your comment has been received and held for approval by the blog owner.

  275. #275 Richard Jefferys
    June 21, 2006

    What’s your point Gene? The fact that HIV causes AIDS is entirely independent of any individual opinions about why exactly CD4 T cells die/become dysfunctional (even celebrity opinions). It is the denialists that persist in claiming that cytopathicity is a prerequisite for pathogenicity (you have much in common with David Ho, for that very reason). So I don’t understand what your quotes are intended to convey.

    What do you think of the Hellerstein paper? What did you mean earlier when you said that CD4 T cell proliferation equates with increases in peripheral blood CD4 T cell counts? When you have the flu and your CD4 and CD8 T cells are proliferating wildly in response to flu antigens, do you think your peripheral blood CD4 T cell count increases?

  276. #276 Gene Semon
    June 21, 2006

    Hi Richard, this one is especially for you. My point involves an alternate reading frame that requires you to read every post I’ve made while suspending (at least for the moment), the heckling of your friends. Read Wilhelm and Hank the same way.

    Being sympathetic to the plight of aidschurch acolytes and hoping that I can move the symbolic logic and discussion of post @June 19, 2006 11:46 AM and post-posts from incomprehension to comprehension, I offer the following additions and considerations: Let X = transcriptionally active HERVs, LINEs and SINES, some with intact open reading frames, others that can be “paraprocessed”*, (e.g. RNA editing, alternate splicing, trans-complementation). Then reframe X => A etc. chain. Realize the possibility that HERVs and HIVs switching divalent cation preferences cannot be excluded and include all posts by Hank, Wilhelm, Perth Group and myself in your assessment of the data from retroviral research and maybe, just maybe, the lightbulb will turn on.

    *POP QUIZ
    From whom did I get that term?

    All this assumes, of course, that antidenialists are interested in more then playing the game of constructive dismissal. I give you all credit for being very good at something.

    Richard, apparently you read what I posted at NAR. Good. Ask Brian Foley why its important that David Who? is wrong and why its back to the future with Duesberg’s extensive, well documented critique of slow viruses.

    Best regards,
    Gene

  277. #277 Gene Semon
    June 21, 2006

    Oh yeah, your questions. Ultimately, the less free energy, fewer T cells. Many roller coasters in between. Complex and varying dynamics from individual to individual. Hypercortisolism sends more T-cells into tissues, where most of them are anyway, plus drives network from TH1 to TH2.

  278. #278 Richard Jefferys
    June 21, 2006

    Thanks Gene, as I surmised you do not have a clue what you are writing about. I have no idea what posts at NAR you’re referring to, I thought you were just quoting Anthony Liversidge? Since you did though, are you going to retract your statement that CD4 T cell proliferation equates with increased T cell counts? You were rather chest-pounding when you thought Viji had something wrong.

    Why don’t you explain why you think David Ho’s errors are so important? Zvi Grossman (who is affiliated with NIAID but is cited by denialists) and many other immunologists (like Mario Roederer, another NIH employee frequently cited by denialists) critiqued Ho’s theories from the get go (check out the letters page from Nature after Ho published his tap-and-drain theory). At one conference, Grossman’s challenges produced a classic piece of petulance from Ho (“that’s Grossman citing Grossman!”). So, is Zvi part of the “orthodoxy”? Does he get a day off when denialists feel the need to cite his work?

    Marc Hellerstein’s work is funded by NIH, but is cited by Rethinking AIDS in defense of Farber’s error-riddled screed. But if Hellerstein’s work challenges the “orthodoxy,” why is he receiving funding from NIH? Shouldn’t he be getting censored?

    This is what happens when you try and misappropriate science in the service of an ideology.

  279. #279 Gene Semon
    June 21, 2006

    Richard,

    Nothing like starting out cross-wired.

    You really have to ask Truthseeker over at NAR that question. I confess to the crime of not putting the appropriate quotation marks and attribution, and you might well be correct and “Truth” wrong on that particular point, for the very reasons I stated above. If, in fact, Truthseeker is in error, then he missed the mark in his satire of Dr Fauci.

    The response I referred to was late at the tail end of the Larry Kramer/apology thread and it was to answer two of your questions.

    My “chest beating”, if you want to call it that, was to draw attention to Viji’s shooting from the hip when dealing with Wilhelm.

    If you want to insist “you do not have a clue what you are writing about”, at least read all my posts and please be specific. Don’t go off half-cocked like you just did. See, that’s the essential problem, uncritical inferences and jumping to conclusions.

    I hope we can stay on the high road,
    Gene

  280. #280 Gene Semon
    June 21, 2006

    More on constructive dismissal. What’s in the previous exchange may be a candidate, depending on Richard’s response.

    Zen . . . And the Art of Debunkery Revised edition, 1997 by Daniel Drasin. http://members.aol.com/ddrasin/zen.html

    EXCERPTS:

    As the millennium turns, science seems in many ways to be treading the weary path of the religions it presumed to replace. Where free, dispassionate inquiry once reigned, emotions now run high in the defense of a fundamentalized “scientific truth.” As anomalies mount up beneath a sea of denial, defenders of the Faith and the Kingdom cling with increasing self-righteousness to the hull of a sinking paradigm. Faced with provocative evidence of things undreamt of in their philosophy, many otherwise mature scientists revert to a kind of skeptical infantilism characterized by blind faith in the absoluteness of the familiar. Small wonder, then, that so many promising fields of inquiry remain shrouded in superstition, ignorance, denial, disinformation, taboo . . . and debunkery.

    What is “debunkery?” Essentially it is the attempt to *debunk* (invalidate) new information and insight by substituting scient*istic* propaganda for the scient*ific* method.

    HOW TO DEBUNK JUST ABOUT ANYTHING

    Portray science not as an open-ended process of discovery but as a holy war against unruly hordes of quackery- worshipping infidels. Since in war the ends justify the means, you may fudge, stretch or violate the scientific method, or even omit it entirely, in the name of defending the scientific method.

    Equate the necessary skeptical component of science with *all* of science. Emphasize the narrow, stringent, rigorous and critical elements of science to the exclusion of intuition, inspiration, exploration and integration. If anyone objects, accuse them of viewing science in exclusively fuzzy, subjective or metaphysical terms.

    Insist that the progress of science depends on explaining the unknown in terms of the known. In other words, science equals reductionism. You can apply the reductionist approach in any situation by discarding more and more and more evidence until what little is left can finally be explained entirely in terms of established knowledge.

    END EXCERPTS

    Sound familiar? This is an advertisement to a comprehensive treatment of this subject at the above URL.

    Of course, Occam’s razor cuts both ways.

  281. #281 Gene Semon
    June 21, 2006

    I would love to answer all the “new” questions, guys but already have. Read, really read the 2004-2006 research and stop shooting from the hip!

  282. #282 Richard Jefferys
    June 21, 2006

    OK, so I found your comment on NAR. Ironically, you cite Marc Hellerstein’s first paper evaluating T cell turnover in HIV infection using deuterated glucose but then claim that:

    “In Part One, the first part of the deductive chain: HIV causes CD4 depletion in-turn causing OI is weakened, i.e. casts doubts on HAART works, therefore HIV causes AIDS.”

    “Part One” refers to your comparison of Hellerstein’s data to David Ho’s tap and drain model. The fact that you believe that Hellerstein’s work somehow contradicts the fact that HIV typically causes CD4 T cell depletion and OIs (and casts doubt on both HAART and HIV causing AIDS) speaks volumes regarding your ability to understand Hellerstein’s data. Since central memory CD4 T cells are critical for protection against opportunistic pathogens, and Hellerstein’s data shows that HIV infection causes a decline in this long-lived CD4 T cell population and an increase in short-lived effector CD4 T cells, how can this be compatible with your interpretation that it weakens the case that “HIV causes CD4 depletion in-turn causing OI.” The Nature Medicine paper states that CD4 T cell production increased after HAART, which rather contradicts your claim that the paper casts doubt on HAART working or HIV causing AIDS.

    The quote you bring forth above refers to people misusing science; I think this is a little different from informing someone that they haven’t understood the paper they are citing. You don’t have to take my word for it, you can write to Marc Hellerstein and ask him.

    Your ideological position is nicely articulated by one of your asides above:

    “POP QUIZ

    a) Which kills more in the good old USA per year, iatrogenic medicine or AIDS?

    b) How many dogs can waste taxpayer money while chasing their tails on the head of a pin?”

    I guess at least you don’t think Marc Hellerstein was wasting taxpayer money. Or maybe you do now?

  283. #283 Wilhelm Godschalk
    June 21, 2006

    McKiernan:
    Wilhelm, seems Peter Duesberg has a different opinion:

    I know. Of course I’m familiar with the two Continuum articles. Peter Duesberg is entitled to his opinion. I agree wih him on many issues, but on this one I side with Stefan Lanka and the Perth Group.
    I’ve always wondered why he ever wrote this. Maybe he was just having a little fun with the apologists (he has a terrific sense of humor). Maybe he made a serious attempt to rake in the prize Continuum Magazine had promised to the first person who proved the existence of HIV.
    But if we seriously look at it – I mean without smoking funny cigarettes – this “molecular cloning” of DNA is a far cry from physically isolating an RNA-containing virus.
    The sentence “In conclusion: HIV has been isolated by the most rigorous method science has to offer.” should have elicited howls of laughter from California to Europe to Australia. And Duesberg must have known that. He was just playing games, I think.
    The other paper you quoted is just a run-of-the-mill 9-author paper where they employ the usual hanky panky with PCR and co-culturing.
    Like Peter Duesberg, I am entitled to my opinion too. Duesberg (however brilliant) belongs to the generation of virus hunters (starting with the ‘war on cancer’). I am 5 years older than Duesberg. We didn’t have these wild goose chases in our time.

  284. #284 Wilhelm Godschalk
    June 21, 2006

    Chris Noble:
    It is nonsense to insist that all other viruses that have been found subsequently must behave like TYMV.

    Riiiiight! So who has made that claim?
    But… if you put any virus in an ultracentrifuge (perish the thought), then it should obey the laws of hydrodynamics, just like they alwys did. And if you shine UV light through a solution of any virus, in a spectrophotometer or a fluorimeter, they show the same behavior with respect to absorption, fluorescence, and light scattering.
    Only when you put them in a host, or a withes’ brew, they start to show different behavior.

    Viji:
    Wilheim, in the MIT paper you referenced, there is no mention of the p24 family of vesicle proteins as equivalent to the HIV p24.

    Eh… hahahahahaha! My dear Viji, that’s because there is no HIV p24. These p24 proteins are all different from each other. And because they are situated at the edge of a membrane, where legend has it the HIV cores get their envelopes, the HIV wizards scratched their pointy heads and thought: “Good, that’s just what we need.” So they just stole one (thinking the rest of the family wouldn’t miss it), sequenced it and filed it in the protein bank under the name “HIV p24″. Then they looked for a piece of DNA that could account for that protein sequence, and declared that as part of the “HIV genome”. Of course it was there, because it was just part of the cellular genome.
    If you start to think about this with an open mind, you’ll slowly get to realize what an out-and-out fraud this is, and how you have been deceived.
    Never mind Chris Noble and Richard Jefferys. They are part of the organization that’s perpetrating this fraud: TAG. They will never contribute anything to science. Their only function is to spread disinformation. And they have been pretty successful for the past 22 years.

  285. #285 Dale
    June 21, 2006

    Gene writes Let X = transcriptionally active HERVs, LINEs and SINES, some with intact open reading frames, others that can be “paraprocessed”*, (e.g. RNA editing, alternate splicing, trans-complementation). Then reframe X => A etc. chain. Realize the possibility that HERVs and HIVs switching divalent cation preferences cannot be excluded and ,,,

    If ‘HIV” were an endogenous retrovirus, it would be present in ~50% of children in whom either parent were HIVpositive (rather than the observed 10-25% of children of affected mothers only) and inheritance would not be affected by either ARV treatment of the mother prior to the child’s birth or by breastfeeding. Moreover, sexual partners of HIV positive individuals would be at no greater risk than the general population of being HIV positive themselves when in fact, partners of HIV positive individuals have a statistically much higher risk of being HIV positive.

    But don’t let data get in the way of your hypotheis.

  286. #286 Gene Semon
    June 22, 2006

    Richard, I supported you over at NAR. Is this anyway for you to behave?

    It seems to me you’re either lazy or illiterate. My comments specifically addressed Ho’s model and HAART, which was the most important justification (Times’ Man of the Year, remember!?) for the cocktails you love so dearly. Now you have a new, brand new guaranteed correct theory. And you’re resorting to ad hominem because obviously I am not part of the revised standard official version of your vanguardist movement. You’ve taken a page from the playbook of Vladimir Illich. Congratulations Richard. You’re sure to make Cardinal.

    In the meantime. I will continue to make posts that are OF A PIECE and consistent with previous posts and, hopefully, move the discussion forward. If you choose to make progress measured in inches and want to belabor points endlessly, beating your chest to impress all of us with your great knowledge of T-cell dynamics, fine.

    Carl T. Bergstrom and Rustom Antia. How do adaptive immune systems control pathogens while avoiding autoimmunity? Trends in Ecology & Evolution . Volume 21, Issue 1 , January 2006, Pages 22-28

    EXCERPTS

    (B)ecause pathogens interfere with immune function, immune systems must be robust against sabotage. We describe here how these challenges are met by two immune systems, the intracellular RNA interference system and the vertebrate CD8 T-cell response. We extrapolate from these two systems to propose principles for strategically robust control.

    By deploying multiple redundant defense pathways, the host can influence the evolutionary trajectory of a pathogen population. Redundant defense mechanisms reduce the selective advantage to the pathogen of knocking out a single mechanism.

    Systems that have to deal with internal subversion (and the retrovirus must be demonstrated to reach that stage)* must go one step further and be strategically robust: that is, they need to function properly despite efforts to sabotage their workings. *(added to text)

    The distinction between robustness and strategic robustness becomes clear through analogy. A robust computer circuit would function effectively even if a few resistors burned out at random. A strategically robust computer circuit would function even if a disgruntled technician tried to sabotage the machine by removing precisely those resistors that were most crucial. (Added to text: if the AIDS virus can be demonstrated to be equivalent to the “disgruntled technician”, without invoking teleology, then we have something like compelling evidence.)

    RNAi is a system of post-transcriptional gene silencing that is broadly conserved across eukaryotes; it appears to have evolved as a form of adaptive immunity to prevent viruses from replicating within infected cells, by targeting foreign nucleic acids. (Added to text: something the classical virologists knew nothing about. Score one for the antidenialists.)

    END EXCERPTS

    Assuming an HIV “hijacks”, what about the armed guards RNAi?

    This paper can be accessed at:

    http://www.barnesworld.blogs.com/ => Science Stuff => Trends in Ecology & Evolution

  287. #287 Gene Semon
    June 22, 2006

    Hey something I can grab onto! Thanks Dale.

    “If ‘HIV” were an endogenous retrovirus, it would be present in ~50% of children in whom either parent were HIVpositive (rather than the observed 10-25% of children of affected mothers only) and inheritance would not be affected by either ARV treatment of the mother prior to the child’s birth or by breastfeeding. Moreover, sexual partners of HIV positive individuals would be at no greater risk than the general population of being HIV positive themselves when in fact, partners of HIV positive individuals have a statistically much higher risk of being HIV positive.”

    The problems with this “data”, as you call it, were addressed in my previous posts re guesstimates, and the specificity problem in Perth and Wilhelm posts; I’m sorry if you take offense at the metaphor but we’re all dancing around on the head of a pin.

    “HIV positives” are measured by the mother’s antibodies, correct? And transmission is transfer of same via mom thru placenta. Your model can only be substantiated by the gold standard of mainstream researchers: full length proviral measurements, i.e. attemts to measure same from momma and poppa (real data) since the kid doesn’t get daddy’s antibodies (unless he’s a pedophile). So its back to GIGO.

  288. #288 Gene Semon
    June 22, 2006

    Richard,

    “the fact that HIV typically causes CD4 T cell depletion”

    Repeating a mantra is your counter argument? See discussions above, especially incremental inductivism.

    “Since central memory CD4 T cells are critical for protection against opportunistic pathogens…”

    OK, but see previous post of today re redundancy. Have CD3 cells, for example, been excluded for backing up the memory/helper function? And what about innate immunity as a back-up against OI?

    “…it weakens the case…” Ho’s case.

    “The Nature Medicine paper states that CD4 T cell production increased after HAART…”

    Ah yes, the leukemic effect. What about the patient’s health?

    “…people misusing science…”

    Yeah, like relying on teleology.

    “…you can write to Marc Hellerstein and ask him…”

    No need. I’ll get around to a re-read to see how your interpretation holds up.

    What “ideological position”? a) is a serious question that has been answered by JAMA. Prioritizing threats to the public health is “ideological”? b), of course is satire. Since I cited Hellerstein at length, that’s hardly an accusation of wasting the taxpayer’s money. In fact, apparently we both agree that refuting Ho was a service!

    OK, but see today’s previous post re redundancy. Have CD3 cells been excluded from playing this role? What about innate immunity and OI (another back-up)?

    “Hellerstein’s data shows that HIV infection causes a decline in this long-lived CD4 T cell population and an increase in short-lived effector CD4 T cells”

    Assuming your interpreation of Hellerstein’s data is the correct one and accepting Perth, Duesberg, Wilhelm, Urnovitz and Lanka, I would say measurements of markers associated with retroviral transcription are associated with the described phenomena in T-cells.

  289. #289 Gene Semon
    June 22, 2006

    And finally, “Farber’s error-riddled screed”. As you know, Richard, responses to the 50 points have been made. If you want to debate any of those (as opposed to starting all over), let’s have at it.

    Whoops, ignore redundant third paragraph from the bottom in previous post.

  290. #290 Richard Jefferys
    June 22, 2006

    Both CD4 and CD8 T cells express CD3, it’s part of the T cell receptor. It’s not a marker for a different subset of cells.

  291. #291 Richard Jefferys
    June 22, 2006

    How is an NIH-funded researcher refuting the David Ho model compatible with the idea of an “orthodoxy”? Since Ho and Hellerstein surely cannot be orthodox simultaneously, which one is represents the “orthodoxy” now, in the view of denialists? It doesn’t seem to be Hellerstein, because he’s cited in that Rethinking AIDS document you’re referring to. This time last year Hellerstein was presenting at an NIAID-sponsored workshop on T cell homeostasis and HIV infection, convened by Zvi Grossman. Who is also cited by Rehinking AIDS.

  292. #292 Gene Semon
    June 22, 2006

    The hits just keep on coming!

    “So, in fact, the denialists are not arguing with the science (since they’re citing it!)”

    Are you really saying, Richard, that theorists cannot use data to advance their argument from a paper in which they disagree with the conclusions?

    See post on constructive dismissal. Like I said, the TAG has definitely mastered a real skill.

  293. #293 Gene Semon
    June 22, 2006

    “If the sequence is endogenous and part of the human genome then it will be present in every single cell of every single person. It isn’t.”

    Chris, you haven’t grasped my model. All kidding aside, it responds to this point. The now much-maligned Gallo ( from “one side” according to Richard), was careful enough, because he actually did know what he was doing, to check HTLV IIIb against the human genome.

  294. #294 Richard Jefferys
    June 22, 2006

    It’s not just the conclusions, Gene. The Hellerstein paper demonstrates the deleterious effects of HIV on the T cell immune system and the salutary effects of HAART in this setting, and it’s being cited by people arguing that HIV is apathogenic and that HAART has no benefit.

  295. #295 Gene Semon
    June 22, 2006

    “(I)f p24 shows up as a “false positive” in placenta and/or organ transplant recipients, this isn’t a practical problem in diagnosing HIV infection as such diagnoses are neither carried out on placental tissue nor made in the absence of a medical history that would reveal whether someone was a transplant recipient.”

    Good point, Dale, but if it shows up as a stress protein in an AIDS risk group, it will be a false positive.

    Cherry-picking: “Smaller Hsp’s (15-28kd stress proteins) bind reversibly to the nuclear skeleton during heat shock and form higher order aggregates.”

    Joan Smith-Sonneborn. The role of the “stress protein response” in hormesis. (1993) Belle Newsletter, V1, N3, 4

  296. #296 Gene Semon
    June 22, 2006

    And viji, you seem like an old friend at this point; all barking and kidding aside, really I have responded to your long-winded post of June 21, 2006 01:35 AM and do understand the distinctions between different retroelements.

  297. #297 Dale
    June 22, 2006

    Gene writes “HIV positives” are measured by the mother’s antibodies, correct? And transmission is transfer of same via mom thru placenta. Your model can only be substantiated by the gold standard of mainstream researchers: full length proviral measurements,

    In New York state there has been mandatory testing of babies born to mothers of unknown HIV status since 1997. HIV positives are initially identified by antibodies but HIV transmission is measured by HIV DNA PCR – not a full length proviral measurement but a proviral measurement nonetheless. Transmission varies from about 26% in cases where neither mother nor infant is treated to about 6% where mother is treated with ARVs prior to labor and infant is treated after birth. Transmission of an endogenous virus from a positive mother would be 50% and would be unaffected by ARV treatment. If the virus is not endogenous, none of its genes including p24 are endogenous.

  298. #298 Chris Noble
    June 22, 2006

    Gene writes:

    Chris, you haven’t grasped my model. All kidding aside, it responds to this point.

    How do you define endogenous?

    The papers you cite demonstrate that HIV Gag, Pol and Env are homologous to other retroviruses so you don’t seem to be denying that it is retroviral. That leaves two possibilities that it is endogenous or exogenous.

    All other endogenous retroviruses that have been found have been incorporated into the human genome early in the evolution of humans. Every human being has these endogenous retroviruses in cells in their body.

    As Dale points out if HIV were endogenous then it would be passed on from mother (and father) to child completely unaffected by HAART.

    DNA replication in humans has much higher fidelity than RNA viruses and only small sequence changes would be expected over time. This is true both within an individual and within a popualtion. This is completely the opposite of what is observed.

    Both Duesberg and the Perth Group frequently point out that HIV DNA is only found in a small percentage of CD4 T-cells. If HIV is an endogenous virus then it should be present in %100 of T-cells.

    If you are going to claim that HIV is endogenous then explain this. Explain what you mean by endogenous.

  299. #299 Chris Noble
    June 22, 2006

    Hank Barnes wrote:

    Umm, Temin is dead.

    Good point. That was a stupid mistake on my part.

    His published papers clearly show his opinion on the subject and the evidence that supports this opinion.

    If you are going to cite a paper by Temin or other “orthodox” scientists in an attempt to argue that HIV does not exist or does not cause AIDS then you should consider the possibility that you have not understood the paper.

    It is arrogance of an enormous magnitude to argue that you know how to interpret the words of a scientist better than the scientist himself.

  300. #300 Hank Barnes
    June 23, 2006

    It is arrogance of an enormous magnitude to argue that you know how to interpret the words of a scientist better than the scientist himself.

    Disagree. Interpreting the data is one thing; buying wholesale the author’s conclusion of his own data is another. Often the conclusion doesn’t faithfully report the data.

    Take Padian. She observed HIV+ people having sex for 6 years. However, none of the sex partners contracted HIV. That’s the data. You can intepret it your way, I’ll interpret it my way.

    If all or most of the sex partners had contracted this “fatal, sexually-transmissible” virus, then, obviously, I’d be supporting the orthodox view.

    If you were a rigorous dispassionate scientist (on this issue), you’d do the converse, Chris.

    Hank

  301. #301 Jeremy
    June 23, 2006

    Same discussion, same participants.

    Some things never change.

    Ya know, “Someday this war’s gonna end…” I hope.

  302. #302 Gene Semon
    June 23, 2006

    “Both CD4 and CD8 T cells express CD3, it’s part of the T cell receptor. It’s not a marker for a different subset of cells.

    Wait a minute, I thought the T-cell receptor was designated alpha/beta; Richard you should know that T-cells can have various expressions of CD4+/-,CD8+/-, or CD3+/-, etc., i.e. not exclusive.

  303. #303 Richard Jefferys
    June 23, 2006

    That’s really great Gene. You just suggested that CD3 – which is known as a pan-T cell marker – was a marker for a subset of T cells somehow different from CD4 and CD8 T cells. Now you’re suggesting that there are CD4 and CD8 T cells that don’t express CD3.

    Please do a PubMed search. Or look at this description of T cell development, which has a nice picture of where CD3 fits into the T cell receptor complex:

    http://www-immuno.path.cam.ac.uk/~immuno/part1/lec08/lec8_97.html

    And since HIV infects T cells and you’re claiming to have some insight into HIV infection that the world’s immunologists have overlooked, your ignorance on this topic should give you pause (not that it will, of course).

  304. #304 Gene Semon
    June 23, 2006

    Viji: “HIV does this in order to hijack human physiological processes for its own replication, this insertion is transient, and at the end of the life cycle there is a free-standing virus particle…”

    Chris: “If you are going to claim that HIV is endogenous then explain this. Explain what you mean by endogenous.”

    Dale: “Transmission of an endogenous virus from a positive mother would be 50% and would be unaffected by ARV treatment. If the virus is not endogenous, none of its genes including p24 are endogenous.”

    Fair enough, let me put flesh on the bones of the previous symbolic chain and explain what I mean by reframing “HIV phenomena”. Unfortunately, I must point out that a rigid exogenous/endogenous distinction and Viji’s “insertion is transient” is a bit of a muddle.

    Let me start with Viji. By definition, any “exogenous” retrovirus, once in its proviral form and covalently bonded within chromosomal DNA is endogenous(!) and remains so for up to millions of years (if it makes it to the germ-line), until it is removed by a recombination mechanism between the two LTRs. It can be transcribed, of course, in a short period of time thereafter by cellular RNA polymerase and be reborn, so to speak, but now we get to the fun part. (Here’s where the well crafted arguments of the Bialy/Duesberg team come into play – see Dean Esmay and Harvey’s book.) The starting point for this is the section of Duesberg’s never-answered 1989 PNAS paper: HIV is a conventional retrovirus without an AIDS gene, which discusses why “accessory genes” are not sufficient to demonstrate that an HIV: can “escape the fate” of being “trapped” by the cell’s transcriptional apparatus; or, to put it another way; has the “ability” to “hijack the cell’s physiological processes”.

    Now, let me cherry-pick a mainstream paper, Piatak M, et al (1993), Science 259, 1749-1754, and propose a hypothetical natural history starting at the point of, say 10-100 entry virions in the future patient who is now a matter of great concern. (Also ignoring objections like no cell free transmission, etc.) The authors estimate, based on infectious titration of their viral load, that 99.998% are defective. But this would apply to the RNA genome, of course, so we can presume that this hardy little group has managed to associate with functional reverse transcriptase and integration enzymes plus obtain entry into some hapless T-cells. When they make it to the proviral stage, they are no different functionally and structurally from defective HERVs.

    Multiplying several low probabilities produces substantially lower ones. Can we see the yawning gap here in terms of the odds of a pathogenic transmission? Why 140 bp of gag, although extremely sensitive, proves nothing? Why denialism flourishes? Note that transcription of the defective DNA (assuming the LTR promoters are intact) in a cell under stress can produce the marker “seropositivity” and would be a true positive. But cross reactions with HERVS in cells under oxidative stress can also occur, in fact have been documented in AIDS patients in the famous PNAS “viruses in all of us” paper. (will provide exact ref)

  305. #305 Dale
    June 23, 2006

    Gene writes and propose a hypothetical natural history starting at the point of, say 10-100 entry virions in the future patient who is now a matter of great concern. (Also ignoring objections like no cell free transmission, etc.) The authors estimate, based on infectious titration of their viral load, that 99.998% are defective. But this would apply to the RNA genome, of course, so we can presume that this hardy little group has managed to associate with functional reverse transcriptase and integration enzymes plus obtain entry into some hapless T-cells. When they make it to the proviral stage, they are no different functionally and structurally from defective HERVs.

    Your scenario has several problems. First Piatak and his collegues estimated the infectivity of viral particles based on an endpoint dilution assay in cells grown in a laboratory. Infectivity in such an assay may or may not accurately reflect infectivity in a human being. Secondly, even if those numbers are an accurate reflection of infectivity, they don’t negate any of the data demonstrating that HIV does not behave like an HERV. If HIV were no different functionally or structurally from a defective HERV then it wouldn’t be infectious (as is clearly demonstrated by transfer from infected to non infected T cells in the laboratory), it wouldn’t replicate (as demonstrated by the appearence of reverse transcriptase activity, increasing viral loads and of heterogeneity in the HIV sequences that are inconsistent with replication by the enzyme that replicates integrated HERVs) and it wouldn’t be transmitted to sexual partners (as demonstrated both epidemiologically and by following transmission cohorts).

  306. #306 Gene Semon
    June 23, 2006

    “And since HIV infects T cells and you’re claiming to have some insight into HIV infection that the world’s immunologists have overlooked, your ignorance on this topic should give you pause (not that it will, of course)”.

    Richard, I believe Polly Matzinger has “overlooked” the SPECIFICS of HIVs, but I’m sure you’ll correct me if I’m wrong.

    “…insight into HIV infection…” See previous post.

    Excellent reference. Thanks.

    Excerpt: “cells which successfully pass this scrutiny become CD4+CD8+ ‘double positive’ cells”

    On T-cell alpha/beta; the “complex” diagram clearly shows CD3 separate from (even though surrounding) alpha/beta plus CD4/CD8 in turn surrounding CD3 – alpha/beta, all as part of the same complex.

    “…not that it will, of course…” Your point, and my possible ignorance re CD3-, is taken. Let’s not rule out other schools of thought; I stand by that.

  307. #307 Richard Jefferys
    June 23, 2006

    I’m beginning to get the impression that perhaps Gene, like Harvey Bialy and Hank, thinks that it is somehow subversive just to keep these dialogues going. For some light relief, here is a bit of classic Peter Duesberg, from his 1993 paper in Biotechology. He is expounding on his attempts to identify cases of “HIV negative AIDS”:

    “Table 1 includes some American and European immunodeficiencies that may not exactly fit the current definition of AIDS defining immunodeficiency without disease, which is <200 T-cells per microliter (CDC, 1992, MMWR 41, RR 17, 1-19), as for example, HIV-free male homosexuals on various recreational drugs with “<600 cells per cubic millimeter” or HIV-negative hemophiliacs with T4/T8 cell ratios of about 1 or <1 (Table 1, refs. 46-61). But even if not all of these cases fit the current definition of AIDS-defining immunodeficiency exactly, they do so prospectively. This is because their T-cells typically continue to decline either because of risk behavior, such as the consumption of recreational drugs, or because of clinical AIDS risks, such as chronic transfusion of foreign proteins as prophylaxis against hemophilia (Duesberg, P.H., 1992, op. cit.).”

    I hope it is clear what Duesberg is saying here. In the Kaslow paper he is citing (ref 14), gay men taking drugs did not display evidence of AIDS unless they were HIV-infected. They had CD4 T cell counts in the normal range. But Duesberg has decided to count them as “HIV-negative AIDS” cases, because – according to him – “their T-cells typically continue to decline either because of risk behavior, such as the consumption of recreational drugs.”

    In other words, my theory predicts their T cells will decline to less than 200 cells, ergo I am counting them as “HIV-negative AIDS” cases in order to support my theory that their drug use will cause their T cells to decline to less than 200 cells. And Duesberg accuses other scientists of circular reasoning! If you can read this and still be surprised that Duesberg can’t get published in a serious journal, then I am at a loss. As you can see, he takes the same approach with the literature on hemophiliacs.

    Another interesting thing is that the reference to what the HIV-negative gay men’s T cell counts actually were is in the PDF of the Biotechnology paper that is on Duesberg’s website here:

    http://duesberg.com/papers/the%20hiv%20gap.pdf

    But in the version that is reproduced in HTML form on the “Virusmyth” website, it reads thusly:

    http://www.virusmyth.net/aids/data/pdbiotech93.htm

    “HIV-free male homosexuals on various recreations drugs with “X cells per cubic millimeter” (Table 1, ref. 14) or HIV-negative hemophiliacs with T4/T8 cell ratios of about 1 or 1 (Table 1, refs. 46-61).”

    Now, why would the Virusmyth website replace “<600 cells” with “X cells”?

    If you go on down through the other references in this paper, I am sure you will that find Duesberg is similarly abusing them. And Duesberg now claims to have documented several thousand “HIV-negative AIDS” cases with this kind of methodology, a claim Celia Farber repeats in her Farber’s article.

  308. #308 Richard Jefferys
    June 23, 2006

    Oh dear, I just invented “Farber’s Magazine” – now there’s a scary thought.

  309. #309 Gene Semon
    June 23, 2006

    “Infectivity in such an assay may or may not accurately reflect infectivity in a human being.”

    Dale,

    You’re not demonstrating infectivity in a human being by this statement.

    Viral load has been debunked here by Wilhelm and plenty of places elsewhere starting with Duesberg/Bialy plus you ignored that part of my post.

    Your last part ignores demonstated HERV K particles in cultures (the “HIV standard”) and HERV K reinfection in vivo.

    Dale, you’re very good at constructive dismissal. I nominate you for Bishop.

  310. #310 Gene Semon
    June 23, 2006

    Hi guys,

    You’re gonna get the last word today for sure. I’ll be reading with consuming interest your latest.

    See ya

  311. #311 Dale
    June 23, 2006

    Gene,

    I will concede that HERVs and exogenous retroviruses can behave very similarly in a number of assays. Most HERVs are defective and don’t replicate but some do. Some produce viral like particles. So the real sticking point is transmission frequencies and the effect of ARVs on those frequencies. HERVs will be passed on from parents to children according to the rules that govern other cellular genes and the frequency of transmission will be unaffected by ARVs. So in looking at two characteristics that will distinguish an HERV from an exogenous retrovirus, HIV behaves like the latter.

  312. #312 Hank Barnes
    June 23, 2006

    Dale,

    Good summary above.

    If, say, a large epidemiological study was done to observe HIV+ men and women having sex with uninfected partners over, say, 6 years, and none of the partners contracted HIV — would this lend evidence to the proposition that HIV was an HERV or an exogenous retrovirus?

    Hank

  313. #313 Richard Jefferys
    June 23, 2006

    No Hank, it wouldn’t. If you really refuse to countenance the fact that risk reduction could produce that result, you might want to look at some studies like this:

    http://www.journals.uchicago.edu/JID/journal/issues/v179n3/980696/980696.html

    Also, in the Nairobi sex worker cohort studied by Frank Plummer’s group, new women entering the cohort have a huge risk of acquiring infection in the first year or so (they have at least 60 unprotected exposures per year). But a minority of the women do not seroconvert, and if they remain uninfected for more than two years, their risk of acquiring HIV infection is 1/10 that of women newly entering the cohort.

    Care to venture a guess as to why that might be?

    I’m actually tempted to ask Nancy Padian if she has any stored samples that could be assayed for HIV-specific T cell responses by the Gladstone (as they did among some of the women in the heterosexual transmission of AIDS study). But somehow, even if the uninfected partners possessed HIV-specific T cell responses (as at least some of them probably would), I doubt that would pursuade you to give it up. Remind me why you ignore the Rakai cohort again? What’s the distinction you make between Californian and Ugandan heterosexual couples?

  314. #314 Hank Barnes
    June 23, 2006

    To distinguish between an endogenous or exogenous virus,

    Dale wrote:

    So, the real sticking point is transmission frequencies and the effect of ARVs on those frequencies

    I gave Dale a hypothetical about sexual transmission, where “no seroconversions” were noted and asked Dale:

    …would this lend evidence to the proposition that HIV was an HERV or an exogenous retrovirus?

    You answered:

    No, it wouldn’t, Hank.

    Please re-read the question, Richard before spouting off.

    Hank

  315. #315 Wilhelm Godschalk
    June 23, 2006

    Chris wrote:
    DNA replication in humans has much higher fidelity than RNA viruses and only small sequence changes would be expected over time. This is true both within an individual and within a popualtion. This is completely the opposite of what is observed.

    This is a recurring theme with him, and it tends to put the reader on the wrong foot. I know he will accuse me (again) of alleging that RNA-viruses don’t mutate (something I never claimed), but the extent of RNA transcription errors (reverse or otherwise) is geatly exaggerated. Let’s forget our fixation on retroviruses for a second, and look at other RNA viruses: The Picorna viruses (to which plant viruses belong, as well as entero viruses such as Polio) are genetically very stable. No wild mutations all over the place. And as always, when I point this out, the many mutations of Influenza virus are brought up. Yes indeed, Flu virus does mutate, and brings us a new strain every year (no, it does not have a built-in calendar, but we humans tend to look at it every year, before the flu season starts). But this kind of mutation is not the same as transcription errors. The Flu virus genome is multithreaded, so in this case the mutations are due to reassortment or recombination.
    In HIV (assuming this beast exists), or any other retrovirus, this mechanism is not operative, so any mutations must arise from transcription errors. Well, even though human DNA to DNA transcription may be more accurate, there is no reason to assume that viral RNA makes a mess of the process.
    But the HIV-hustlers need this mutation-like-crazy principle for their pet virus. They are sloppy experimenters; they brought a new dimension to the term “experimental error”. So they must find an explanation for the fact that every time they do an experiment, they get different results. “Ah! But HIV mutates very fast!” is the explanation.
    Yeah, sure. HIV has another remarkable feature: It is big enough to cover your ass.

    I wouldn’t feel right without making a few remarks about endogenous and exogenous proteins and nucleic acids.
    “Exogenous” means the stuff (whatever) comes from outside. But after something has been shown to be exogenous, why, in the name of Theophrastus Bombastus von Hohenheim, does that necessarily mean it must come from HIV, or any virus? The bacteria that live happily in your colon are certainly exogenous, right? Lots of foreign protein and nucleic acid there… How about the fungus that is present in your lungs (and which causes PCP if you give it half a chance)? And, of course, there are enteroviruses multiplying in our intestine. And, eh… is sperm exogenous? Well, for some of us, it is. So tell me, guys, why is it that, whenever a protein is found that could not be coded for by the human genome, you are so sure that it comes from HIV?
    And as far as the endogenous stuff is concerned: I think the geneticists are overstating their case. They know too little and talk too much. I can’t possibly believe that a whole human being is already mapped out in the DNA at birth. I’m pretty sure there are a lot of other factors that are not being considered. The human body can be many things, but two things it is not: Simple and Tidy.

  316. #316 Richard Jefferys
    June 23, 2006

    Since Dale was talking about the frequency of transmission from mother to child, Hank, the answer would still be: no, it wouldn’t.

  317. #317 Richard Jefferys
    June 23, 2006

    Since you neglected to provide it, Hank, I went and found your justification for ignoring the Rakai data. Here it is in all it’s glory:

    “Chris Noble,

    Your Ugandan study on heterosexual transmission is interesting, thanks.

    But, it seems awful late in the game (published in 2005, regarding results in 1994)

    By the mid-1980’s, the scientific community had already declared that HIV was heterosexually transmissible. Padian began her work 10-year study on this topic in 1985. I assert that her results, actually refuted the working-hypothesis.

    The question is, What study of heterosexual transmission in the early 1980’s formed the foundation to support the scientific assertion that AIDS was a sexually transmitted disease? Your cite of Rakai is interesting, but dislocated from the historical development of the disease.

    Barnes, Hank”

    That’s just stellar Hank. The Rakai data are data.

    J Infect Dis. 2005 May 1;191(9):1403-9. Epub 2005 Mar 30.

    Rates of HIV-1 transmission per coital act, by stage of HIV-1 infection, in Rakai, Uganda.

    Wawer MJ, Gray RH, Sewankambo NK, Serwadda D, Li X, Laeyendecker O, Kiwanuka N, Kigozi G, Kiddugavu M, Lutalo T, Nalugoda F, Wabwire-Mangen F, Meehan MP, Quinn TC.

    Heilbrun Department of Population and Family Health, Columbia University Mailman School of Public Health, New York, New York 10032, USA. mwawer@jhsph.edu

    BACKGROUND: We estimated rates of human immunodeficiency virus (HIV)-1 transmission per coital act in HIV-discordant couples by stage of infection in the index partner. METHODS: We retrospectively identified 235 monogamous, HIV-discordant couples in a Ugandan population-based cohort. HIV transmission within pairs was confirmed by sequence analysis. Rates of transmission per coital act were estimated by the index partner’s stage of infection (recent seroconversion or prevalent or late-stage infection). The adjusted rate ratio of transmission per coital act was estimated by multivariate Poisson regression. RESULTS: The average rate of HIV transmission was 0.0082/coital act (95% confidence interval [CI], 0.0039-0.0150) within approximately 2.5 months after seroconversion of the index partner; 0.0015/coital act within 6-15 months after seroconversion of the index partner (95% CI, 0.0002-0.0055); 0.0007/coital act (95% CI, 0.0005-0.0010) among HIV-prevalent index partners; and 0.0028/coital act (95% CI, 0.0015-0.0041) 6-25 months before the death of the index partner. In adjusted models, early- and late-stage infection, higher HIV load, genital ulcer disease, and younger age of the index partner were significantly associated with higher rates of transmission. CONCLUSIONS: The rate of HIV transmission per coital act was highest during early-stage infection. This has implications for HIV prevention and for projecting the effects of antiretroviral treatment on HIV transmission.

  318. #318 Dale
    June 23, 2006

    Hank writes If, say, a large epidemiological study was done to observe HIV+ men and women having sex with uninfected partners over, say, 6 years, and none of the partners contracted HIV — would this lend evidence to the proposition that HIV was an HERV or an exogenous retrovirus?

    Such a study could only be interpreted as support for the proposition that HIV was not sexually transmitted if there was no other evidence that HIV IS sexually transmitted. I’ve mentioned to you before several such lines of evidence including but not restricted to (1) Padian’s own retrospective data and (2) transmission cohort studies in which lines of transmission are supported not only by the self reported histories of the individuals involved but by sequencing of the viruses. As far as using such a study to support the notion that HIV is an endogenous virus, well it doesn’t really address the question since it doesn’t look at the transmission of virus between parents and children.

    Wilhelm writes Let’s forget our fixation on retroviruses for a second, and look at other RNA viruses: The Picorna viruses (to which plant viruses belong, as well as entero viruses such as Polio) are genetically very stable. That may be true Wilhelm but since picorna viruses don’t use the same enzymes that HIV do to replicate they really can’t be used to argue about mutation rates in HIV.

  319. #319 Richard Jefferys
    June 23, 2006

    Here’s a prior study from the Rakai cohort.

    Lancet. 2001 Apr 14;357(9263):1149-53.

    Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda.

    Gray RH, Wawer MJ, Brookmeyer R, Sewankambo NK, Serwadda D, Wabwire-Mangen F, Lutalo T, Li X, vanCott T, Quinn TC; Rakai Project Team.

    Departments of Population and Family Health Sciences, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. rgray@jhsph.edu

    BACKGROUND: The probability of HIV-1 transmission per coital act in representative African populations is unknown. We aimed to calculate this probability overall, and to estimate how it is affected by various factors thought to influence infectivity. METHODS: 174 monogamous couples, in which one partner was HIV-1 positive, were retrospectively identified from a population cohort in Rakai, Uganda. Frequency of intercourse and reliability of reporting within couples was assessed prospectively. HIV-1 seroconversion was determined in the uninfected partners, and HIV-1 viral load was measured in the infected partners. Adjusted rate ratios of transmission per coital act were estimated by Poisson regression. Probabilities of transmission per act were estimated by log-log binomial regression for quartiles of age and HIV-1 viral load, and for symptoms or diagnoses of sexually transmitted diseases (STDs) in the HIV-1-infected partners. RESULTS: The mean frequency of intercourse was 8.9 per month, which declined with age and HIV-1 viral load. Members of couples reported similar frequencies of intercourse. The overall unadjusted probability of HIV-1 transmission per coital act was 0.0011 (95% CI 0.0008-0.0015). Transmission probabilities increased from 0.0001 per act at viral loads of less than 1700 copies/mL to 0.0023 per act at 38 500 copies/mL or more (p=0.002), and were 0.0041 with genital ulceration versus 0.0011 without (p=0.02). Transmission probabilities per act did not differ significantly by HIV-1 subtypes A and D, sex, STDs, or symptoms of discharge or dysuria in the HIV-1-positive partner. INTERPRETATION: Higher viral load and genital ulceration are the main determinants of HIV-1 transmission per coital act in this Ugandan population.

  320. #320 Richard Jefferys
    June 23, 2006

    And one more:

    N Engl J Med. 2000 Mar 30;342(13):921-9.

    Viral load and heterosexual transmission of human immunodeficiency virus type 1. Rakai Project Study Group.

    Quinn TC, Wawer MJ, Sewankambo N, Serwadda D, Li C, Wabwire-Mangen F, Meehan MO, Lutalo T, Gray RH.

    National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA.

    BACKGROUND AND METHODS: We examined the influence of viral load in relation to other risk factors for the heterosexual transmission of human immunodeficiency virus type 1 (HIV-1). In a community-based study of 15,127 persons in a rural district of Uganda, we identified 415 couples in which one partner was HIV-1-positive and one was initially HIV-1-negative and followed them prospectively for up to 30 months. The incidence of HIV-1 infection per 100 person-years among the initially seronegative partners was examined in relation to behavioral and biologic variables. RESULTS: The male partner was HIV-1-positive in 228 couples, and the female partner was HIV-1-positive in 187 couples. Ninety of the 415 initially HIV-1-negative partners seroconverted (incidence, 11.8 per 100 person-years). The rate of male-to-female transmission was not significantly different from the rate of female-to-male transmission (12.0 per 100 person-years vs. 11.6 per 100 person-years). The incidence of seroconversion was highest among the partners who were 15 to 19 years of age (15.3 per 100 person-years). The incidence was 16.7 per 100 person-years among 137 uncircumcised male partners, whereas there were no seroconversions among the 50 circumcised male partners (P<0.001). The mean serum HIV-1 RNA level was significantly higher among HIV-1-positive subjects whose partners seroconverted than among those whose partners did not seroconvert (90,254 copies per milliliter vs. 38,029 copies per milliliter, P=0.01). There were no instances of transmission among the 51 subjects with serum HIV-1 RNA levels of less than 1500 copies per milliliter; there was a significant dose-response relation of increased transmission with increasing viral load. In multivariate analyses of log-transformed HIV-1 RNA levels, each log increment in the viral load was associated with a rate ratio of 2.45 for seroconversion (95 percent confidence interval, 1.85 to 3.26). CONCLUSIONS: The viral load is the chief predictor of the risk of heterosexual transmission of HIV-1, and transmission is rare among persons with levels of less than 1500 copies of HIV-1 RNA per milliliter.

  321. #321 Richard Jefferys
    June 23, 2006

    Apologies, the last part got snipped.

    (P<0.001). The mean serum HIV-1 RNA level was significantly higher among HIV-1-positive subjects whose partners seroconverted than among those whose partners did not seroconvert (90,254 copies per milliliter vs. 38,029 copies per milliliter, P=0.01). There were no instances of transmission among the 51 subjects with serum HIV-1 RNA levels of less than 1500 copies per milliliter; there was a significant dose-response relation of increased transmission with increasing viral load. In multivariate analyses of log-transformed HIV-1 RNA levels, each log increment in the viral load was associated with a rate ratio of 2.45 for seroconversion (95 percent confidence interval, 1.85 to 3.26). CONCLUSIONS: The viral load is the chief predictor of the risk of heterosexual transmission of HIV-1, and transmission is rare among persons with levels of less than 1500 copies of HIV-1 RNA per milliliter.

  322. #322 Gene Semon
    June 24, 2006

    Revisiting Hellerstein and Piatak

    Let’s go back to what is, after all, fundamental in this debate.

    Three mechanisms are proposed for why HAART works based on a discrediting of David Ho’s speculative dynamics, (the indirect cause of how much unnecessary liver disease, BTW?), and direct, but incomplete, measurements of T-cell dynamics. One of these, HIV cell-killing is eliminated by Duesberg (“mediated” or not, whatever THAT means).

    Here are the two distinctly stated mechanisms of Hellerstein to explain “the increase in fractional replacement and absolute production rate of blood T cells in the HAART group”: 1) “reduced adherence of dividing T cells to lymphoid tissues, allowing redistribution of these dividing cells into the circulating pool;” 2)”disinhibition of T-cell profileration in tissues (the leukemic effect)*, allowing greater release of dividing cells into the circulating pool.” *(parens added)

    Now, clearly, considering Duesberg’s refutation, as confirmed by nondenialists Strohman and Urnovitz plus leaving the two remaining mechanisms; the syllogism HAART works, therefore HIV causes AIDS, collapses.

    Dale, you’re misinterpreting Piatak, confused over “tissue culture”. Read the fine print; most possible direct ex vivo measurements were made of “infectivity” ,(excluding human subjects, of course).

  323. #323 Gene Semon
    June 24, 2006

    Wilhelm says, “As far as the endogenous stuff is concerned: I think the geneticists are overstating their case. They know too little and talk too much. I can’t possibly believe that a whole human being is already mapped out in the DNA at birth. I’m pretty sure there are a lot of other factors that are not being considered. The human body can be many things, but two things it is not: Simple and Tidy.”

    I think we should all keep this in mind as we explore the newly discovered sequences of the human genome.

  324. #324 Gene Semon
    June 24, 2006

    Who’s ignorance?

    Simon H-U, Plotz SG et al. Abnormal clones of T cells producing interleukin-5 in idiopathic eosinophilia. New England Journal of Medicine.(1999)341, N15, 1112-20

    Table 3 is absolutely fascinating, listing the different possibilities of T cell immunophenotypes, consistent with the abstaction I previously posted.

    “In patient 3, an additional 33.9 percent of cells were CD3-, CD4+ lymphocytes…”

    “Additional DNA was extracted from purified CD3- T cells with low amounts of CD4…”

    Well, you get the picture.

    One thing about that always-present temptation to shoot from the hip, the rounds can ricochet back.

  325. #325 Gene Semon
    June 24, 2006

    “So the real sticking point is transmission frequencies…”

    Dale, I appreciate the concession, but (there’s always a but) I don’t think you’ve grasped the point on the equivalency of transcriptional regulation of the provirus, regardless whether it’s exogenous or endogenous.

    Don’t be distracted by Richard, you really need to look uo the “…conventional retrovirus…” Duesberg argument I previously posted.

  326. #326 Dale
    June 24, 2006

    Gene,
    1. I think you may have misread Piatak. Viral infectivity was measured by end point dilution culture. That is definately a cell culture assay.

    2. I appreaciate that as a provirus within a cell HIV may be replicated and transcribed in much the same manner as an endogeneous retrovirus. But do you appreaciate that an endogenous retrovirus will not be serially transmitted between sexual partners nor will it be transmitted from mother to child at less than 50% frequency (unless of course it’s toxic) and whatever the mother to child transmission frequency it should not be affected by ARVs nor should a certain percentage of infected children become infected after birth?

    3. Re CD3negative T cells … I think the title of the paper you choose says it all ” Abnormal clones of T cells …”

  327. #327 Richard Jefferys
    June 24, 2006

    Way to search PubMed Gene, I freely and without reservation admit to not having previously read that paper. I wonder if you’d care to speculate as to why they used the word “abnormal,” or wrote in the paper: “the CD3-CD4+ immunophenotype is abnormal because the CD3 molecule normally occurs on all CD4+ T cells”? Do you think there is something broadly applicable here:

    “Each patient had a unique subgroup of T cells with an aberrant immunophenotype. Nine patients (Patients 1, 4, 6, 9, 10, 12, 13, 14, and 15) had abnormal CD3+CD4+CD8- T cells, three patients (Patients 5, 8, and 16) had abnormal CD3+CD4-CD8+ cells, and three patients (Patients 2, 11, and 15) had abnormal CD3+CD4-CD8- cells (Table 3). CD3-CD4+ T cells were found in two patients (Patients 3 and 7).”

    So this was two of the 60 individuals with idiopathic eosonphilia that were studied. Did you find a lot of other examples in PubMed? Are you arguing that T cell immunologists should be considering CD3-CD4+ T cells as a new subset? How do you think these cells would participate in an immune response without CD3? Unfortunately you’re only making it clearer that you’re not understanding what you’re reading.

    And if you look back up this skyscraper of a thread, you’ll find your original inquiry was about the role of CD3+ T cells, as compared and contrasted with CD4+ and CD8+ T cells.

    And, once again, the Marc Hellerstein paper does not in any way contradict the idea that HAART works, just the opposite, people can read the papers for themselves thankfully, without the assistance of your bizarre and erroneous interpretations. Talking of bizarre, what an earth do you mean by “the leukemic effect”? Are you suggesting that there is a connection between antigen-specific or homeostatic T cell proliferation and the proliferation that occurs in leukemia?

  328. #328 Gene Semon
    June 24, 2006

    Wilhelm,

    Thanks for your post of 6/23, 8:22PM. Brilliant! I feel like I’m at university with a very learned professor.

  329. #329 Gene Semon
    June 24, 2006

    “HIV transmission within pairs was confirmed by sequence analysis.”(Rakai data)

    Richard, how many base pairs? RNA? DNA? Controls for cross reactions?

  330. #330 Gene Semon
    June 24, 2006

    “That may be true Wilhelm but since picorna viruses don’t use the same enzymes that HIV do to replicate they really can’t be used to argue about mutation rates in HIV.”

    Dale,

    But what if they’re phylogenetically related?

    Richard,

    You have such a sly sense of humour, accusing Dueberg of circular reasoning for his expansion of the definition of AIDS right after CDC does the same thing.

  331. #331 Richard Jefferys
    June 24, 2006

    I think the word pairs refers to the discordant couples (i.e. two people=a pair). I would hope that the information about the sequence analysis is in the paper.

  332. #332 Richard Jefferys
    June 24, 2006

    The CDC expanded the definition of AIDS to include drug using gay men with T cell counts in the normal range? When did that happen?

  333. #333 Gene Semon
    June 24, 2006

    Richard, in some circumstances, redundant functioning (my original point) of a system is abnormal! An emergency cooling system for a chemical plant reactor is not normally turned on.

    Thanks for considering my entire argument before shooting from the hip again.

    Dale,

    I know they used a tissue culture. You’re still missing the point.

  334. #334 Gene Semon
    June 24, 2006

    “And, once again, the Marc Hellerstein paper does not in any way contradict the idea that HAART works, just the opposite, people can read the papers for themselves thankfully, without the assistance of your bizarre and erroneous interpretations.”

    And once again, you’re shooting from the hip. The post and text are clear no matter how you want to spin it.

    Once again, have the last word and a nice night. Take a break from your heckling, really guys, people can think for themselves.

  335. #335 Richard Jefferys
    June 24, 2006

    Hellerstein’s studies, blessedly, are much clearer than your posts. So let’s give the last word to Marc Hellerstein:

    “Effective LT (long term) ARV therapy restored CD4+ T cell survival rates to normal.”

    http://www.jci.org/cgi/content/full/112/6/956

  336. #336 Dale
    June 24, 2006

    Gene writes “That may be true Wilhelm but since picorna viruses don’t use the same enzymes that HIV do to replicate they really can’t be used to argue about mutation rates in HIV.”
    Dale,
    But what if they’re phylogenetically related?

    But they aren’t phylogenetically related in any significant way; one being an RNA virus that replicates without a DNA intermediate (using RNA dependent RNA polymerase) and the other being an RNA virus that replicates through a DNA intermediate (using reverse transcriptase and DNA dependent RNA polymerase).

    Gene also writes I know they used a tissue culture. You’re still missing the point.

    I assumed your point initially was that viral loads as measured by PCR are much higher than infectious virus as measured by end point dilution assays. My point was that there is no way of knowing how good an estimate of in vivo infectivity that an end point dilution assay is. And your point, that I continue to miss … was really what?

  337. #337 Wilhelm Godschalk
    June 24, 2006

    >”But they aren’t phylogenetically related in any significant way; one being an RNA virus that replicates without a DNA intermediate (using RNA dependent RNA polymerase) and the other being an RNA virus that replicates through a DNA intermediate (using reverse transcriptase and DNA dependent RNA polymerase).”

    All true, Dale. But I still don’t know exactly what your point is. Do you mean RNA –> RNA transcription is less prone to errors than RNA –> DNA reverse transcription? If that’s so, I’m not aware of it. Why would that be?

  338. #338 Dale
    June 24, 2006

    I haven’t checked the literature Wilhelm so I don’t know what the relative error rates are of RNA dependent RNA polymerase versus reverse transcriptase – but why should you expect them to be the same when they are, as we seem to agree, completely different enzymes?

  339. #339 Chris Noble
    June 25, 2006

    Wilhelm Godschalk wrote on 6/23, 8:22PM

    But this kind of mutation is not the same as transcription errors. The Flu virus genome is multithreaded, so in this case the mutations are due to reassortment or recombination.

    Gene Semon writes

    Wilhelm,
    Thanks for your post of 6/23, 8:22PM. Brilliant! I feel like I’m at university with a very learned professor.

    What is your definition of learned? Wilhelm just makes this stuff up. He never provides references for his assertions.

    The seasonal variation in the influenza virus is due primarily to antigenic drift (point mutations etc) not antigenic shift (reassortment or recombination). This is due to the high mutation rate of all RNA viruses.

    Mutation rates among RNA viruses.

  340. #340 Chris Noble
    June 25, 2006

    Wilhelm Godschalk wrote:

    The Picorna viruses (to which plant viruses belong, as well as entero viruses such as Polio) are genetically very stable. No wild mutations all over the place.

    I have previously given Godschalk several references that demonstrate that poliovirus like all other RNA viruses has extremely high mutation rates.


    Molecular Evolution of a Type 1 Wild-Vaccine Poliovirus Recombinant during Widespread Circulation in China

    “Polioviruses are among the most rapidly evolving viruses known. The most important mechanism for the rapid evolution of RNA viruses is a high rate of base misincorporation by the viral RNA polymerases, which generally lack 3’?5′ exonuclease proofreading mechanisms (8, 9). Base misincorporation rates in the range of 10-5 to 10-4 per base pair per replication have been reported for numerous poliovirus alleles (7, 9, 44). The high mutability of poliovirus genomes, coupled with the frequent occurrence of genetic bottlenecks (8) during poliovirus replication in the human intestine (21, 31), results in exceptionally rapid rates of evolution (~10-2 substitutions per site per year) during person-to-person transmission (J. Jorba, L. De, J. Kim, and O. M. Kew, Abstr. 18th Annu. Meet. Am. Soc. Virol., p. 148, 1999). Most of this evolution appears to be random genetic drift, as >80% of nucleotide substitutions within the coding region generate synonymous codons (14, 31, 36, 40; Jorba et al., Abstr. 18th Annu. Meet. Am. Soc. Virol., 1999).”

    Godschalk responds by just repeating his assertion over and over again without providing a single reference.

    Making this assertion once could be due to ignorance. Repeating it over and over again can only be due to delusion or dishonesty.

  341. #341 Chris Noble
    June 25, 2006

    More on the “stability” of picorna viruses.

    Evolution of circulating wild poliovirus and of vaccine-derived poliovirus in an immunodeficient patient: a unifying model.

    Poliovirus infection normally lasts a few weeks during which some evolution make take place. In immunodeficient patients the infection is often persistent and can last several years. During this time a similar degree of evolution compared to HIV is seen.

  342. #342 Chris Noble
    June 25, 2006

    Gene Semon writes:

    The starting point for this is the section of Duesberg’s never-answered 1989 PNAS paper: HIV is a conventional retrovirus without an AIDS gene, which discusses why “accessory genes” are not sufficient to demonstrate that an HIV: can “escape the fate” of being “trapped” by the cell’s transcriptional apparatus; or, to put it another way; has the “ability” to “hijack the cell’s physiological processes”.

    Groan. You started with the Perth Group – HIV doesn’t exist – HIV p24 is really just a cellular protein – now you are going to Duesberg. Can’t you just form a coherent hypothesis and stick to it.

    Duesberg’s – HIV doesn’t have an AIDS gene – argument is a stupid one.

    SIVmac and various HIV/SIVmac hybrids also do not have an “AIDS gene”. However if you infect macaque monkeys with these viruses they suffer CD4 loss, immunesuppression, AIDS and death. This is entirely reproducible. SIVmac and SHIV are available from AIDS reagent programs. Hundreds of labs around the world are doing experiments using thes viruses.

    People that deny this evidence are in denial and can only be described as Denialists.

    And what do you mean by “never answered”. Checking science citations shows that out of come 89 papers citing Duesberg’s 1989 PNAS article around 10 directly address Duesberg’s claims.

    Why do people keep on insisting that Duesberg has never been answered? That no debate has taken place?

  343. #343 Dale
    June 25, 2006

    Chris, thanks for posting the references about poliovirus mutation rates.

  344. #344 Chris Noble
    June 25, 2006

    Dale wrote:

    Chris, thanks for posting the references about poliovirus mutation rates.

    In my post at 8.02 PM the citation I meant to give was this one.

    Mutation rates among RNA viruses

    Doing a literature search for mutation rates in poliovirus shows many more similar articles. Any text book in virology will tell you that all RNA viruses have high mutation rates due to the lack of a proof-reading mechanism.

    Why Godschalk continues to deny this is beyond belief. Perhaps because he finds that his bullshit impresses uncritical minds like Gene Semon.

  345. #345 Chris Noble
    June 26, 2006

    Hank Barnes wrote:

    Take Padian. She observed HIV+ people having sex for 6 years. However, none of the sex partners contracted HIV. That’s the data. You can intepret it your way, I’ll interpret it my way.

    You have come down from 10 years to 6 years but this is still a misrepresentation. It has been continuously shown to you that the average follow up was significantly less than this.

    It has also been pointed out to you that Padian was actively seeking to reduce risk behaviour in this group. To a large degree she succeeded.

    It has also been pointed out to you that experimental data shows that transmission risk of HIV is directly related to HIV viral load. Even Duesberg points out that HIV should be less transmissible after the initial acute infection.

    You also ignore the retrospective part of the study that demonstrated that the seroconversion of the previously negative partner occurred during a peiod where the couple was monogamous and without other risks for infection.

    You ignore the evidence that you don’t like.

    You also ignore the Rakai data. For what reason?

    Studies like Padian’s demonstrate that in that particular population at that stage of infection HIV has a similar transmission risk to herpes simplex.

    For some reason you aren’t claiming that herpes simplex doesn’t exist or cannot be sexually transmitted. Why?

  346. #346 Gene Semon
    June 26, 2006

    More from the uncritical mind.

    Chris, Wilhelm’s point is reinforced by “the enzymes most related to reverse transcriptases are the RNA-directed RNA polymerases identified in various RNA viruses, in particular the polio-like goup.” Which are, of course, picornaviruses.

    Xiong & Eikbush, (1990) EMBO, V9, N10, 3356

    Average mutation rates are meaningless when one is assessing virulence. (This is where proving stuctural stability comes into play.) Why? Because an RNA virus that loses its replicase gene stability becomes DEFECTIVE (You’ve heard of those kinds of viruses, right guys, or is that bullshight too.) Now, what happens when a virus is defective? It can no longer replicate, unless it is “rescued”.

    BTW, this is what the old hands meant when they referred to the Rous Sarcoma-Avian Leukosis retrovirus complex.
    But nothing they ever said is worth a damn because we have PCR.

    Try to at least be creative in your attacks so we have some entertainment value when you have nothing substantive.

  347. #347 Gene Semon
    June 26, 2006

    “I think the word pairs refers to the discordant couples (i.e. two people=a pair). I would hope that the information about the sequence analysis is in the paper.”

    Yes Richard, I see the ambiguity in the quoted statement from Dakai. You should know the answer on DNA bp.

    My response re functional redundancy of “abnormal” T cells didn’t make it to the thread on Sat. An emergency cooling system for a chemical reactor is not “normally” turned on.

  348. #348 Gene Semon
    June 26, 2006

    “The CDC expanded the definition of AIDS to include drug using gay men with T cell counts in the normal range? When did that happen?”

    Richard, you made another uncritical inference. I thought normal was 1000; so what if Dueberg playfully extended 200 to 600.

  349. #349 Dale
    June 26, 2006

    So if I understand you correctly Gene, you state that a virus that mutates so as to lose certain key functions will lose its ability to replicate. That seems pretty obvious but what’s your point? Presumably as long as each round of viral replication produces more than one infectious virus, the viral pool will expand. The data says HIV mutates and replicates throughout the course of progression to AIDS so if your theory says it shouldn’t, there is clearly something wrong with your theory.

  350. #350 Gene Semon
    June 27, 2006

    “That seems pretty obvious but what’s your point?”

    Absolutely, Dale, I owe you more here. Chris posted, “Most of this evolution appears to be random genetic drift, as >80% of nucleotide substitutions within the coding region generate synonymous codons”. And that’s the heart of the matter, evolution by purifying selection; the ratio of nonsynomous to synonymous codon substitutions being much less than 1, which is consistent with picorna viruses are “genetically very stable. No WILD mutations all over the place.” Here’s more back-up for Wilhelm: “(I)n vivo and in vitro estimates of the average error frequencies of viruses RNA replicases and reverse transcriptases also suggest misincorporation frequencies of the order of 10(exp-3) to 10(exp-5).” (Emerging Viruses, S. Morse, ed,(1993) Oxford University Press, pg 206 – John Holland)

    Chris, you’re a real piece of work. If you’d bother to read my posts without an uncritical mind, you wouldn’t be so quick to jump to conclusions or the attack. Did I say anywhere that HIV doesn’t exist? Because I brought in the Perth Group, I must agree with their conclusion? Can I form a coherent hypothesis cocsistent with everything I’ve posted? You’re either lazy or illiterate. Clearly, ALL evidence considered, retroviral transcriptions are secondary to toxic stressors as agents in the etiology of chronic diseases. How’s that? As far as injecting monkeys with “AIDS reagents”, we need more details to look at dose-response, artifactual vs more realistic models, etc. See Howard Urnovitz, HHS fails to make the case that HIV causes AIDS, at chronicillnet.org for more critique of these animal studies. According to Perth Group, it would be necessary to isolate HIV/SIV from the animals to fulfill Koch’s postulates.

  351. #351 Gene Semon
    June 27, 2006

    Response to Richard 6/24, 4:26PM

    There is a distinction between “arguing” and defining. I originally stated the possibility of CD3- cells and you replied that CD3 is part of the T cell receptor (not mentioning alpha/beta), by definition on each and every T-cell. I find examples of CD3- cells in ONE NEJM paper at hand and you hand wave about “abnormal”.

    My earlier post said “by deploying multiple redundant defense pathways, the host can influence the evolutionary trajectory of a pathogen population. Redundant defense mechanisms reduce the selective advantage to the pathogen of knocking out a single mechanism.”(authors) This was, for your consideration, a network model discussing adaptive responses and functional redundancies of T cells. “Three patients” with “abnormal CD3+CD4-CD8- cells” are suggestive of functional redundancy for the helper/memory function. I make an analogy to an emergency cooling system for a chemical plant reactor, not normally turned on. So nothing here is inconsistent with the idea that detailed understandings of lymphocyte dynamics have different schools of interpretation, which should be a given when evaluating such papers as Hellerstein.

    The leukemic effect? You’re really exercised over this one. I would say it’s an effect consistent with severe, life threatening hypersensitivity reactions of NNRTIs. Other effects consistent: eosinophilia(!), lymphadenopathy, general malaise, flu-like symptoms, etc. And let’s not forget that “(mechanism and long term consequences of) redistribution/accumulation of body fat including central obesity, dorsocervical fat enlargement (buffalo hump), peripheral wasting, facial wasting, breast enlargement (are currently unknown)” (PDR, 2006)

  352. #352 Chris Noble
    June 27, 2006

    Gene you should consider the possibility that you do not understand what you are reading.

    All RNA viruses have high mutation rates because the RNA polymerases lack a proof reading mechanism. This is true for RNA replicases and reverse transcriptases.

    Poliovirus and FMDV are both picornaviruses and they have some of the highest evolution rates observed.

    The mutation rate of FMDV is so high that it is close to the error catastrophe.

    This completely contradicts Godschalk’s bald assertion that these viruses do not have high mutation rates.

    The citations that you gave say that all RNA viruses have high mutation rates.

    Take a deep breath and attempt to say something coherent.

  353. #353 Gene Semon
    June 28, 2006

    Chris, nice try.

    It is you my good friend, who is in over his head.

    Here’s more confirmation of Wilhelm’s points that have completely eluded you. Really guy, it’s time to leave the Bizarro World of HIV/AIDS science.

    Excerpts from below reference:

    “The human endogenous retroviruses of the so-called HERV-K family come closest to being biologically active. . . Although the HERV-K element was first introduced into the human germ line more than 25 million years ago, as judged from its distribution in different primates, several members contain a complete genome with long terminal repeats and open reading frames encoding Gag, Pol, and Env proteins and three chromosomes are candidates for harboring a completely intact HERV-K locus . . . specific enzymatic activities have been reported for the HERV-K dUTPase, protease, and endonuclease, and we now report data for the two remaining enzymatic activities, that of the reverse transcriptase polymerase and its RNase H domain. Reverse transcriptase enzyme activity has been found in a variety of HERV-K-containing biological samples.

    “We and others previously found that purifying or negative selection seems to operate on the HERV-K genomes. At least in some of the subgroups, there is a remarkable conservation of the open reading frames, and this result was confirmed in the present study for the HML-2 RT genes. Furthermore, of the mutations that are present, a strong prevalence of synonymous nucleotide substitutions was noted. The biological significance of this retrovirus family is substantiated further by the finding that multiple members are transcriptionally active. This also holds for the ACTIVE* RT species identified in this study, which were cloned by an RT-PCR strategy with cellular RNA as input. The cloning of several full-length HERV-K RT sequences allowed us to readdress some of the issues concerning the apparent conservation of these genes. Most strikingly, we noticed that some HERV-K elements have preserved their RT-encoding capacity despite the presence of deletions and/or substitutions that destroy the reading frame. Alignment of the RT sequence of clone 10.2 with that of HERV-K10 indicates that three 1-nt deletions are present that are unique for this clone. Whereas any of the individual mutations would cause a frameshift during translation of the RT protein, the combination of all three mutations restores the reading frame and allows the expression of full-length RT with a mutant 8-amino-acid stretch. A somewhat similar situation is seen in clone 10.1, where a 2-nt insertion is combined with a 1-nt insertion to restore the RT reading frame, so that only 3 amino acids are read out of frame.” *(emphasis added)

    (Berkhout, B, M Jebbink, J Zsíros; Identification of an Active Reverse Transcriptase Enzyme Encoded by a Human Endogenous HERV-K Retrov. Journal of Virology, March 1999, p. 2365-2375, Vol. 73, No. 3)

    Dale,

    “My point was that there is no way of knowing how good an estimate of in vivo infectivity that an end point dilution assay is. And your point, that I continue to miss … was really what?”

    Piatak, “For HIV-1 propagated in vitro, total virions have been reported to exceed culturable infectious units by factors of 10(exp4) to 10(exp7) (25), ratios similar to those we OBSERVED IN PLASMA.” (emphasis added)

    Now, the point is that on the “estimate”, if you use the LOW BOUND cited by Piatak, the “99.998% defective” in previous post becomes 99.99%. Substitute this number into the statement I made and it doesn’t change the argument.

    25. SP layne et al, Virology 189, 695 (1992); AS Bourinbaiar, Nature 349, 111 (1991); JA McKeating, JP Moore, ibid, p660

  354. #354 Gene Semon
    June 28, 2006

    Hank, Duesberg is not an appropriate citation for evidence of anything pertaining to HIV or AIDS as Duesberg has published no clinical or laboratory studies that contain original data.
    Posted by: Dale | June 6, 2006 04:23 PM

    I just came across this howler. You really believe this, Dale?! Have you ever heard of Popper’s Conjectures and Refutations and similar works by critical rationalists?

    Thanks for the laughs.

  355. #355 Dale
    June 28, 2006

    Gene, I’m glad you find me amusing as I find you equally so. Because in trying to make your point about Piatak’s paper, you are confusing the source of the virus (either grown in culture or obtained from patient plasma) with the assay used for measuring viral infectivity. The assay is performed in cell culture. In fact, if you read the Bourinbaiar reference you cited you will find reference to the acronym TCID as a measure of viral infectivity. The TC stands for “tissue culture”. Moreover, I note that Bourinbaiar makes the same point I did but slightly differently – namely that TCID measurements may not be accurate reflections of viral infectivity in vivo.

    As far as my statement to Hank, I’d be happy to change my opinion if you or anyone else would provide a citation to any original research (not an analysis of other people’s data but original research) related to either HIV or AIDS, published by Dr. Duesberg.

  356. #356 HankBarnes
    June 28, 2006

    Dale,

    I’d be happy to change my opinion if you or anyone else would provide a citation to any original research (not an analysis of other people’s data but original research) related to either HIV or AIDS, published by Dr. Duesberg

    The original research done by Gallo was deemed fraudulent.

    And, the original reasearch done by Montagnier, convinced him that HIV was insufficient to cause AIDS.

    “There are too many shortcomings in the theory that HIV causes all signs of AIDS,” says Luc Montagnier.

    In June, when Montagnier, a French AIDS researcher announced his rejection of the established theory, he should have provoked a sensation. After all, Montagnier discovered HIV in the first place.

    Montagnier now believes that HIV is “a peaceful virus” that becomes a killer only when combined with another bug-a bug he has already isolated and identified. This finding received none of the attention of his original discovery.

    Hank Barnes

  357. #357 Dale
    June 28, 2006

    Hank,
    What does Gallo have to do with the topic at hand. Point me to Duesberg’s original research on HIV or AIDS and I will retract my comment.

    As far as Montagnier (who also has nothing to do with the topic at hand) goes, may I point you to the following:
    NEJM 349, 2283

    If you don’t recognize it, its a 2003 paper by Gallo & Montagnier titled “The discovery of HIV as the cause of AIDS”.

    Whatever Montagnier may have believed back in the late 80s, it would appear he’s changed his mind.

  358. #358 Richard Jefferys
    June 28, 2006

    Montagnier was a member of the organizing committee for the Durban Declaration.

    Hank, since you’re here, I was wondering if you’d care to declare whether or not you’re a member of the Federalist Society? I ask because you’re incredibly solicitous of gay men that support your views on HIV, but the People for the American Way report on the Federalist Society has this to say about their perspectives on gay men and people with AIDS:

    “Charles J. Cooper, who chairs the organization’s practice group on civil rights, is a well-known opponent of traditional anti-discrimination efforts. In fact, Cooper co-wrote an opinion while serving in the Reagan Justice Department that federal law did not prevent employers from refusing to hire people with AIDS if those employers cited a “fear of contagion, whether reasonable or not.” An article on the Society’s Web site by Princeton University professor and leading Federalist Society member Robert George and attorney Bill Saunders attacks the U.S. Supreme Court’s 1996 Romer v. Evans decision on anti-gay discrimination for curbing the ability of a state “to employ its ‘police power’ to protect public morals” George and Saunders write that if the repeal of state sodomy laws encourages the Supreme Court “to raise homosexuality to protected status, perhaps such conduct should not be de-criminalized in the first place.”

    Source: “The Federalist Society: From Obscurity to Power.”
    A Report by the People For the American Way Foundation
    August 2001
    http://www.pfaw.org/pfaw/general/default.aspx?oid=7754

  359. #359 Wilhelm Godschalk
    June 28, 2006

    Chris wrote:
    >”Wilhelm just makes this stuff up. He never provides references for his assertions.”

    Most of what I write I just quote from memory or personal knowledge. I sometimes provide references. But usually I tend to avoid the PubMed papers, because they are mostly of inferior quality (and written by 14 or so scientific prostitutes). It’s sad, but some day soon we’ll have to throw 25 years of biomedical science away.

    >”The seasonal variation in the influenza virus is due primarily to antigenic drift (point mutations etc) not antigenic shift (reassortment or recombination). This is due to the high mutation rate of all RNA viruses.”

    I’m trying to give a scholarly answer to this crock, but the only word that comes to mind is “bullshit”. It’s simply not true. Eh… who was making things up again?

    >”I have previously given Godschalk several references that demonstrate that poliovirus like all other RNA viruses has extremely high mutation rates.”

    Yes, yes, I remember those references very well. Just exercises by the usual crowd with DNA fixation.
    Get a load of this:

    !RNA was extracted from cell lysates with Ultraspec 3 (Biotexc) and was reverse transcribed using random hexamer primers (Boehringer Ingelheim) with avian myeloblastosis virus reverse transcriptase (Promega). DNA copies of selected genomic portions were amplified by PCR with appropriate primers (the primer sequences are available upon request), and the PCR products were purified with the QIAquick system (Qiagen) and were directly sequenced either automatically (Applied Biosystems) or manually by using the Sequenase kit, version 2.0 (U.S. Biochemicals).

    Meaning they took a fraction of the poop, supposedly containing the polio virus, put it on a cell culture, let it sudder for a while, and the lysed the cells. Whatever came out of those cells was reverse transcribed to DNA. Ah! now they finally has something they knew how to work with!
    By the way, can you imagine anything more irrelevant than reverse transcribing polio-RNA? Polio is not a retrovirus, of course, but they just HAD to have DNA, because that’s the only stuff they know how to work with. A little PCR, sequencing the DNA, and poof! Lots of mutations…
    Well, I’ll gladly believe there was lots of different crap. But I have a question: Did any of this lead to real mutant infectious polio virus particles? Nooooo-o, but there was lots of different DNA, and every strand could be sequenced and placed in the gene bank.
    For the virologists of today, a strand of DNA equals a virus. And if the virus really contains RNA, no problem; we just make DNA out of it by reverse transcription.

    We should all be grateful to Chris that he presented a complete paper, not just an abstract. But if you read this “Materials and Methods” section, be honest: Do you really get the impression that this is genetic drift at work, or just an extrapolation based on messy lab work?
    It is certain that none of these so-called mutations is producing any infectious virus strains. So even if frequent point mutations took place, they would be totally without any practical consequence. It’s like a factory making widgets. Some widgets will turn out to be defective, but they are just thrown away, and are never sold to the public.
    I repeat: All this harping on mutations only serves to cover up sloppy lab work.

  360. #360 Dale
    June 29, 2006

    Wilhelm writes All this harping on mutations only serves to cover up sloppy lab work.

    In other words, Wilhelm, you acknowledge that RNA viruses have high mutation rates as measured by the only means known to assess such things. So what was all that business about earlier when you stated that RNA viruses like poliovirus had stable genomes?

  361. #361 Gene Semon
    June 29, 2006

    Dale,

    Nice evasion. Good work. Now make a counter argument on the subject of defective viruses and how they can be pathogenic!

    More to come on those missing gp120 knobs as we revisit earlier posts on this thread.

  362. #362 Gene Semon
    June 29, 2006

    “(Y)ou are confusing the source of the virus (either grown in culture or obtained from patient plasma) with the assay used for measuring viral infectivity. The assay is performed in cell culture. In fact, if you read the Bourinbaiar reference you cited you will find reference to the acronym TCID as a measure of viral infectivity. The TC stands for “tissue culture”. Moreover, I note that Bourinbaiar makes the same point I did but slightly differently – namely that TCID measurements may not be accurate reflections of viral infectivity in vivo.”

    Dale,

    You are the confused one. I stated previously that tissue culture was used to make an observation ex vivo, which means as close as you can get to directly observing what’s going on in vivo. I quoted Piatak’s numerical range ESTIMATE and used the most conservative (no Richard, I don’t support the Federalist Society) percentage number to clearly state the extraordinarily low odds of infectious transmission, as pointed out by Duesberg/Bialy in the Maddox-allowed response to Ho and Wei in 1995 (referencing Piatak).

    But you guys are so good at backpedaling and smoke-screening that today I don’t laugh but have to express a grudging admiration for your skills in keeping so many people snowed.

  363. #363 Chris Noble
    June 29, 2006

    Godschalk writes:

    Most of what I write I just quote from memory or personal knowledge. I sometimes provide references. But usually I tend to avoid the PubMed papers, because they are mostly of inferior quality (and written by 14 or so scientific prostitutes). It’s sad, but some day soon we’ll have to throw 25 years of biomedical science away.

    But you do not have any personal knowledge of the mutation rates of viruses such as poliovirus and FMDV. All you have is bald assertions.

    On the other hand I have provided several papers demonstrating that all RNA viruses have high mutation rates. There are many, many more. I have selected some that are available gratis on the internet in the hope that people not at an academic institution will read them. They are no more “PubMed papers” than papers published in any peer-reviewed journal. This has to be one the most bizarre criticisms yet.

    Any textbook on virology will say that all RNA viruses have high mutation rates. Every single paper will also state this. There is a simple reason. RNA viruses do not have a proof reading mechanism to correct the errors that occur with the RNA replication.

    On the other hand we have one Wilhelm Godschalk saying this is not the case because “I said so”. Can you produce one single paper to support your assertion? No. All you have is “personal knowledge” which is so personal that nobody else in the world shares it.

    All I can say is. Bullshit!

    Godschalk also writes:

    I’m trying to give a scholarly answer to this crock, but the only word that comes to mind is “bullshit”. It’s simply not true. Eh… who was making things up again?

    Pick up a text book on virology. Visit the websites of the agencies responsible for producing influenza vaccines.

    Here is one paper that talks about both antigenic shift and antigenic drift.

    Influenza Vaccine – Outmaneuvering Antigenic Shift and Drift

    Of more relevance to this year’s experience is the phenomenon of antigenic drift. Drift is a subtler process than shift and involves the accumulation of mutations within the antibody-binding sites in the hemagglutinin (see Figure), the neuraminidase, or both that abrogate the binding of some antibodies. Because of these mutations, the resulting viruses cannot be inhibited well by antibodies against previous strains, and it is easier for them to spread throughout a partially immune population. Antigenic drift occurs in both influenza A and influenza B viruses, but the pattern observed is somewhat different for the different viruses. Whereas drift variants of A (H1) viruses and B viruses often cocirculate with multiple coexisting lineages, influenza A viruses of the H3 subtype evolve more rapidly. Antigenic-drift variants of the H3 viruses occur more often, and new variants tend to replace older variants quickly, so that the evolution of the H3 hemagglutinin is more linear than that of other subtypes.2

    In addition to influencing the nature of the yearly influenza epidemic, antigenic drift must be taken into account when strains are being considered for inclusion in influenza vaccines. Strain selection is an ongoing and complex process, involving the coordinated efforts of national and international organizations. Surveillance for new influenza strains is conducted year-round by the Centers for Disease Control and Prevention and the World Health Organization. The HA1 regions of the hemagglutinin gene of new viruses are sequenced, and their reaction with serum from experimentally infected ferrets is tested. The extent of epidemic activity of new viruses is assessed in an attempt to predict which viruses will emerge as predominant in the next year’s influenza season. If a substantially new variant is identified, it must be prepared as an influenza vaccine in time for the next vaccination season.

    The annual variation in influenza vaccine is determined predominantly by antigenic drift.

  364. #364 Wilhelm Godschalk
    June 29, 2006

    >”In other words, Wilhelm, you acknowledge that RNA viruses have high mutation rates as measured by the only means known to assess such things.”

    No, Dale. I just pointed out that there’s a lot of different crap in those cell cultures.

    >”So what was all that business about earlier when you stated that RNA viruses like poliovirus had stable genomes?”

    They do. If you don’t believe me, find a large number of different polio strains (whole particles, please!), isolate RNA from all of them, and (try to) sequence that.
    All this reverse transcribing, followed by PCR and sequencing the DNA seems a little artificial to me.

  365. #365 Chris Noble
    June 29, 2006

    Godschalk writes:

    Most of what I write I just quote from memory or personal knowledge. I sometimes provide references. But usually I tend to avoid the PubMed papers, because they are mostly of inferior quality (and written by 14 or so scientific prostitutes). It’s sad, but some day soon we’ll have to throw 25 years of biomedical science away.

    For clarification it should be pointed out that Godschalk cannot find a single reference to support his claim that RNA viruses such as poliovirus do not have high mutation rates. This is why he does not give a citation. He is also willing to ignore every single paper and textbook written on the subject because they are written by “scientific prostitutes”. We are also supposed to throw 25 years of biomedical science away. Why? Because it disagrees with Godschalk’s “personal knowledge”.

  366. #366 Dale
    June 29, 2006

    Gene writes which means as close as you can get to directly observing what’s going on in vivo.
    Exactly! And neither you nor I nor the people doing the experiments have any way of telling how good ‘as close as you get’ really is. What they and I (and you should) know is that HIV is infectious in vivo and that viral load correlates with viral infectivity. That’s what observation tells them and since the purpose of theories is to explain observations and make predictions, if your theory says HIV shouldn’t be infectious in vivo then there is clearly something wrong with your theory.

  367. #367 Chris Noble
    June 29, 2006

    Godschalk writes:

    All this reverse transcribing, followed by PCR and sequencing the DNA seems a little artificial to me.

    Why? These techniques are all standard.

    If you want to back in time then here is an old reference.

    Multiple genetic changes can occur in the oral poliovaccines upon replication in humans.

    No PCR!

    RNA was extracted from poliovirions purified in sucrose gradients.

    Oligonucteotide maps of the digested RNA showed multiple changes during a single human passage.

    This is afterall the reason why live oral poliovirus vaccine can lead to an outbreak of neourovirulent polio in undervaccinated populations. Poliovirus has an extremely high mutation rate.

  368. #368 Gene Semon
    June 30, 2006

    “What they and I (and you should) know is that HIV is infectious in vivo and that viral load correlates with viral infectivity. That’s what observation tells them and since the purpose of theories is to explain observations and make predictions, if your theory says HIV shouldn’t be infectious in vivo then there is clearly something wrong with your theory.”

    Dale,

    You really don’t get it. What part of 99.99% defective don’t you understand. Look, there is clearly something wrong with “viral load”, if it doesn’t measure the env gene since according to the orthodox model, gp120, a product of the env gene is REQUIRED for infectivity. The huffing and puffing you guys did earlier cited a paper that measured 115bp (that’s out of 10,000 bp – full length genome) of the gag gene. Branched DNA (used by Ho and Wei, Nature, 1995) measures the pol gene ONLY.

    Now, consider “isolation” as defined by:

    Robey WG, Arthur LO, et al, Proc. Natl. Acad. Sci. USA [1986] V83, 7023-7027

    Excerpts:

    “Initial purification studies using sucrose-banded ‘virions’ showed that VERY LITTLE* gp120 was present. The levels observed were 0.06-0.10 ug/mg of virus protein. However, purification of HIV gp120 to homogeneity was possible using infected cells or cell culture fluids as the source of the glycoprotein. The purified material is immunogenic in goats, horses, and rhesus monkeys . . . .” (quotation marks mine) (EMPHASIS ADDED)

    “In previous studies gp120 was readily detected in either cell extracts or cell culture fluids but was not significantly present in sucrose-gradient purified virions.” (Robey, WG, Safai, B . . . . Gallo, RC . . . .[1985] Science, V228, 593-595)

    “Extensive experience in the production of large quantities of HIV has shown that purified virion preparations contain many contaminating cellular proteins and very little gp120. Because of this lack of gp120 in purified virions, membrane fractions from infected cells were used as the starting material for the large-scale isolation of the glycoprotein.”

    Remember previous posts re complex transcriptions of proviral DNA?

    So, the case of the missing viremia, meaning surrogate markers do not demonstrate infectious particles, goes on and Duesberg still stands.

    Is it too much for you to grasp that the burden of proof is on your side?

  369. #369 Dale
    June 30, 2006

    Gene, Once again I think your point escapes me. Viral load is not a direct measure of infectivity, even though the two generally correlate? Hiv viruses may not be particular stable during sucrose banding? I’ll agree to either of those points but neither speaks to the question of whether HIV is infectious or not. The burden of proof on that point has been met over and over again by epidemilogical and molecular biological studies of transmission cohorts.

  370. #370 Gene Semon
    July 1, 2006

    “I’ll agree to either of those points but neither speaks to the question of whether HIV is infectious or not. The burden of proof on that point has been met over and over again by epidemilogical and molecular biological studies of transmission cohorts.” Dale

    “‘We are still very confused about the mechanisms that lead to CD4 depletion, (but) at least now we are confused at a higher level of understanding’ (says) immunologist Paul Johnson of Harvard Medical School.”
    (Michael Balter, Science, V278, 1399-1400, 11/21/97)

    Finally it hits me. Dale has reached that ultimately sublime space in the Bizzaro World of HIV/AIDS science of being confused (higher level or not) in his understanding. Or as Harvey B puts it: what kind of scientist continues to believe in a theory that doesn’t explain or predict.

    And how do the “epidemilogical and molecular biological studies of transmission cohorts” lead to this conclusion: “During the past few years it has become clear that apparently harmless, and possibly protective, encounters with HIV can occur;” (Jonas Salk, Peter A. Bretscher, Peter L. Salk, Mario Clerici, Gene M. Shearer, Science, V260, 1270, 5/28/93)?

  371. #371 Dale
    July 1, 2006

    Gene, You have more wonderfully irrelevant quotes than any dissident/skeptic/denialist I have ever exchanged comments with. As far as Harvey B.’s quote – you should ask him what kind of scientist he is and that will provide you to the answer to his question.

  372. #372 Chris Noble
    July 2, 2006

    Gene Semon writes:

    And how do the “epidemilogical and molecular biological studies of transmission cohorts” lead to this conclusion: “During the past few years it has become clear that apparently harmless, and possibly protective, encounters with HIV can occur;” (Jonas Salk, Peter A. Bretscher, Peter L. Salk, Mario Clerici, Gene M. Shearer, Science, V260, 1270, 5/28/93)?

    Have you written to the authors to ask them about your interpretation of their article? You should consider the possibility that you have no understanding of articles that you cite.

    Cell-mediated immunity is also of vital importance in malaria. Not only can harmless and even protective encounters with Plasmodium falciparum occur but it is being proposed as a method of vaccination.

    Sub-patent infection with Plasmodium falciparum can lead to a protective cell-mediated immunity.

  373. #373 Chris Noble
    July 2, 2006

    Gene Semon writes:

    So, the case of the missing viremia, meaning surrogate markers do not demonstrate infectious particles, goes on and Duesberg still stands.

    Where do you think the RNA is coming from if not from infectious particles? Is it magically contrcuting itself from nothing?

    High mutation rates in RNA viruses mean that these viruses exist as a “quasispecies”. A mutation rate of ~10^-4 for a virus with ~10^4 bps means that on average each virion will have one base-pair substitution. A large percentage will be non-infectious.

    This is also true for other viruses such as poliovirus and FMDV which both have extremely high mutation rates.

    Nobody is saying that viral load measured by RNA is equivalent to measuring infectious virions. The only people that make this assertion are “rethinkers” contructing strawman arguments.

  374. #374 Wilhelm Godschalk
    July 3, 2006

    I see that Chris Noble has been very busy again spinning yarns. So it’s time again for some rebuttals

    Any textbook on virology will say that all RNA viruses have high mutation rates. Every single paper will also state this. There is a simple reason. RNA viruses do not have a proof reading mechanism to correct the errors that occur with the RNA replication.

    Tell somebody who gives a damn. It’s quite possible that there are some point mutations. But what maniac would go to the trouble of measuring a mutation rate? These point mutations (or genetic drift, as you like to call it) lead to defective virus particles, so they are of no consequence.

    Furthermore, you say: “All RNA viruses”. Well that includes the plant viruses then. But you never hear of mutations playing any kind of a role in plant virology. Only when it comes to animal viruses such as polio and influenza, the whining about mutations manifests itself. Small wonder, because those are the viruses where the money is. So that’s where the whole repertoire of fairy tales and outright lies is played out.
    Flu virus is different; reassortment and recombination are possible. But polio is just a plain, humble picorna virus, and there is no reason, that could come up in a normally functioning brain, to assume that it would behave differently than the other picorna viruses (that happen to be out of the money). I’m sure you are aware of the controversy in which polio vaccines have been involved, ever since the days of Jonas Salk. It’s the same ol’ shit again, just like “HIV”. Just because it’s a big-money virus (real or virtual), it’s touted all of a sudden that it possesses magical qualities. Well, it just ain’t so, no matter how stubbornly you try to push your benefactors’ stupid theories down our throats.

    Can you produce one single paper to support your assertion?

    What? proving that there are NO mutations? Like proving there’s no Santa Claus? Totally unimportant. There may be mutations taking place, but they don’t lead to anything infectious. Too many researchers with five thumbs on each hand and shit for brains blame their faulty technique on some poor virus’ frequent mutations. In all cases where they claim 100 different strains of one and the same virus, it’s just a matter of never getting the same result when an experiment is repeated over and over again. – Irreproducibility.

    Visit the websites of the agencies responsible for producing influenza vaccines.

    Oh please! Have some pity! Those are the scoundrels responsible for murdering people in the name of AIDS, and scaring millions of people shitless over a totally ridiculous concept of bird flu.
    Oh, and before I forget: My criticism on the PubMed papers is only based on the fact that they are all recent. Didn’t I say somewhere that the last 25 years of virus research should be thrown away?

    Here is one paper that talks about both antigenic shift and antigenic drift.

    Right. This is a review article, written by an M.D. John Treanor mentions point mutations somewhere, but does not present any evidence for it. So these things just seem to be true because he says so… (something you criticize me for) Well, I say these are not point mutations leading to new strains. And I can’t think of a single reason why John Treanor should have even remotely more authority than I have. (Maybe because he makes more money on this crap?)

    Why? These techniques are all standard.

    Sure. But sequencing, PCR, etc. are all DNA techniques. Very useful when DNA is involved. But in the case of an RNA virus, producing DNA for the sole reason that that’s the only material they can work with, is a little roundabout.
    Let’s face it: They can’t deal with RNA. Now that’s nothing to be ashamed of; it is difficult. But that’s no reason to snow us under with irrelevant DNA work and trying to hammer into our skulls that their DNA (from godknows what origin) is equivalent to an RNA-containing virus.

    By the way, thanks for that 1981 reference. That illustrates my point. No PCR (of course), but they isolate and analyze the RNA by chopping it into pieces and making oligonucleotide maps. I hope it’s clear that these maps won’t always produce the same results. If you find a spot less, or one in a different location, it is a little farfetched to conclude that a mutation has taken place. If the RNA-chain is cut in a different location, you get different oligonucleotides. Why, oh why do they always draw conclusions first, before they do the experiment?

  375. #375 Chris Noble
    July 5, 2006

    Godschalk writes:

    Tell somebody who gives a damn. It’s quite possible that there are some point mutations. But what maniac would go to the trouble of measuring a mutation rate? These point mutations (or genetic drift, as you like to call it) lead to defective virus particles, so they are of no consequence.

    The majority of point mutations in RNA viruses such as influenza and poliovirus are neutral. They do not effect the viability of the virus. There are some highly conserved regions where mutations lead to the inability of the virus to replicate or infect host cells etc. But these regions represent only a small percentage of the genome.

    Genetic drift is very important. It is the process that leads to the seasonal variation in influenza. It is also the process that lead to the various isoforms of the hemagglutin proteins H1 – H16 and the various isoforms of the neuraminidase proteins N1 – N9.
    Where do you think the different subtypes of hemagglutinin and neuraminidase came from? Did the Intelligent Designer create them or did they evolve?

    Here is an older paper regarding the evoultion of influenza A viruses

    Evolution of human influenza A viruses over 50 years: rapid, uniform rate ofchange in NS gene.

    PS. You haven’t come up with a single reference to support your claim that poliovirus does not have a high mutation rate.

  376. #376 Dale
    July 5, 2006

    Sure. But sequencing, PCR, etc. are all DNA techniques. Very useful when DNA is involved. But in the case of an RNA virus, producing DNA for the sole reason that that’s the only material they can work with, is a little roundabout.

    Now *that* is hilarious! Francis Crick must be rolling over in his grave.

  377. #377 Gene Semon
    July 6, 2006

    Chris asks, “Where do you think the RNA is coming from if not from infectious particles? Is it magically contrcuting itself from nothing?”

    At first, you guys are entertaining, but then you start to get tiresome.

    You ignore what I say in other posts to focus on a FRAGMENT of the argument on the transcriptional behaviour of retroviral proviral DNA, which CLEARLY EXISTS, even if you choose J. McDonald’s classification system published in Genome Research, where he states that “complex infectious retroviruses” are a sub-taxon of retrotransposons. These retrovirus-like genes were found in the nematode worm so this means they have been with animals since before the Cambrian Explosion. (HIV as “living fossil”, remember?)

    Here’s more on Piatak, which, of course, you’re free to ignore.

    From Dean Esmay – cc and paste:

    Ho and Wei have been falsified. Ho and Wei are the two Nature papers published in 1995 claiming to confirm HIV as cause of AIDS and disprove Duesberg. Unfortunately, they did not deal at all with Duesberg’s points and relied on a novel assay – branched DNA signal (no polymerase amplification) – to measure pol RNA, which they assumed to be equivalent to HI virions.

    Here is a quote from Piatak et al (Science, V259, 1993, 1749): “Circulating levels of plasma virus determined by PCR . . . exceeded by an average of nearly 60,000-fold titers of infectious HIV-1.” And, in vivo “titers of culturable virus” survive “viral envelope shedding (and) deterioration of other viral components”; many in the “60,000” are “genotypically defective virus”. This was pointed out in the Maddox-allowed response to Ho and Wei by Duesberg and Bialy in Nature, reinforcing Duesberg’s original point of insufficient biochemical activity to cause ANYTHING. Of course, ignored by the AIDS establishment.

    Consider recent publication: among retrovirus-like sequences in the HUMAN GENOME, “about 8,000 pol containing elements have been identified to date”. (Seifarth et al, Journal of Virology, January 2005, V79, 341). Latent retroviruses, in other words, is a condition shared by ALL humans.

    Clearly, the assumption of virion equivalency is invalid, since the pol RNA can be transcribed in the lymphocytes of the patients studied as, e.g. a response to toxic stressors. Circulating nucleic acids, not particle associated, have been detected in cancer patients.

    (End cc and paste)

    Pachl, C et al, RAPID AND PRECISE QUANTIFICATION OF HIV-1 RNA IN PLASMA USING A BRANCHED DNA SIGNAL AMPLIFICATION ASSAY, Journal of AIDS and Human Retrovirology, 8, 446-454, 1995, EXCERPT:

    “The viral RNA is detected directly at its physiological level, without amplification of the target sequence.” NO POLYMERASE CHAIN REACTION IN THIS ASSAY*

    Principles of the bDNA Assay: “. . . the bDNA method is based on the hybridization of HIV-1 viral RNA in plasma to 49 oligonucleotide probes (target probes). Each target probe includes 33 bases complementary to the most conserved regions of the HIV-1 pol gene, based on the available pol sequences from 18 HIV-1 isolates [subgroups A, B, and D]. . . . The RNA probe complex is detected with the use of a chemiluminescent substrate and light emission is proportional to the amount of RNA target captured in the microwell.”

    “Quantitation Standard: The standard used for quantitation of HIV-1 RNA in the bDNA assay is a single-stranded DNA molecule encoding the gag and pol genes of HIV-1(SF2) inserted into a phagemid vector. This single-stranded DNA standard was quantitated in the bDNA assay by comparison to a 9.0-kb HIV-1(IIIB) RNA transcript standard, which was transcribed in vitro from plasmid pBKBH10S (provided from the National Institutes of Health AIDS Research and Reference Reagent Program), with the use of a commercially available kit. This HIV-1(IIIB) RNA transcript was quantitated with use of absorbance at 260 nm and hybridization in probe excess. The standard curve (Relative Luminescence vs HIV RNA Eq/ml) used in the assay was prepared by dilution of the single-stranded DNA standard into recalcified plasma to generate a four-point standard (calibration) curve from 1 X 10(4) to 1.6 X 10(6) HIV-RNA Eq/ml.”

    Figure 2 clearly shows the bDNA assay measures pol RNA only, not full-length “HIV” RNA. Moreover, “. . .the equivalence of HIV-1 plasma RNA to viral particles HAS NOT BEEN DIRECTLY SHOWN* . . .” and “it is reasonable to ASSUME* that the HIV-1 RNA measured by the bDNA assay is particle associated.” (emphasis added) Most importantly, “the broad range of HIV-1 RNA levels at any given CD4+ T-cell level indicates that CD4+ T-cell counts cannot be used to predict viral load.”

    *(EMPHASIS ADDED)

    END EXCERPT

    Take note of the ASSUMPTION that is the quicksand of this assay.

    So, Chris, can you at least SEE the counter-argument re cross reactions (especially if you take another look at previous posts) given the well established facts of mRNA AND SEPARATE Env transcriptions of same?

  378. #378 Gene Semon
    July 6, 2006

    And here’s another one I’ve dug out of the archives. It goes best with the exchanges at Dean Esmay.

    Response to HIV Campaign

    “During the past few years it has become clear that apparently harmless, and possibly protective, encounters with HIV can occur.” (1)

    Introduction

    After participating in a blog at Dean’s World with esteemed and learned scientists defending the AIDS viral sex and blood plague, I read in my newspapers the alarm of public health officials over a new drug-resistant strain of this putative plague retrovirus in one patient! What kind of epidemic curve can we draw from that?

    It’s old news, guys, rooted in the flawed 1995 refuted-by-everybody Nature publication of the eminent Dr David Ho (Time Magazine’s man of the year) who assured us that “drug-resistant” variants of the harmless passenger HIV were on the way. Well, 10 years later we still have flat HIV incidence according to best CDC guesstimates. This drug resistance is explained below as well documented cellular response to stressors, in other words same old boring problem of bio-markers and toxemia.

    Can we put the virus hunting on hold, a temporary moratorium, so that public health departments can investigate environmental contamination and chronic diseases? Plenty to chew on at http://www.chronicillnet.org: Howard Urnovitz,PhD where he recommends that scientists and public health officials stop putting round pegs in square holes, i.e. look into the dynamic or fluid genome!

    Farr’s Law and AIDS

    Important fact left out of all discussions of “pandemic” transmission of an AIDS virus is that “data” is constructed from falsified math model of exponential runaway based on Farr’s Law. Whether incidence or prevalence is ESTIMATED, flat HIV curves as published by CDC falsify Farr’s exponential-increase model.

    In 1840, William Farr postulated a math model which he referred to as a “law of epidemics”, the “first measure of epidemic theory”. He stated: “Epidemics appear to be generated at intervals in UNHEALTHY PLACES, spread, and go through a regular course, and decline; but of the cause of their evolutions no more is known than of the periodic paraoxysms of ague . . . If the latent cause of epidemics cannot be discovered, the mode by which it operates may be investigated. The laws of its action may be determined by observation.”

    The “incidence” data in above paper is for AIDS, not HIV. It is significant that “HIV incidence” is omitted from the author’s discussion. Most important, “We have made no effort to calculate confidence limits for these projections. We humbly submit that we do NOT KNOW HOW TO ACCOUNT* for the error due to biases in the reporting system. Furthermore, we believe it would be futile and meaningless to place a 95% confidence interval based on random error about the projections that extend out for a decade. To do so would suggest a greater confidence in both the method used and the data available than is justified.” (2) *(emphasis added)

    The authors conclude, “the use of the normal curve was chosen partly in respect to the Farr-Brownlee tradition but more practically because of the stark SIMPLICITY* of the method. Others have also discussed the complexity of modeling the infinite number of events, circumstances and relationships that have conspired to create the epidemic of AIDS. There is reluctance to accept simple explanations of complex phenomenon.” (ibid) *(emphasis added)

    According to Farr and an important postulate of Koch as stated by Huebner, “In order that a virus be regarded as an established cause of a specific human illness, the following” condition is at least “necessary: constant association with specific illness. If the disease in question is a well-defined and recognizable entity, the agent should be constantly associated therewith. If tissues of the host are available at a suitable time during the course of the illness, the agent should be found in the diseased areas.” (3) Farr’s Law, in turn is founded on the observation of obvious biological effects spread from one victim to another – said “effects” missing in the case of HIV, which cannot be directly detected in transmission even with the most sensitive of assays.

    Total endemic infection rate of all HIV variants as harmless passenger viruses remains unknown. Complicating this problem is that functionally homologous endogenous retroviral sequences can have the same protective function as the exogenous sequences. In any case, the measurement: – full-length HIV DNA considering all known and UNKNOWN variants of the unrooted “sunburst” phylogeny – is not sufficiently SENSITIVITE.

    Assuming a gold standard of “seroconversion” based on correlation with “HIV disease” or “AIDS” as a highly sensitive surrogate for incidence data is not sufficiently SPECIFIC. Test-kit proteins derived from human blood and cells with AIDS associated viruses, (e.g. hepatitis, herpes, HTLV,) and autoantibodies guarantee a high false positive rate, as compared to the most accurate measurement, still to be defined in the case of HIV. This unstated, but presumed gold standard is not a trivial matter, since false positive rate can be high or 100%. This is why tests are not diagnostic for HIV infection nor AIDS as stated by manufacturers in disclaimers that accompany the kits.

    Therefore, no AIDS virus can be claimed based on epidemiological data.

    HIV Debunk

    Peter Duesberg’s much maligned arguments are falsifications of hypothetical mechanisms postulated for an AIDS virus in “constant association” with the multiple disorders falling into AIDS construct. They are based on the following never-refuted-by-anyone biological properties of retroviruses, as detailed in his 1987 – 89 papers in Cancer Research and PNAS:

    a) Exogenous and endogenous retroviruses are isogenic, meaning canonical gag, pol and env genes are functionally homologous;

    b) Transmission between organisms cannot be cell-free; in sex, an undetectable donation of lymphocytes with proviral passenger HIVs to partner must take place. In order for “efficient transmission”, proviral DNA must be transcribed in allogeneic, transplanted lymphocytes and integrated into host immune cells via mediated gp120 cell-entry.

    c) A SECOND proviral transcription is alleged to produce a viral load based on antigenemia of gag p24 or mRNA transcripts of pol RNA. As stated by Salk et al “protective effect” of these transcriptions may include emergency DNA repair or blocking of a pathogen. “It is possible that cellular factors induced or activated by a variety of agents are primarily responsible for triggering a cascade of events . . . (reactivating viral expression from latency).” An “SOS-like stress response could be a general inducer of the HIV LTR.” (4)

    d) No specific AIDS gene or set of genes has ever been identified; proposed candidates not withstanding. The citing of “accessory” or “trans-activator” genes is not sufficient evidence since functional genomic analysis will produce the same result in all animal retroviruses, based on the well established property of retroviral cellular gene transduction.

    In reference 5 Duesberg et al present and explain the flat HIV incidence curve – the cause of much sound and fury (see deanesmay.com). As the best approximation of the CDC’s epidemiological guesses in conjunction with above arguments, Duesberg, Bialy et al have falsified AIDS sex and blood plague virus

    It should be understood by all public health officials and journalists reporting on HIV that so called epidemiological data are nothing more than guesses, and bad ones at that. HHS and WHO have not responded to scientific and detailed challenges that debunk surrogate anti-HIV, falsified models of an AIDS virus.

    1. Jonas Salk, Peter A. Bretscher, Peter L. Salk, Mario Clerici, Gene M. Shearer, Science, V260, 1270, 5/28/93

    2. DJ Bregman and AD Langmuir, Farr’s Law Applied to AIDS Projections, JAMA, V263, 1522 (1996)

    3. Robert J Huebner, Criteria for etiologic association of prevalent viruses with prevalent diseases: the virologist’s dilemma, Annals New York Academy of Sciences, V67, 430, (1957)

    4. Valerie, Delers et al; Activation of Human Immunodeficiency Virus Type 1 by DNA Damage in Human Cells; Nature, V333, 78-81 (1988)

    5. PETER DUESBERG, CLAUS KOEHNLEIN, and DAVID RASNICK, 2003 The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition, J. Biosci. 28 383-412]

  379. #379 Dale
    July 6, 2006

    Gene,
    You ignore what I say in other posts to focus on a FRAGMENT of the argument on the transcriptional behaviour of retroviral proviral DNA, which CLEARLY EXISTS, even if you choose J. McDonald’s classification system published in Genome Research, where he states that “complex infectious retroviruses” are a sub-taxon of retrotransposons. These retrovirus-like genes were found in the nematode worm so this means they have been with animals since before the Cambrian Explosion. (HIV as “living fossil”, remember?)
    Show me the evidence that HIV sequences have been with humans since before the 1950s and I’ll take your argument more seriously. Yes there are retrovirus-like genes and retrovirus-like elements that are endogenous to human cells but there is no evidence that HIV is one of them and plenty of evidence that it isn’t.

    Here’s more on Piatak, which, of course, you’re free to ignore.
    Ho and Wei have been falsified. Ho and Wei are the two Nature papers published in 1995 claiming to confirm HIV as cause of AIDS and disprove Duesberg. Unfortunately, they did not deal at all with Duesberg’s points and relied on a novel assay – branched DNA signal (no polymerase amplification) – to measure pol RNA, which they assumed to be equivalent to HI virions.

    Yes, Ho and Wei have been falsified. Within about a month of publication. Falsified by orthodox scientists. Old news.

    Here is a quote from Piatak et al (Science, V259, 1993, 1749): “Circulating levels of plasma virus determined by PCR . . . exceeded by an average of nearly 60,000-fold titers of infectious HIV-1.” And, in vivo “titers of culturable virus” survive “viral envelope shedding (and) deterioration of other viral components”; many in the “60,000” are “genotypically defective virus”. This was pointed out in the Maddox-allowed response to Ho and Wei by Duesberg and Bialy in Nature, reinforcing Duesberg’s original point of insufficient biochemical activity to cause ANYTHING. Of course, ignored by the AIDS establishment.

    Demonstrates that viral particles as measured by PCR are likely not in one to one correspondence with infectious virus. This is true of many viruses as Chris Noble has pointed out previously. It’s probably more the rule than the exception. You ignore that Piatak also found a correlation between high levels of infectious virus and high viral loads. Where viral loads were high, infectious virus was high. Duesberg’s point originally was that there didn’t seem to be enough HIV in the peripheral blood to account for the eventual depletion of CD4+ T-cells. The flaw in Duesberg’s argument was and is in assuming that there is only one model by which a virus can cause a disease. Ain’t so.

    Consider recent publication: among retrovirus-like sequences in the HUMAN GENOME, “about 8,000 pol containing elements have been identified to date”. (Seifarth et al, Journal of Virology, January 2005, V79, 341). Latent retroviruses, in other words, is a condition shared by ALL humans.
    Clearly, the assumption of virion equivalency is invalid, since the pol RNA can be transcribed in the lymphocytes of the patients studied as, e.g. a response to toxic stressors. Circulating nucleic acids, not particle associated, have been detected in cancer patients.

    The sequences of HIV pol are unique to HIV. So the fact there are other ‘pol containing elements’ is irrelevant. If HIV pol is a response to ‘toxic stressors’ why does it behave like an infectious agent? Why do ‘toxic stressors’ appear in individuals who have had sex with others expressing the same ‘toxic stressors’ at but not in individuals

    “During the past few years it has become clear that apparently harmless, and possibly protective, encounters with HIV can occur.” (1)
    The operative word here is ‘can’. It’s a rare event.

    After participating in a blog at Dean’s World with esteemed and learned scientists defending the AIDS viral sex and blood plague, I read in my newspapers the alarm of public health officials over a new drug-resistant strain of this putative plague retrovirus in one patient! What kind of epidemic curve can we draw from that?
    That was a false alarm. Some over eager public official jumped the gun.

    It’s old news, guys, rooted in the flawed 1995 refuted-by-everybody Nature publication of the eminent Dr David Ho (Time Magazine’s man of the year) who assured us that “drug-resistant” variants of the harmless passenger HIV were on the way. Well, 10 years later we still have flat HIV incidence according to best CDC guesstimates.

    And you’re going to tell me that Americans haven’t changed their sexual behaviour over the past 20 years in response to HIV/AIDS? Funny but that’s not what the surveys indicate. Not to mention that while the overall numbers may have remained relatively static infection rates among various subgroups of Americans have been changing.

    Farr’s Law and AIDS
    Important fact left out of all discussions of “pandemic” transmission of an AIDS virus is that “data” is constructed from falsified math model of exponential runaway based on Farr’s Law. Whether incidence or prevalence is ESTIMATED, flat HIV curves as published by CDC falsify Farr’s exponential-increase model.
    In 1840, William Farr postulated a math model which he referred to as a “law of epidemics”, the “first measure of epidemic theory”. He stated: “Epidemics appear to be generated at intervals in UNHEALTHY PLACES, spread, and go through a regular course, and decline; but of the cause of their evolutions no more is known than of the periodic paraoxysms of ague . . . If the latent cause of epidemics cannot be discovered, the mode by which it operates may be investigated. The laws of its action may be determined by observation.”
    The “incidence” data in above paper is for AIDS, not HIV. It is significant that “HIV incidence” is omitted from the author’s discussion. Most important, “We have made no effort to calculate confidence limits for these projections. We humbly submit that we do NOT KNOW HOW TO ACCOUNT* for the error due to biases in the reporting system. Furthermore, we believe it would be futile and meaningless to place a 95% confidence interval based on random error about the projections that extend out for a decade. To do so would suggest a greater confidence in both the method used and the data available than is justified.” (2) *(emphasis added)
    The authors conclude, “the use of the normal curve was chosen partly in respect to the Farr-Brownlee tradition but more practically because of the stark SIMPLICITY* of the method. Others have also discussed the complexity of modeling the infinite number of events, circumstances and relationships that have conspired to create the epidemic of AIDS. There is reluctance to accept simple explanations of complex phenomenon.” (ibid) *(emphasis added)
    According to Farr and an important postulate of Koch as stated by Huebner, “In order that a virus be regarded as an established cause of a specific human illness, the following” condition is at least “necessary: constant association with specific illness. If the disease in question is a well-defined and recognizable entity, the agent should be constantly associated therewith. If tissues of the host are available at a suitable time during the course of the illness, the agent should be found in the diseased areas.” (3) Farr’s Law, in turn is founded on the observation of obvious biological effects spread from one victim to another – said “effects” missing in the case of HIV, which cannot be directly detected in transmission even with the most sensitive of assays.
    Total endemic infection rate of all HIV variants as harmless passenger viruses remains unknown. Complicating this problem is that functionally homologous endogenous retroviral sequences can have the same protective function as the exogenous sequences. In any case, the measurement: – full-length HIV DNA considering all known and UNKNOWN variants of the unrooted “sunburst” phylogeny – is not sufficiently SENSITIVITE.
    Assuming a gold standard of “seroconversion” based on correlation with “HIV disease” or “AIDS” as a highly sensitive surrogate for incidence data is not sufficiently SPECIFIC. Test-kit proteins derived from human blood and cells with AIDS associated viruses, (e.g. hepatitis, herpes, HTLV,) and autoantibodies guarantee a high false positive rate, as compared to the most accurate measurement, still to be defined in the case of HIV. This unstated, but presumed gold standard is not a trivial matter, since false positive rate can be high or 100%. This is why tests are not diagnostic for HIV infection nor AIDS as stated by manufacturers in disclaimers that accompany the kits.
    Therefore, no AIDS virus can be claimed based on epidemiological data.

    What can be concluded from all that is not that “no AIDS virus can be claimed” but that any mathematical model projecting how the virus will spread is based on necessarily incomplete assumptions. HIV can be directly detected in transmission using PCR and sequencing to follow transmission cohorts. It is true that the “endemic infection rate of HIV as a harmless passenger virus remains unknown but there is NO evidence for ANY large groups of individuals in whom HIV might be a harmless passenger virus. LTNPs are estimated to be at most 10% of the population of HIV+ individuals.

    HIV Debunk
    Peter Duesberg’s much maligned arguments are falsifications of hypothetical mechanisms postulated for an AIDS virus in “constant association” with the multiple disorders falling into AIDS construct. They are based on the following never-refuted-by-anyone biological properties of retroviruses, as detailed in his 1987 – 89 papers in Cancer Research and PNAS:
    a) Exogenous and endogenous retroviruses are isogenic, meaning canonical gag, pol and env genes are functionally homologous;
    the ‘canonical genes may be functionally homologous but their DNA sequences are very different. The redundancy of the genetic code and all that.
    b) Transmission between organisms cannot be cell-free; in sex, an undetectable donation of lymphocytes with proviral passenger HIVs to partner must take place. In order for “efficient transmission”, proviral DNA must be transcribed in allogeneic, transplanted lymphocytes and integrated into host immune cells via mediated gp120 cell-entry. if HIV passes from one individual to another as a provirus or a cell free virus that is then somehow integrated into host immune cells where it replicates and then goes on to enter other host cells … as far as I can tell, that’s infection.
    c) A SECOND proviral transcription is alleged to produce a viral load based on antigenemia of gag p24 or mRNA transcripts of pol RNA. As stated by Salk et al “protective effect” of these transcriptions may include emergency DNA repair or blocking of a pathogen. “It is possible that cellular factors induced or activated by a variety of agents are primarily responsible for triggering a cascade of events . . . (reactivating viral expression from latency).” An “SOS-like stress response could be a general inducer of the HIV LTR.” (4) The operative word being ‘could’. No evidence that it is.
    d. No specific AIDS gene or set of genes has ever been identified; proposed candidates not withstanding. The citing of “accessory” or “trans-activator” genes is not sufficient evidence since functional genomic analysis will produce the same result in all animal retroviruses, based on the well established property of retroviral cellular gene transduction. Show me where functional genomic analysis shows that other human retroviruses have these same “accessory” or “trans-activator” genes and I’ll seriously consider this argument.

    In reference 5 Duesberg et al present and explain the flat HIV incidence curve – the cause of much sound and fury (see deanesmay.com). As the best approximation of the CDC’s epidemiological guesses in conjunction with above arguments, Duesberg, Bialy et al have falsified AIDS sex and blood plague virus

    In reference 5 Duesberg confuses incidence and prevalence (a glaring error that Bialy didn’t notice until Nick Bennett pointed it out to him) and furthermore ignores the fact that CDC estimates of HIV prevalence are calculated based on the hypothesis that HIV causes AIDS. One cannot be inconsistent with the other as Bialy tried to insist, because especially in the early years, one was based on the other. Still is to some extent because while all states report AIDS cases, not all states report HIV infections.

  380. #380 Wilhelm Godschalk
    July 6, 2006

    Now *that* is hilarious! Francis Crick must be rolling over in his grave.

    I don’t think so. I’ve met Francis Crick in Cambridge, England, and he was not that kind of a guy. Although totally obsessed with DNA, as were his apostles ever since, he wasn’t so small-minded not to admit that RNA is a bitch to work with.
    So everybody who dabbles at RNA-viruses,will go to any length to link them up with DNA, because thst’s so much easier to work with. PCR and sequencing are automated now, so you need only one hand to do the assay. The other one holds the instruction manual.
    You’re better at discussing nitpicking bullshit than facing fundamental issues, Dale.

  381. #381 Hank Barnes
    July 6, 2006

    Not to add distraction to this informative, entertaining and unending thread, but…..

    There’s a good piece in LA Times about researching HIV+ folks who are completely healthy. Of course, the story misses the point that these folks eschew the toxic drugs, but, hey, glacial progress as they say:

  382. #382 Dale
    July 6, 2006

    Wilhelm, I’m not suggesting that he or anyone else who’s ever worked with RNA would not admit RNA is a bitch to work with. I’m suggesting that he would be unlikely to question the validity of reverse transcribing RNA to DNA in order to sequence it just because reverse transcriptase and PCR weren’t techniques used when he was a young graduate student. Which is what you appear to be doing.

  383. #383 Chris Noble
    July 6, 2006

    Gene you really don’t get it.
    There is a difference between functional homology and sequence similarity.

    All pol genes have functional homology to each other. That doesn’t mean they are identical or that they are all equally similar to each other.

    You previously cited this paper.

    Origin and evolution of retroelements based upon their reverse transcriptase sequences.

    Fig 3 shows a phylogenetic tree of retroviruses based on pol-RT. HIV is clearly on one branch together with SIV, FIV, EIAV, CAEV, visna and BIV.

    A probe consisting of 33 bps is very specific.

    Again if the “HIV sequences” were of endogenous origin then everybody would have “HIV DNA” in every cell in their body. They don’t. HIV is not endogenous.

    No matter how much you frantically wave your hands in the air it won’t change reality. HIV is not endogenous.

    I previously asked you to define want you meant by endogenous. You have not done so.

  384. #384 Chris Noble
    July 7, 2006

    Gene writes:

    Exogenous and endogenous retroviruses are isogenic, meaning canonical gag, pol and env genes are functionally homologous;

    There are three possibilities.
    1) You don’t understand the meaning of isogenic.
    2) You don’t understand the meaning of functional homology.
    3) You don’t understand either terms.

    In any case you are throwing around terms that you don’t understand.

  385. #385 truthmachine
    July 8, 2006

    Dear Tara, Chris, Dale, et. al.,

    Please stop wasting your time on these cretins and jackasses that you could instead spend on research or even just enjoying yourselves. Arguing on a blog with HIV/AIDS deniers is futile and neurotic. Let it go.

  386. #386 Chris Noble
    July 8, 2006

    Gene Semon wrote:

    No WILD mutations all over the place.” Here’s more back-up for Wilhelm: “(I)n vivo and in vitro estimates of the average error frequencies of viruses RNA replicases and reverse transcriptases also suggest misincorporation frequencies of the order of 10(exp-3) to 10(exp-5).” (Emerging Viruses, S. Morse, ed,(1993) Oxford University Press, pg 206 – John Holland)

    It is worthwhile looking at what these misincorporation frequencies mean.

    For an RNA virus with ~10000 base pairs the probability of the genome being replicated with 100% accuracy is given by (1-mf)^10000.

    For what is a typical value of mf = 10^-4 (see numbers for FMDV below) it equals (0.9999)^10000 = 0.368. In other words only 37% of the genomes replicated will be identical with the original. 73% will have one or more mutations. The majority of genomes will be “mutants”. If this is not “WILD mutation” then I don’t know what is.

    Both poliovirus and FMDV (two picornaviruses) operate close to the “error catastrophe” limit. In fact this has been proposed as an antiviral treatment in itself. Ribavarin is a mutagenic ribonucleoside. It is incorporated by viral RNA polymerases and greatly increases the mutation frequency. In cases like poliovirus and FMDV which are already operating close to the “error catastrophe” it can push these viruses over the edge and effectively reduce the amount of infectious virus.

    An Antiviral Mechanism Investigated with Ribavirin as an RNA Virus Mutagen for Foot-and-mouth Disease Virus

    Table 1 shows that for two genes the normal mutation frequencies were 0.7*10^-4 and 2.1*10^-4. This rose to 5.6*10^-4 and 22.5*10^-4 respectively with 1000 microM of ribavarin. This resulted in a loss in infectious virus of 99.7%

    Similar papers have demonstrated even more dramatic effects for poliovirus.

    At this point it might be a good opportunity for me to stop adding more words to this thread and find something more productive to do. I hope that I have demonstrated to most people that people like Wilhelm and Gene far from being “defenders of the scientific method” are actually profoundly antiscience. In their fervour to attack the science involving HIV and AIDS they are prepared to jettison all of modern virology.

    Wilhelm Godschalk would have people believe that thousands of scientists working in hundreds of labs around the world doing experimental research on poliovirus and FMDV are all incompetent idiots who should just take his personal word for it that RNA viruses don’t mutate.

    The truly sad thing is that Godschalk does get a few people to listen to him. These people are often HIV+ and have little training or understanding of science. The antiscience nonsense can be attractive to people who desperately want to deny that they are infected with a potentially fatal virus. Godschalk hands out medical advice to these people.

  387. #387 Gene Semon
    July 10, 2006

    Dale,

    A long and reasoned response, actually scientific and appreciated. As Harvey B would say, now we’re in the thick of it. Good. However, I have answered some of these in the previous posts and some points are addressed in Wilhelm’s.

    Only time for preliminary, right now, but will scrutinize details off-line.

    It was Howard Temin, who published on retroviral recombination every time the DNA is transcribed from RNA by the mechanism of template switching. This is one explanation for a continuous spectrum of genetic subtypes which begs the question which HIV are you talking about when you say, “The sequences of HIV pol are unique to HIV”.
    There are additional reasons for many (how many, do you know?) genetic subtypes.

    “And you’re going to tell me that Americans haven’t changed their sexual behaviour over the past 20 years in response to HIV/AIDS?” Certainly not, but what’s your point? Terror campaigns, in case you haven’t noticed, are extant. Are they all based on reality, or moves to take away our traditional liberties? And why would all those benvolent people in the Reagan administration want to end the sexual revolution by scamming the lefties, anyway?

    “… the ‘canonical genes may be functionally homologous but their DNA sequences are very different. The redundancy of the genetic code and all that.” Which is consistent with everything I’ve posted.

    “if HIV passes from one individual to another as a provirus or a cell free virus that is then somehow integrated into host immune cells where it replicates and then goes on to enter other host cells … as far as I can tell, that’s infection.” Big if there. If gp120 braks off right away, there goes your cell-free transmission. Otherwise, harmless passenger. And it doesn’t “replicate”.

    “An ‘SOS-like stress response could be a general inducer of the HIV LTR.’ (4) The operative word being ‘could’. No evidence that it is.” (4) is the evidence; have you done the comprehensive search to back up your bold conjecture? What about documented reverse transcriptase emergency DNA repair?

    Re protective response, you say, “The operative word here is ‘can’. It’s a rare event.” But what about all the papers on HIV and apoptosis? Isn’t that protective after the lymphocyte has done its job? And blocking a receptor that is used by a DNA virus? Protection? What about iRNA, who knows where that line of enquiry is going to lead? gp120 downregulation cannot be excluded as being an appropriate response at the right time in a lymphocyte/monocyte response.

    “Show me where functional genomic analysis shows that other human retroviruses have these same ‘accessory’ or ‘trans-activator’ genes and I’ll seriously consider this argument.” The point here, considering everything I’ve posted, is that functional cell-culture analysis is a model system for the more complex in vivo reactions. The “endogenous side” of the research is exploding and my prediction is that a “convergence” will occurr in the not-too-distant future. Of course, I stand by Duesberg as the leading authority on genomic analysis.

    “In reference 5 Duesberg confuses incidence and prevalence (a glaring error that Bialy didn’t notice until Nick Bennett pointed it out to him) and furthermore ignores the fact that CDC estimates of HIV prevalence are calculated based on the hypothesis that HIV causes AIDS. One cannot be inconsistent with the other as Bialy tried to insist, because especially in the early years, one was based on the other. Still is to some extent because while all states report AIDS cases, not all states report HIV infections.”

    And it wouldn’t be any fun if you didn’t commit another whopper. Prevalence is the only thing you can get from HIVAb measurements, assuming we can ignore the specificity problem. As I pointed out to Dr Bennett, there is no incidence- transmission DATA (based on measurements of primary HIV infection – full-length only thank you) only guesses. The flat curve model which DOES NOT track with Farr’s exponential is based on Duesberg’s expert judgement considering the CDC’s flat curves as reproduced at Dean Esmay.

  388. #388 Gene Semon
    July 10, 2006

    Chris says, “There is a difference between functional homology and sequence similarity.

    “All pol genes have functional homology to each other. That doesn’t mean they are identical or that they are all equally similar to each other.

    “In any case you are throwing around terms that you don’t understand.”

    Since I choose now to break the chain of “you don’t get its”, let’s go to the substance.

    See response to Dale. Look at my other posts. Yes, Chris, sequence and functional homolgy not the same thing, but HIV is not singular sequence. Get it? (Whoops, just broke my promise!)

    Chris also says, “For what is a typical value of mf = 10^-4 (see numbers for FMDV below) it equals (0.9999)^10000 = 0.368. In other words only 37% of the genomes replicated will be identical with the original. 73% will have one or more mutations. The majority of genomes will be ‘mutants’.”

    But you left out the nonsynonymous to synonymous ratio, (dN/dS) i.e. mutations that lead to an amino acid substitution (nonsynonymous) are more likely to be deleterious to the protein’s function than mutations that do not (synonymous). If dN/dS is much less than one, this would indicate genetic stability as a result of purifying selection.

    And, of course, you finish your post with some brilliant handwaving and ranting about antiscience. Yes, Chris, I’m part of the conspiracy to destroy science as we know it as any fool can see from my posts. My comments re confused scientists, as Dale says , are irrelevant. Of course.

  389. #389 Wilhelm Godschalk
    July 10, 2006

    “I’m suggesting that he would be unlikely to question the validity of reverse transcribing RNA to DNA in order to sequence it just because reverse transcriptase and PCR weren’t techniques used when he was a young graduate student.”

    He wouldn’t question it? When I met him, he was already the ultimate authority on DNA. Reverse transcription was still unknown, and merely suggesting its existence would have been regarded as swearing in church. It wouldn’t have entered my mind at the time. Let’s face it, Dale: I’m no Howard Temin.

  390. #390 Wilhelm Godschalk
    July 10, 2006

    “The truly sad thing is that Godschalk does get a few people to listen to him. These people are often HIV+ and have little training or understanding of science. The antiscience nonsense can be attractive to people who desperately want to deny that they are infected with a potentially fatal virus. Godschalk hands out medical advice to these people.”

    That’s exactly what’s intended. These people with little understanding of science have been brainwashed and browbeaten by the orthodoxy. I’m proud to be among those who are in a position to provide some counter-information, so they can make more informed decisions. These people are NOT infected by a potentially fatal virus. Telling them, in an official capacity, that they are is downright criminal.

    And I, of all people would be anti-science? Well, I can assure you that it’s mainly my love for science that drives me. The way science has been murdered for the past 25 years, by people who only have monetary motives, is a disgrace. And I hope to see the day when science is put back on track, from the medieval state it is in now.

    And then… comes the final sting, about giving medical advice. That’s how I know you, Chris, slimy as ever.
    First you tried to catch me as a fraud by checking with the University of Leiden, if I really got a Ph.D. there. That was confirmed of course.
    And now you’re trying to maneuver me in a position where I can be accused of practicing medicine without a license. Well, you can try, in your sneaky way, but that won’t work either. Go ahead! Let’s make a big stink about it. I can use the publicity, so I can reach more people who have been told they’ve been infected by a nasty virus. People whose lives are being destroyed, so that the pharma industry and a group of pharma flunkies can make a buck.

  391. #391 Chris Noble
    July 10, 2006

    Godschalk writes:

    First you tried to catch me as a fraud by checking with the University of Leiden, if I really got a Ph.D. there. That was confirmed of course.

    No. I personally did not doubt that you had obtained a Ph.D. from the University of Leiden. You made a claim that you currently had access to laboratories at the University of Leiden and could do experiments on HIV isolates. I emailed the relevant people (that you yourself provided as contacts) and I found that none of them had seen you for a quarter of a century. You have no access to these labs. You have no authorisation to do these experiments. You are not affiliated with any university. Like most of the claims you have made these are false.

  392. #392 Dan
    July 11, 2006

    The truly sad thing is that Godschalk does get a few people to listen to him. These people are often HIV+ and have little training or understanding of science. The antiscience nonsense can be attractive to people who desperately want to deny that they are infected with a potentially fatal virus. Godschalk hands out medical advice to these people.”

    Chris,
    you’re full of shit.

    Wilhelm doesn’t have any “followers”. And the people I know that enjoy his online company are all “HIV negative”.

    In all my years dealing with the “AIDS” paradigm,
    I’ve not met ANYBODY desperate to deny they’re infected with “HIV”. You live in a fantasy world, Chris. But it suits your purposes.

  393. #393 Chris Noble
    July 11, 2006

    Dan writes:

    Chris,
    you’re full of shit.

    Wilhelm doesn’t have any “followers”. And the people I know that enjoy his online company are all “HIV negative”.

    In all my years dealing with the “AIDS” paradigm,
    I’ve not met ANYBODY desperate to deny they’re infected with “HIV”. You live in a fantasy world, Chris. But it suits your purposes.

    I am afraid that you are the one living in a fantasy world.

    Godschalk proudly stated in the post above that it is exact intention to tell people that they are not infected with a potentially fatal virus ie. HIV. He has done this on many occasions. He has also told HIV+ people not to take ARVs.

    Here are Winstone Zulu’s words describing his own period of HIV Denial.

    I was already looking for a way out, something that meant I wasn’t inevitably going to die. So here were these people saying, ‘It’s all been this vast mistake. It’s not what causes Aids.’ Looking back, I think it was about wishing Aids away.

  394. #394 Dan
    July 11, 2006

    Good for you, Chris. You found one example of somebody desperate to “deny” their serostatus.

    In my own travels through “AIDS”-land for the past 24 years, I haven’t met anybody who fits this description.

    We don’t seem to agree on terminology. It looks as if anybody who reads a post of Wilhelm’s on the internet becomes a “follower”, by your standards.

    I don’t perceive Wilhelm as having “followers”. Some of us enjoy and appreciate his company online, but we’re adults, and all capable of independent thought.

    Mischaracterizing is certainly a helpful tool for you.

  395. #395 Dale
    July 11, 2006

    Gene writes And it wouldn’t be any fun if you didn’t commit another whopper. Prevalence is the only thing you can get from HIVAb measurements, assuming we can ignore the specificity problem. As I pointed out to Dr Bennett, there is no incidence- transmission DATA (based on measurements of primary HIV infection – full-length only thank you) only guesses. The flat curve model which DOES NOT track with Farr’s exponential is based on Duesberg’s expert judgement considering the CDC’s flat curves as reproduced at Dean Esmay.

    If you read what I wrote I didn’t mention HIV incidence, only prevalence. And if estimates of prevalence are based on limited sampling of HIVAb status then estimates of incidence are indeed as you say, only crude guesses. Farr’s “law” of epidemics was modeled on assumptions that don’t necessarily apply to HIV

  396. #396 Chris Noble
    July 12, 2006

    Dan writes:

    We don’t seem to agree on terminology. It looks as if anybody who reads a post of Wilhelm’s on the internet becomes a “follower”, by your standards.

    We don’t seem to agree on reality.

    The only person who has used the term “follower” to this point in the thread is you.

    I sincerely hope that nobody gives any credence to the totally unsupported opinions of Godschalk on HIV and AIDS.

    The credulity that you display makes me fear for the worst.

  397. #397 Gene Semon
    July 12, 2006

    Look at this response (7/11-6:08PM) from Dale. We appear to be “converging” on certain points, which to me is more convincing evidence that he actually is the person I’m guessing he is.

    Let’s revisit Dale’s “Duesberg’s point originally was that there didn’t seem to be enough HIV in the peripheral blood to account for the eventual depletion of CD4+ T-cells. The flaw in Duesberg’s argument was and is in assuming that there is only one model by which a virus can cause a disease. Ain’t so.”

    Once again Dale sheds a great light on the heart of the matter. I have argued that eventual depletion of CD4+ cells, which we now know resists overly simplistic characterizations plus complicated by possible functional redundancy (CD3+CD4-CD8- cells documented), is primarily an energy deficiency post-hypercortisolic-phase syndrome. It may also be the case, considering Polly Matzinger’s danger model, that T-cells in the blood can be produced on demand from the recognition of danger by the neuro-immunoregulatory network. So, perhaps low cell-count with no danger not a problem. Root-Bernstein, an HIV realist, has proposed a model of too many antigens overstimulating the network as a primary etiological factor in AIDS, with (category) HIV phenomena as the effect, not cause of this process (consistent with Duesberg).

    Dale aso says, “Show me the evidence that HIV sequences have been with humans since before the 1950s and I’ll take your argument more seriously. Yes there are retrovirus-like genes and retrovirus-like elements that are endogenous to human cells but there is no evidence that HIV is one of them and plenty of evidence that it isn’t.”

    Of course the Los Alamos gang claims to have done just that, dating the SIV to HIV transition back to 1931. I would be surprised if Dale is not familiar with this which raises the prospect of a debate between him and Brian Foley for which I would be happy to sell tickets.

    Here I will cheerfully concede that I am not in a position to judge phylogenetic reconstructions, but if someone like Lynn Margulis is skeptical, so am I. Mikkel H. Schierup and Jotun Hein have discussed the problem with not taking retroviral recombination properly into account, so that there may be many MRCAs and an innaccurate “molecular clock”. This indicates that horizontal transfer of retroviruses way back into primate evolution cannot be excluded, which brings us back to Peter Duesberg’s model. Mutualism would be established by millions of years of evolution, thus a flat HIV curve is best estimate.

    And, finally, Farr’s exponential was fitted to AIDS incidence by epidemiologists who passed JAMA’s peer review.

  398. #398 Dale
    July 12, 2006

    And, finally, Farr’s exponential was fitted to AIDS incidence by epidemiologists who passed JAMA’s peer review.

    Now you seem to be confusing incidence with prevalence. Even Duesberg saw AIDS incidence fitted to “Farr’s exponential”. It’s HIV prevalence (mislabeled HIV incidence) that his Figure in the 2003 J. Biosci. paper purports to show does not. HIV incidence estimates were and maybe even still are, very crude and aren’t the same thing as HIV prevalence.

  399. #399 Dan
    July 12, 2006

    “I sincerely hope that nobody gives any credence to the totally unsupported opinions of Godschalk on HIV and AIDS.
    The credulity that you display makes me fear for the worst.”

    I do enjoy it when you have these moments of honesty, Chris. Yes, I’m sure you fear for the worst, the worst being *your* absolute loss of credibility when your beloved paradigm comes crashing down.

  400. #400 Dale
    July 12, 2006

    Gene wrote Of course the Los Alamos gang claims to have done just that, dating the SIV to HIV transition back to 1931. I would be surprised if Dale is not familiar with this which raises the prospect of a debate between him and Brian Foley for which I would be happy to sell tickets.
    The Los Alamos gang ‘estimated’ the SIV to HIV transition back to 1931 plus or minus about 10 years based on certain assumptions about the molecular clock and based on extrapolation. Extrapolation is notoriously inaccurate compared to interpolation and in any case there is a huge difference between saying HIV first entered the human population in 1930 or 1940 or 1950 versus saying it’s been there for thousands or even hundreds of years.

    You want me to believe that ‘something’ causes AIDS and that subsequently AIDS patients develop ‘HIV’ seropositivity and ‘viral loads’ through reactivation of endogenous retroviral sequences. The problem with that argument as I keep trying to explain is that it doesn’t explain why that ‘something’ behaves like an infectious agent; why transfusion recipients and sexual partners of AIDS patients are at so much higher risk than the general population of developing AIDS.

  401. #401 Chris Noble
    July 12, 2006

    Dale writes:

    You want me to believe that ‘something’ causes AIDS and that subsequently AIDS patients develop ‘HIV’ seropositivity and ‘viral loads’ through reactivation of endogenous retroviral sequences.

    I have been trying to get a coherent explanation of this bizarre hypothesis for some time now.

    The Perth Group seem to believe that sperm, cigarette smoke and other “oxidising agents” all cause cancer. Somewhere around 1980 these same agents began causing AIDS. The theory offers no explanation or predictive ability as to why these agents cause cancer in some cases and why they cause AIDS in other cases. In the cases where these agents cause AIDS they also reshuffle the human genome to assemble DNA coding for proteins that just by chance happen to have more similarity to proteins in exogenous retroviruses such as SIV, EIAV, visna etc than to anything in the human genome. The reshuffling also seems to be somehow effected by the reshuffling that occurs in people that they have sexual relations with. Just by chance the “HIV” DNA in some people appears to be amazingly similar to the “HIV” DNA in people they have sex with. These proteins are then expressed leading to the presence of both RNA and antibodies in sera. The exact of mechanism of this amazingly non-random “reshuffling” has yet to be explained.

    Of course this “reshuffling” is much more belieavable than the existence of an exogenous retrovirus.

  402. #402 Gene Semon
    July 13, 2006

    Dale and Chris,

    The problem now is that (category) “AIDS incidence” is itself not singular and it would make more sense to separate out the individual epidemic and endemic curves. Is pneumonia the same disease as cancer simply because high risk groups have both. Don’t many cancer patients die from “complications”? And what’s the story on KS – the original signal disease of the CDC “task force” – at this point? Is KS the same as “HIV Disease”? And of course we have “idiopathic” CD4 cell depletion.

    Shuffling, stress proteins and the dynamics of the genome are infant sciences which at least require the accurate sorting of diseases and escape from the Bizarro Science of AIDS. (Category) HIV is not “infectious” in the classical epidemiological sense but retroviruses and LTR retrotransposons are capable of “horizontal” transmission between organisms; confusion back to Dale and Chris since the time of discovery of these phenomena do not equate to the time of “incidence”. The point of a flat curve is that it doesn’t match an exponential whether it is incidence or prevalence; surely, endemic means an equilibrium has been established.

    Harmless passengers, genetic taxicabs with reverse transcription function, (which, after all, go all the way bach to the RNA World) are very unlikely to CAUSE DISEASE, but more likely part of “evolution encoded”. Cell culturing INDICATES processes in vivo, not a predictor of “infectious replication”; correlation is most definitely not causation and the ontological rebuttalism of the Perth Group can hardly be a “straw man” when applied to those hypotheses where the conclusions are already assumed and there’s a constant struggle with new observations (since Margaret Heckler’s press conference), prevalent throughout the history, as documented so well and in such great detail by Peter Duesberg.

  403. #403 Dale
    July 13, 2006

    The point of a flat curve is that it doesn’t match an exponential whether it is incidence or prevalence; surely, endemic means an equilibrium has been established.

    The ‘point’ Gene is that the AIDS curve that Duesberg published in his J. Biosci. paper looked very much like the curve for a ‘classical microbiological induced epidemic’ that he published in the same paper.

    The ‘point’ Gene is that prevalence can be flat while incidence increases if deaths per year equal new cases per year.

    Of course the real reason the HIV prevalence curve published by Duesberg is flat is because the early estimates of HIV prevalence (calculated based on AIDS incidence and certain assumptions about time from infection to diagnosis) were very crude.

    But the real ‘point’ is that there is absolutely no evidence that HIV has been in the human population for a long period of time nor is there any evidence that HIV is harmless.

  404. #404 Dale
    July 13, 2006

    The point of a flat curve is that it doesn’t match an exponential whether it is incidence or prevalence; surely, endemic means an equilibrium has been established.

    The ‘point’ Gene is that the AIDS curve that Duesberg published in his J. Biosci. paper looked very much like the curve for a ‘classical microbiological induced epidemic’ that he published in the same paper.

    The ‘point’ Gene is that prevalence can be flat while incidence increases if deaths per year equal new cases per year.

    Of course the real reason the HIV prevalence curve published by Duesberg is flat is because the early estimates of HIV prevalence (calculated based on AIDS incidence and certain assumptions about time from infection to diagnosis) were very crude.

    But the real ‘point’ is that there is absolutely no evidence that HIV has been in the human population for a long period of time nor is there any evidence that HIV is harmless.

  405. #405 Gene Semon
    July 14, 2006

    Test comment. Last post wiped out.

  406. #406 Gene Semon
    July 14, 2006

    Dale, The point here is that disseminated KS, toxoplasmosis, PCP or candida fungal infections, lymphoma, lymphoid interstitial pneumonia, PML, etc. can cause “incidence” and death “increases if deaths per year equal new cases per year” without “laboratory tests for HIV”.

    Again, please read Huebner ref posted above for limitations of cross-sectional epidemiology when dealing with prevalent viruses.

    Gallo made a falsifiable claim that HTLViii was uniquely different from HTLVs i and ii, because it was capable of cell-free transmission. This, too, collapsed under the scrutiny of Duesberg and Perth Group. Elementary logic dicates that one cannot prove a negative, ie “harmless”.

    My previous posts are clear on (category)HIV as a special case of LTR retrotransposon/retrovirus horizontal transfer from animal to animal going back millions of years. If all this bores you or interferes with YOUR special perceptions, there’s nothing I can do.

  407. #407 Dale
    July 14, 2006

    Gene writes The point here is that disseminated KS, toxoplasmosis, PCP or candida fungal infections, lymphoma, lymphoid interstitial pneumonia, PML, etc. can cause “incidence” and death “increases if deaths per year equal new cases per year” without “laboratory tests for HIV”. In other words a flat line for prevalence along with a bell shape curve for incidence is consistant with an infectious epidemic. So you would appear to agree that AIDS (ignoring laboratory tests for HIV) behaved like an infectious epidemic according to Farr’s law and to Figure 1 in Duesberg’s J. Biosci. paper.
    You also appear to concede that HIV may be transmitted both laterally and longitudinally although you refuse to put the label ‘infectious’ on lateral transmission, even though I think one would be hardpressed to identify any biological agent that may be transmitted laterally that doesn’t fit the definition of ‘infectious’.

    Your arguments about the properties of ‘special cases’ of prevalent retroviruses would perhaps eliminate HIV as a cause of AIDS if you provided any evidence that HIV is a prevalent virus. Which I note, you don’t. Lots of references to how horizontally transmissible (i.e. infectious) retroviruses might behave but the sticking point here remains the lack of evidence that HIV has been ‘prevalent’ in any population for more than several decades. This would not be a difficult point to demonstrate if it were true. It wouldn’t require a lot of funds and it wouldn’t require any special permission from anyone to work with HIV. There is at least one large project out there to collect DNA samples from large numbers of individuals to study multifactorial genetic disorders. So why doesn’t one of the many dissident scientists look for HIV sequences in those individuals. As I have read more than once, even high school students can perform PCR reactions.

  408. #408 Gene Semon
    July 15, 2006

    Dale, here’s what I originally stated, “According to Farr and an important postulate of Koch as stated by Huebner, ‘In order that a virus be regarded as an established cause of a specific human illness, the following” condition is at least “necessary: constant association with specific illness. If the disease in question is a well-defined and recognizable entity, the agent should be constantly associated therewith. If tissues of the host are available at a suitable time during the course of the illness, the agent should be found in the diseased areas.”(3)’

    ‘3. Robert J Huebner, Criteria for etiologic association of prevalent viruses with prevalent diseases: the virologist’s dilemma, Annals New York Academy of Sciences, V67, 430, (1957)’

    Now, constant association means constant association so your argument doesn’t not pass muster by the standard of Huebner’s postulates (all NINE of them if you care to read the paper) and these are imbedded in the Duesberg, Rasnick, Koenlein, Bialy critiques of your very bad hypothesis.

    “doesn’t fit the definition of ‘infectious'”. Accurate renaming, of course, goes hand-in hand with rethinking, something you appear to be incapable of: (I really wish I didn’t have to say this, but you say I’m not providing evidence and I say you’re ignoring and evading substantive points which I’ve made. I don’t doubt your awareness of the vast number of papers on HIVs and HERVs, not to mention the primate stuff, which just doesn’t fit into this forum. As I originally stated (somewhere), all I’m providing is a seconding of the “dissidents” and a rough sketch, sighting shots towards a reframe of the vast amount of data on retrotransposons/retroviruses). Finally, is “acquiring genomes”, as covered by Lynn Margulis’ evolutionary theory, the same thing as “infectious” when discussed in the context of diseases?

    I understand your dilemma, Dale, if you really are a top dog within institutionalized science. Trust me, I’ve been there and know, first hand, what a Bizarro World it actually is. (I’m talking about the denialism practiced by our good friends in the chemical industry.)

    As far as you’re last paragraph, I’m with you. It should be obvious by now that I’m an advocate for pluralism and that the Hooper, Elswood, Stricker and Kyle model re the source of exogenous HIV/SIVs should be taken seriously and funded. (I believe in a “weak” Hooper principle.) You appear to be saying they have not been refuted by the Los Alamos gang. Take note that Howard Urnovitz has addressed this issue as well at his websites. Obviously, the flat curve is a simplification and sharp spikes from contaminated vaccines and blood transfusions cannot be excluded from causing “autoimmune” phenomena.

  409. #409 Gene Semon
    July 15, 2006

    Joshua Lederberg also has something to say on the meaning of “infectious”. (SS Morse-ed, Emerging Viruses, Oxford University Press, 1993, 3-9)

    EXCERPTS

    (T)he historiography of epidemic disease is one of the last refuges of the concept of SPECIAL CREATIONISM*, with SCANT ATTENTION* to dynamic change on the part of the agents of disease.

    (T)he very essence of the virus is its fundamental entanglement with the genetic and metabolic machinery of the host.

    The vertebrate immune system illustrates how the hypermutability of immunoglobulin genes is a trick relearned in evolution – and matched by the trypanosome’s versatility in varying its surface antigens.

    The eukaryotic cell is now recognized as a synmbiosis, those elements (chromosomal) very likely having been evolved from what were once free living microbes.

    At one time much polemical energy was spent arguing whether some of these entities were viruses, on the one hand, or cytogenes on the other, as if these were disjunctive concepts. The word plasmid was invented in 1952 to help moot a logically empty controversy … and was intended to apply as well to mitochondria and temperate viruses.

    END EXCERPTS *(emphasis added)

  410. #410 Gene Semon
    July 15, 2006

    And here’s the refutation of the falsifiable claim, repeated here, that defective or “mutated” HIVs can be pathogenic.

    Excerpted from David Rasnick, INHIBITORS OF HIV PROTEASE USELESS AGAINST AIDS BECAUSE HIV DOESN’T CAUSE AIDS Reapprasing AIDS August 1996
    http://www.virusmyth.net/aids/data/drinhibit.htm:

    No Mutation to Resistant Forms

    In 1994 I attended the Gordon Conference on Proteolytic Enzymes in New Hampshire where HIV protease inhibitor results were discussed. John Kay provided interesting information on the clinical trials of Roche’s HIV protease inhibitor Ro 31-8959. He made the astounding claim that Roche had synthesized 800 tons (that’s right: tons) of this compound. When given the opportunity to change his statement, he stuck to 800 tons. The clinical trail consisted of 400 AIDS patients receiving 2g of the Roche inhibitor per day. After 18 months there was not clinical difference between the group given the protease inhibitor and the controls. Kay announced that Roche was putting an information blackout on further reports on the HIV protease inhibitor clinical trials due to the disappointing results.

    The vogue explanation for the failure of the inhibitors to benefit AIDS patients is that HIV replicates so fast that it eventually develops mutant forms of protease that resist the inhibitors. Even to this day, however, no one has ever found a resistant HIV protease in any patient, even in patients that are claimed to have them! The only inhibitor-resistant HIV proteases anybody has ever examined are those produced in the lab using genetic engineering. Nevertheless, the mutation explanation, just like the HIV theory itself, was completely accepted–without question–as soon as it was proposed.

    The mutation theory is preposterous, but not just because its premise–that HIV replicates hyperactively–is false. The mutation theory is preposterous because it is illogical. Enzyme inhibitors work only because they are shaped like the substrates the enzymes act upon: when an inhibitor fits snugly into an enzyme’s active site, then the substrate cannot. This is now inhibitors keep an enzyme from performing its task, which in this case is to produce HIV. Imagine one of these resistant, lab-created HIV proteases. It resists inhibitors because its active site is shaped in such a way that inhibitors cannot fit inside. That’s great. But how in the world is the substrate going to fit? Remember, the inhibitor and the substrate have the same shape; they appear identical to the active site, the way a lock cannot tell the difference between a key and a copy of a key.

    Yet a representative from Vertex presented a poster showing that some of these lab-created mutants did indeed retain most of their ability to act upon particular substrates. But could such a mutant still produce virus?

    I reminded him that in order for an HIV protease to produce a new virus, it had to cleave eight different substrates, and pointed out that the ability to cut just one of those substrates did not represent the overall ability of the enzyme to produce HIV. Yet he was claiming that some of these resistant proteases were as much as 90% effective when compared to non-mutated protease. But these claims of high effectiveness were always for just one of the eight substrates. In every case, the effectiveness on the other substrates was absurdly low, numbers like 0.1%, or 0.01%, or even 0.001%. In order to calculate the total effectiveness of these mutant proteases, you must multiply together all eight percentages. And when you multiply even a very large percentage like 90% by a bunch of tiny percentages like 0.1%, what you end up with is essentially zero.

    In other words, these drug-resistant proteases were effectively non-functional. They could not produce viruses.

    At the discussion session the next day I argued that the Vertex data did no support the hypothesis that mutations of the HIV protease are responsible for the lack of clinical efficacy of the inhibitors: the drug-resistant proteases were just as inactive as if their active sites were plugged with inhibitors. Other explanations are called for.

    I went on to propose that the HIV protease inhibitors were performing as designed–blocking HIV production–without being undermined by the emergence of drug-resistant mutant strains. The reason that these drugs did not alleviate AIDS is that HIV is not the cause of AIDS.

    During private discussions, none of my colleagues found any flaws with my reasoning and even thought it was right. I left the meeting thinking that these fellows would continue the analysis where I left off. Well, that, of course, didn’t happen. The HIV protease mutation hypothesis has become more entrenched with time.

    None of the inhibitor-resistant mutant HIV proteases reported so far has come anywhere near the minimum level of overall activity necessary to produce relevant numbers of viable virus. It is extremely unlikely that mutations substantial enough to protect the protease against inhibition will at the same time leave virtually unimpaired its ability to produce viable viruses. The conclusion of my analysis is that inhibitor-resistant mutant HIV proteases are very unlikely to contribute to viral viability in vivo. Therefore, the failure of the HIV protease inhibitors to alter the progression of AIDS is not due to inhibitor-resistant mutations of this enzyme. *

  411. #411 DAle
    July 15, 2006

    None of the inhibitor-resistant mutant HIV proteases reported so far has come anywhere near the minimum level of overall activity necessary to produce relevant numbers of viable virus. It is extremely unlikely that mutations substantial enough to protect the protease against inhibition will at the same time leave virtually unimpaired its ability to produce viable viruses. The conclusion of my analysis is that inhibitor-resistant mutant HIV proteases are very unlikely to contribute to viral viability in vivo. Therefore, the failure of the HIV protease inhibitors to alter the progression of AIDS is not due to inhibitor-resistant mutations of this enzyme. * Gene -You seem to think that theoretical analysis trumps real life observation. Oh were it so simple! Once again … if your theory ‘proves’ that something that has been demonstrated to happen can’t BE happening … it’s time to modify your theory.

  412. #412 Chris Noble
    July 15, 2006

    No Mutation to Resistant Forms!

    And bumblebees can’t fly!

    When Rasnick wrote that in 1996 it was not supported by the evidence.

    To cite that article now in 2006 is just plain stupid.

    You can purcahse a series of HIV infectious molecular clones containing 12 different drug resistance mutations.

    You can then test these isolates for drug resistance.

    This of course beats a purely theoretical arguemnt from Rasnick that ultimately stems from his blind dogma that HIV cannot cause AIDS.

  413. #413 Charles
    July 17, 2006

    This is fabulous and important material on the molecular biology of HIV, but it tells us absolutely nothing about AIDS cases and the fact that there never has been – and never will be – an “AIDS epidemic” among heterosexuals and non-drug using Americans.

    This fact was accurately predicted 12 years ago, of course, in the definitive “Sex in America” survey by Robert Michael, et. al. (Little Brown, 1994).

    Since 1981, in California – the state where AIDS was born – there have been over 26,000 reported cases of “AIDS,” but only a microscopic 263 of them (around 10 per year) have been attributed to female heterosexual contacts.

    How does our resident sexpert Tara Smith explain this anomaly? Gird your loins for more of her testy, edgy, tsk-tsk name-calling and question-dodging.

    Evidently oblivious to her very own research findings, safe sex missionary Nancy Padian continues to proselytize about “safe sex” as the way to “fight AIDS” in Africa, as if Africans’ genitalia are somehow different from those of, say, westerners.

    My point is that people in San Francisco and all across California freely and widely engage in recreational heterosexual activities all the time and despite the STD numbers, the number of AIDS cases continues to plummet.

    This may be terrible news to priggish, prim folks in the cloistered midwestern world of Tara Smith, but that is what the AIDS numbers indicate. There should be rejoicing and partying at the good news about the plummeting number of AIDS cases in California or America, but among the AIDS-is-everywhere dogmatists one can only expect vituperation, growling, barking and clenching of teeth.

    The death of a paradigm is never a pretty sight.

  414. #414 Charles
    July 17, 2006

    I should have said in San Francisco (not California) since 1981 there have been over 26,000 cases of AIDS and only 263 have been attributed to heterosexual females. Sorry for that.

  415. #415 Dale
    July 17, 2006

    Charles,

    AIDS does not spread through indiscriminate sexual activity but through sexual activity between individuals who are discordant for HIV status. The majority of cases in SF are MSM, most of whom likely don’t have a lot of sex with females. In fact the number of AIDS cases among heterosexual non drug using males in SF is about 40% the number among heterosexual non drug using females.

  416. #416 mgr
    July 17, 2006

    Charles: care to source that?

    It looks to me like lying with geography.

    http://aidshotline.org/crm/asp/refer/statistics/stats_transmission.asp

    I prefer internal comparisons–

    SF AIDS transmission heterosexual/homosexual –323/19,522

    Cal AIDS transmission heterosexual/homosexual–7,420/92,335

    Cal w/o SF AIDS heterosexual/homosexual 7,097/ 72,813

    This of course does not indicate a trend within these numbers, but the difference is a little disparate (like two orders of magnitude) between the two values. I would suspect that the ratio for California has increased over time–that the reports of heterosexual transmission has increased while homosexual has decreased (simply because the population of homosexuals is smaller and potentially played out with the initial infection).

    Only a prude or a fool would extrapolate the experience of city with a large population of homosexuals to larger demographic trends elsewhere where the bias gets swamped.

    Mike

  417. #417 Gene Semon
    July 18, 2006

    Dale says, “Gene -You seem to think that theoretical analysis trumps real life observation. Oh were it so simple! Once again … if your theory ‘proves’ that something that has been demonstrated to happen can’t BE happening … it’s time to modify your theory.”

    And Chris chimes in, “No Mutation to Resistant Forms!

    “And bumblebees can’t fly!

    “When Rasnick wrote that in 1996 it was not supported by the evidence.

    “To cite that article now in 2006 is just plain stupid.

    “You can purcahse a series of HIV infectious molecular clones containing 12 different drug resistance mutations.

    “You can then test these isolates for drug resistance.

    “This of course beats a purely theoretical arguemnt from Rasnick that ultimately stems from his blind dogma that HIV cannot cause AIDS.”

    So the experiment worked and I obtained the predictable responses from the learned gentlemen I’ve been debating. Once again, I have to congratulate Dale for getting to the heart of the matter.

    Your incremental inductivism is nothing more than a disguised faith. Clones are genetic engineering; your “real life observation” does not meet Huebner’s postulate “(2) Origin of virus: The virus must originate in the human specimens under study and must be shown by repeated isolation to be present therin and not in the experimental animals, CELLS OR MEDIA* employed to grow it”. (*emphasis added) Note also stated virus is singular,like Gallo’s original HTLViii, not plural like HIVs stated in arguments previous. Nothing more than indirect, unvalidated non-specific measurements and fragments of measurement support your hypothesis. The measurement problem of many, many HERVs and many, many possible HIVs, like getting to moving targets to hit each other, is certainly not going to be resolved by high school students deploying PCR. I stand by evidence presented and theorizing from same plus data in the literature.

  418. #418 mgr
    July 18, 2006

    GS–

    regarding those clones

    “A panel of 12 prototypical infectious multidrug resistant HIV-1 reverse transcriptase (RT) clones. The panel includes clones with each of the published nucleoside analog RT mutations in the combinations that occur most frequently in HIV-infected individuals. 1.0 ml of glycerol stock.”

    Engineered or whatever, the clones appear to be of human stock or media in origin, so that it appears that somewhere, sometime, Hueber’s Postulate was fulfilled.

    Mike

  419. #419 Gene Semon
    July 18, 2006

    “Engineered or whatever, the clones appear to be of human stock or media in origin, so that it appears that somewhere, sometime, Hueber’s Postulate was fulfilled.”

    But Mike, this is precisely the point at hand, what kind of human cells are we talking about? How were the clones derived from “the combinations that occur most frequently” i.e. manufactured? The description you quote is consistent with the interpretations of my previous posts, which are intended to be of a piece, and “somewhere, sometime” hardly seems satisfactory.

  420. #420 dale
    July 18, 2006

    uses are drug-resistant

  421. #421 Chris Noble
    July 18, 2006

    Gene, you are really going to utterly incredible lengths to avoid admitting you are wrong.

    All of the RT mutations were found experimentally in HIV isolated from people taking NRTIs.

    The DNA coding for RT was extracted and amplified from these isolates and then inserted into an infectious molecular clone – pNL4-3. These molecular clones are isogenic (in the correct use of the word) with pNL4-3 apart from the different RT mutations.

    You can waffle and obfuscate as much as you want. These NRTI resistant HIV mutants exist. To deny this is just plain stupid. There is no polite way of saying this.

  422. #422 Senor Liam
    July 18, 2006

    Yo Noble.

    It’s great stuff. It really is. Really.

    It is, of course, wildly and criminally irrelevent wherever AIDS is diagnosed, in the sewers of Uganda, for example, or still-essentially apartheided Soweto,

  423. #423 LS
    July 18, 2006

    Oh, there’s more, but this blog software won’t let me post more than 8 words at once.

  424. #424 senor liam
    July 18, 2006

    We’ll pick it up another time. My comments were to competition in the field. See you then. Blogverboten, apparently.

  425. #425 Corn-Catt
    July 18, 2006

    You can waffle and obfuscate as much as you want. These NRTI resistant HIV mutants exist. To deny this is just plain stupid. There is no polite way of saying this.

    That’s just super, Chris.

    You’re performing your job well, Mr. Chris. Keeping all attention focused on laboratory minutiae, to divert attention away from the 800-pound gorilla of a failed paradigm.

  426. #426 Chris Noble
    July 18, 2006

    Corn-Catt writes:

    You’re performing your job well, Mr. Chris. Keeping all attention focused on laboratory minutiae, to divert attention away from the 800-pound gorilla of a failed paradigm.

    Gene recycled a specific argument about the alleged impossibility of NRTI resistant HIV mutations.

    This argument keeps on popping up time after time since Rasnick first put it forward despite being whacked again and again.

    In typical “rethinker” fashion Rasnick’s argument which was once an “800 pound gorilla” is now just “laboratory minutiae” after it has been demonstrated to be false.

    Meanwhile, Rasnick and Gene will never admit to being wrong and after a few months somebody will recycle exactly the same argument again.

    Anyone for another round of whack-a-mole?

  427. #427 Dale
    July 19, 2006

    Gene, the ‘clones’ aren’t the real life observation; the patients are. The ‘clones’ that are engineered based on sequences obtained from the patients and are shown in the laboratory to be drug resistant provide an explanation of why some patients fail to respond to particular antiretrovirals.

  428. #428 mgr
    July 19, 2006

    GS–Dude, it’s time you asserted an alternative that makes sense. Pouring forth logical scepticism when the scientific standard is skeptical pragmatism is easy, and certainly helps to confuse the uninformed observer.

    Seems to me that you have no experience with microbiology or virology based upon your comments–otherwise you would realize that Huebner is no more the QA/QC methods a lab follows to guarantee the organism isolated is obtained from the subject rather that via lab contamination of the media or cell line.

    To question the QA/QC in the instance of AIDS is to question the QA/QC universally applied to all infectious virus–do you really intend to question the measles, mumps, rubella, and polio paradigm? I’d really like to hear your alternative explanation for measles since I am a survivor of encephalis brought on by a failure to vaccinate for measles (yes, I am aware it’s anecdotal evidence). I will bet you that with logical scepticism (not scientific) I could show that it’s QA/QC did not strictly fulfill Huebner either. The pragmatic point is “So what!, apparently it works.”

    I think the results of experiments showing any alternative explanation to the infectious disease model for AIDS are in–if you consider parents allowing an HIV+ child to not recieve the current medical standard of care, and provide the postulated alternative treatments, and the outcome is that the child dies an experiment. These alternative explanations do not offer any pragmatic reduction or cessation of suffering nor prolongation of life.

    The hypothesis–HIV, a retro virus causes the disease AIDS, has been confirmed as holding to the model of infectious disease causation as understood by Koch. It’s transmission from one human to another includes sexual contact. Get over it.

    Mike
    Mike

  429. #429 ls
    July 19, 2006

    The hypothesis–HIV, a retro virus causes the disease AIDS, has been confirmed as holding to the model of infectious disease causation as understood by Koch. It’s transmission from one human to another includes sexual contact. Get over it.”

    Beautiful assertion. All evidence to the contrary. And absolutely irrelevent in the lives of people you stick with the brand/diagnosis.

    So, Get over it.

    Live with the differences, there are at least two schools of thought on this issue, and there’s room for both, Horatio.

    Competition! Get used to it, dummy. It’s the American way, after all.

  430. #430 mgr
    July 19, 2006

    ls–where to start–I have not seen one shred of evidence from your word processor the entire time I have been lurking that this ‘assertion’ is inaccurate (I believe that it would be a conclusion following from my arguments above, but addressing syllogisms with one’s whose stock in trade is ad hominen, would be to go over your head).

    C’mom show me how I am wrong.

    Mike

  431. #431 Chris Noble
    July 20, 2006

    I’ll correct myself.

    Rasnick’s article was about resistance to protease inhibitors.

    The link I gave was for infectious molecular clones of HIV with NRTI resistance.

    However, you can also order both molecular clones and virus with resistance to protease inhibitors from http://www.aidsreagent.org/

    You can also find many papers on protease inhibitor resistant HIV found experimentally in HIV infected people in pubmed

  432. #432 Gene Semon
    July 20, 2006

    Chris says, “All of the RT mutations were found experimentally in HIV isolated from people taking NRTIs.”

    “(F)ound experimentally” is your new magic word but, unfortunately, does not exclude artifacts. “(I)solated” is not directly from fresh tissues or patients blood which all of your rhetorical handwaving and smokescreening will never cover up. Surely, by now, we can agree that demonstration of reverse transcription is not “isolation” of a UNIQUE disease agent. What is there to “admit” on my part? That I can be snowed by you guys like all too many others have been?

    “Anyone for another round of whack-a-mole?”

    Meaning you guys will never stop assuming your conclusions? You can say “whack” and “recycle” all you want but it is you, my friend Chris, backing an unproven hypothesis.

    And Mike, I can say that your post is well-written and your substantive point is you want me to get over something. But what is throwing QA/QC at me supposed to prove. I will cheerfully concede that I don’t know most of the fine details in this vast set of techniques. But let me assure you that I know engineering when I see it and a lot of allegedly intelligent people have been scammed into believing it’s discovery.

    “The pragmatic point is ‘So what!, apparently it works.'”

    As in the vaccination they came up with just like “measles”, “polio”, etc. BTW, Huebner has 2 epidemiolgical postulates (7)a. and b. and all are specifically for viruses. A workable vaccine is postulate (8)”Prevention by specific vaccination”.

    And finally Dale, normally on the precise side says “uses are drug-resistant” meaning users or an agreement with me?

    “The ‘clones’ that are engineered based on sequences obtained from the patients and are shown in the laboratory to be drug resistant provide an explanation of why some patients fail to respond to particular antiretrovirals.”

    I actually find this persuasive, Dale, but the question always remains, how good a model for in vivo is in vitro (too many steps from the actual phenomena – which is Rasnick’s point) and, of course, there’s Hellerstein’s 2 reasons for why HAART works without an anti-RV effect. I think they don’t respond because their HIV is not the cause of their illness.

  433. #433 Dale
    July 21, 2006

    Gene asks “how good a model for in vivo is in vitro?”

    Well Gene, many people, including myself, would consider an in vitro model (in this case the drug resistance of the viruses that were engineered based on sequences obtained from patients) that predicts the in vivo system that it is modeling (i.e. the response of the patients to particular combinations of antiretroviral drugs); an in vitro model system that does that is pretty damn good! Because at least in many cases, it’s not that those patients don’t respond to ANY retrovirals but that they don’t respond to the ones that the laboratory experiments with the viruses predict they won’t respond to.

  434. #434 Gene Semon
    July 24, 2006

    Dale, your response, as usual, has provoked a few reflections of the “if only it were so variety.”

    As always, I appreciate your reasonable answer. We are not going to resolve in this forum the risk-benefit issues which are at the heart of this particular stage in our debate, but let’s not kid ourselves, this Pandora’s box has been opened in related areas such as cancer drugs and the original treatments for PCP/KS patients who were treated with sulfonamides. The first problem with in vitro modeling, which claims both “specific” and “side” effects is that in vivo, there are only effects. The second, I don’t see a complete response to Rasnick’s point which is backed up by “HIV experimental findings” of the past several years, i.e. hypermutation during transcription which is a death sentence not an escape route. I can source these if you want.

    The next issue involves competing models of the immune system. Is a CD4 count below 300, with no other symptoms, a surrogate for imminent immune collapse? And what about the lack of correlation with pol RNA in the blood, as mentioned above in the branched DNA paper? It’s you who’ve conceded that the original basis for HAART has been falsified.

    And since you place a great value on the conclusions of experimentalists, let’s introduce Dr. Gerald B. Dermer on “why cancer research fails(:) The (human tumor) cell lines loss of differentiation is reversed when they are returned to the in vivo environment … It appears that the stability of chromosomes within cells is dependent on the acquisition by the cell’s cytoplasm of a degree of differentiation that is only possible in living animals. These findings suggest that the ultimate control over both differentiation and chromosomal stability within a cell resides in signals coming from other cells in the body. Some of these signals are chemical, others are electrical, and still others are mechanical. They are received first by the cell membrane, are modified in the cytoplasm, and finally are sent to the nucleus in the form of regulatory proteins.” (The Immortal Cell, 1994, Avery Publishing Group) It should be clear, at this point, that chromosomal stability has everything to do with reverse transcription phenomena

    And, once again, Robert Huebner (in collaboration with George Todaro, perhaps the “discoverers” of human retroviruses when you throw in Howard Temin), who were discussing what they called virogenes, now referred to as endogenous retroviruses: “In cell culture, at least two factors are involved in the control of virus production. One is the probability of induction of virus information from an individual cell. This we presume depends on the ‘strength’ of the repressor. A cell susceptible to iduction would be one with a low level of repressor activity. Various agents we now know can overcome the repressor activity and result in the production of type-C viruses (retroviruses)*. Whether the culture (or the animal) is at risk as a result of virus induction depends on a second determinant, the ability of the induced virus to infect neighboring cells and spread like a conventional virus.” *(parens added)

    END OF PART ONE

  435. #435 Gene Semon
    July 24, 2006

    PART TWO

    Picking it up with Huebner and Todaro, “Highly susceptible mice, like the AKR and C58 strains (leukemic DBA/2 strain was used by E deHarven for the republished EM’s – Continuum Winter 1997)*, have cells that are unusually susceptible to infectious expressions of ‘induced’ endogenous virus. Within these animals, once enough virus has developed, it could spread horizontally to adjacent uninduced cells. Strains with low incidence of leukemia, like BALB/c and random bred Swiss mice, even if they have natural expression of infectious virus, may not be susceptible to spread of infection by the virus induced from a few of their cells to other cells in the body.
    “Eventually, with time, mouse leukemia viruses (retroviruses)* have developed by EXPERIMENTAL MANIPULATION** that are capable of growing in cells of most mouse strains; these established viruses very likely have been selected for the following properties: their ability to INTERACT WITH SPECIFIC CELL RECEPTORS, HIGH LEVELS OF REVERSE TRANSCRIPTASE, and INSENSITIVITY TO CELLULAR CONTROL** systems. Whether the postulated repressor is in the virion itself is not known. The reverse transcriptase may have been important at some point in evolution for the maintenance of the infectious virus, but may well now have little role in the perpetuation of the virus information in noninbred species under natural conditions.” (Huebner and Todaro, PNAS, V69, N4, 1009-1015) *parens added, **emphasis added

    Several comments are suggested by the Huebner/Todaro analysis. If humans are “highly susceptible” to wild type HIV strains (perhaps it’s this combination that doesn’t exist), than a direct ex vivo measurement, with an EM of purified particles following deHarven’s protocols (http://www.virusmyth.net/aids/news/edhlettercont.htm), should be obtainable. Also, HIV cell culturing and current technology DOES PROVIDE VALUABLE INFORMATION, we now know there are many “repressors” and “levels” of “repressor activity” associated with retroviral transcriptions, which appear to me as the place where the “in vitro model system” is “pretty damn good”.

    As far as “predicting the in vivo system that it is modeling” for chemotherapies, in addition to the problem of reducing the collapse of “cell mediated immunity” to CD4 cell depletion, we have a 3-steps removed problem: (1) the “immortal cell line”, per Dermer; (2) the stimulation of the cell-culture; and (3) indirect measurements applied to the cells and supernatants; all discussed in exquisite, (some might say excrutiating) detail by our good friends from Australia.

    END OF PART TWO

  436. #436 Dale
    July 25, 2006

    Gene, the issue isn’t whether or not harmless but infectious microorganisms exist but how to distinguish a harmless microorganism from a harmful one. The former will be present in healthy and disease populations are roughly equivalent frequencies and will not be predictive of present or future disease. HIV fulfills neither of these conditions; being present in >99% of individuals who suffer from a form of progressive immunosuppression characterized by loss of a particular class of T cells and <1% of the general American population. >90% of those who are HIV infected develop this progressive immunosuppression while progressive loss of CD4+ T cells among those who aren’t HIV infected is very rare.

    Similarly, the question isn’t whether or not in vitro model systems always predict the behaviour of in vivo systems (they don’t) but what it means when an in vitro system does predict the behaviour of an in vivo system (as the presence of drug resistant HIV viruses in patients predicts the response of the patient to some antiretrovirals and not to others).

  437. #437 Wilhelm Godschalk
    July 27, 2006

    “Gene, the issue isn’t whether or not harmless but infectious
    microorganisms exist but how to distinguish a harmless microorganism
    from a harmful one.”

    You may be right about that, Dale. But let me ask you a fundamental
    question: What is the etiology of bacterial diseases? By what
    mechanism do they cause disease? In the case of Clostridium botulinum I
    have a pretty good idea, because these bacteria excrete a powerful
    toxin. And chemical damage is usually eay to pinpoint. But what about
    other types of bacteria?

    “HIV fulfills neither of these conditions; being present in >99% of
    individuals who suffer from a form of progressive immunosuppression
    characterized by loss of a particular class of T cells and 90% of those
    who are HIV infected develop this progressive immunosuppression while
    progressive loss of CD4+ T cells among those who aren’t HIV infected is
    very rare.”

    I object strongly to inclusion of “HIV” or any virus in the category
    “micro-organisms” A virus is not a micro-organism, or any kind of
    organism. But let’s look at the point you stress:
    You say that HIV occurs in 99% (!) of individuals suffering from
    progressive immunosuppression. Well, I don’t believe Gallo found a
    percentage that high, but even so, 99% or even higher, of these same
    individuals had E. coli and other bacteria as part of their intestinal
    flora. Plus some ever-present enteroviruses. Does that mean that any
    of these caused the progressive immunosuppression? That’s an
    ass-backward way of doing statistics, and you’re way too smart not to
    know that.

  438. #438 Dale
    July 27, 2006

    Wilhelm, what makes

    p(HIV) in AIDS population = > 99%

    p(AIDS) in HIV infected population =>90%

    statistically and biologically significant is THIS :

    p(HIV) in general population = <1%

    p(AIDS) in general population = <1%

  439. #439 Gene Semon
    July 27, 2006

    Dale,

    My preliminary response to this refers to the argument summed from my previous postings that we have very incomplete data on the endemic HTLV’s, (yes, new sub-taxons are necessary), but the most educated guesses; i.e. one million prevalence flat curve still CDC-current for human exogenous retrovirus means “not predictive” of the AIDS Farr-Brownlee curve. As in SIV(agm), the flat curve goes further back, my guess would be a gradual increase to present flatness at the beginning of the Industrial Revolution.

  440. #440 Wilhelm Godschalk
    July 27, 2006

    Wilhelm, what makes
    p(HIV) in AIDS population = > 99%
    p(AIDS) in HIV infected population =>90%

    I wouldn’t know, Dale. Probably the same as:

    p(having a nose) in total mortality = > 99%
    p(people who die) in total population with a nose = > 99%

    Do you get my drift?

  441. #441 Dale
    July 27, 2006

    Wilhelm,

    That didn’t work too well, did it. My previous post was supposed to read:

    Wilhelm, what makes
    p(HIV) in AIDS population = > 99%
    p(AIDS) in HIV infected population =>90%
    statistically and biologically significant is THIS :
    p(HIV) in general population = <1%
    p(AIDS) in general population = <1%

  442. #442 Dale
    July 27, 2006

    And once again it refused to post correctly. The point was that the probability of HIV or AIDS in the general population is less than 1% in the USA. And it is those probabilities compared with the probability of HIV in the AIDS population or the probability of developing AIDS in the HIV infected population (both of which are greater than 90%) that makes the correlation significant.

  443. #443 Dale
    July 27, 2006

    Gene,
    Once again – there is NO evidence that HIV was present in ANY human population much before the 1950s.

    As far as that ‘flat line’ prevalence curve that Duesberg published – there are so many reasons why using that curve to argue that HIV is not infectious are flawed it’s hard to know where to begin.

    So in no particular order of importance:
    1. The early CDC estimates of HIV prevallence were based on very limited data and when published included huge error bars that Duesberg completely ignored. The HIV prevalence estimates I’ve seen for 1986 were something like between 500,000 and 1,000,000. With those kind of error bars and only 5 data points, you could draw any kind of line you want through the data – straight, exponetential, loop-de-loop.

    2. In smaller populations in which HIV prevallence was measured rather than estimated, increases in prevalence between the mid to late 80s up until ~ 1992 have been seen. (in study of Johns Hopkins ER for example prevalence almost doubled between 1988 and 1992)

    3. Since approx. 2000, HIV prevallence has been increasing because HIV infected individuals are living longer so even the CDC estimates no longer give a ‘flat line’ prevalence curve.

    4. Even if that ‘flat line’ prevalence curve had been a relatively accurate measure of HIV prevalence in the USA between 1985 and 2000 – at some point in any epidemic, prevalence may be relatively constant because new cases are offset by deaths (look at the CDC statistics for mid 80s to mid 90s). So you can’t take 4 or 5 data points collected over a 15 year period and attempt to extrapolate back several hundred years to argue HIV has been in human populations since the Industrial Revolution.

  444. #444 Chris Noble
    July 30, 2006

    If I can just emphasise some of the points that Dale makes about the “flat” graph.

    The data for the 1985 point that Duesberg magically rounds off to 1 million is Curran et al, Science 229:2720(1985), 1352-1357

    The estimate (that is quite clearly an estimate) is based on extrapolation from 6875 members of the San Francisco CDC cohort.

    In this cohort the seropositivity was found to have increased from 4% in 1978 to 68% in 1984. This is hardly indicative of stable prevalence.

    More importantly this rise in HIV infection precedes a rise in AIDS cases. When individuals are followed those who are infected with HIV (>90%) develop AIDS (before AZT was prescribed) and those who are not infected HIV do not develop AIDS.

    This is true in every single subgroup where detailed information is available. HIV infection precedes AIDS. Those infected with HIV develop AIDS (even when defined purely upon clinical criteria independent of HIV serology) and those who are not infected with HIV do not develop AIDS.

    Just to emphasise again: we have very good data on specific subgroups such as the San Francisco cohort with blood samples going back to 1978. This cohort has also been followed to see what happens to those that are infected with HIV and those that are not. This data supports with overwhelming certainty that a) HIV was extremely rare or not-present in the US before the 1970s b) HIV precedes AIDS in time and place c) HIV causes AIDS.

    It is beyond comprehension that Duesberg can ignore this data and claim that the magic 1 million prevalence figure for HIV can be extrapolated back 200 years. We simply do not have good estimates of HIV prevalence for the last 30 years.

    The early estimates were based on testing on specific subgroups such as homosexual men and drug users. The extrapolation to the total population has large uncertainties. Even current estimates have uncerntainties of more than +/- 10% and include a sizeable number of people that do not know they are infected with HIV. These people have obviously not been tested despite the picture Duesberg attempts to paint.

    Bizarrely, Duesberg accepts the extrapolations and estimates but ignores the more detailed and comprehensive data on subgroups like the San Francisco cohort where individuals have been followed over time even when the estimates are in fact derived from this very data. No it is not just bizarre and beyond comprehension it borders on criminal. At some point Duesberg must know he is being “economical” with the truth. However, I should never underestimate the ability of people to delude themselves.

  445. #445 Gene semon
    July 31, 2006

    I never said that the flat curve was anything else but an approximation. Subgroup seropositivity measurements are not the same as population-wide transmission-incidence data which doesn’t exist. So how can there be error bars?

    Delusions back to HIV?AIDS glorified polling.

  446. #446 Gene Semon
    July 31, 2006

    Dale, as far as where to begin with flat and exponential model comparisons, unfortunately, there is nothing better than guesses from the CDC or the inadequate extrapolations from subgroups as cited by Chris. The CDC’s current “HIV prevalence”, according to recent New Scientist piece, is still one million.

    According to textbook: When x = agent and y = disease, the statistical link between x and y in an epidemiological study is described in terms of the euphemism “associated”, as in x is “associated” with y. Only if there exists multiple epidemiological studies involving the SAME or SIMILAR x’s in which SIMILAR or CONSISTENT y’s are observed, would it be reasonable to infer the existence of a causal relation. Clearly CDC SURVEILLANCE definitions (JAMA, 1987) violate the similarity principle as detailed by Duesberg. What happens, for example when you separate out KS and amyl nitrite usage curves? Presto, an association is revealed.

    Comparing the flat and exponential curves is a shorthand approximation saying that specific sameness and association of agent and disease is not proven in the case of HIV?AIDS (really, it’s all circular); i.e. it is necessary to demonstrate specific disease agent producing a specific disease in a specific population exposed to a specific situation.

    Reducing complex phenomena like “cell mediated immunity” to a single surrogate marker or (category) HIV to a single agent is a trick, not a proof. HIV?AIDS are fake singulars.

  447. #447 Chris Noble
    July 31, 2006

    Gene writes:

    I never said that the flat curve was anything else but an approximation. Subgroup seropositivity measurements are not the same as population-wide transmission-incidence data which doesn’t exist. So how can there be error bars?

    There are or should be error bars on the estimates of HIV prevalence in the US that Duesberg/Rasnick/Bialy plot in the “flat” graph. DRB do not put error bars on the graph and make outrageous claims about being able to extrapolate back 200 years. They deliberately create the impression that the “orthodoxy” support their errorbarless graph. This together with mislabelling the graph “incidence” displays such an ignorance of epidemiology and mathematics that should raise at least a flicker of doubt in the minds of readers.

    While we do not have accurate data on prevalence and incidence of HIV in the US population for the past 30 years we do have accurate data for subgroups like the SFCCC. In fact the data point for 1985 in the DRB “flat” graph comes is based on the SFCCC. Why do DRB focus on population estimates and ignore the detailed data on which the estimates are based?

    In the SFCCC we have records going back to 1978 showing not only who was HIV positive but also fairly accurately when they seroconverted. This shows a non-flat rapidly increasing pervalence that precedes a rapidly increasing incidence of AIDS and death. Following this cohort over time shows that 10-15 years after seroconversion over 90% had either died from AIDS, been clinically diagnosed with AIDS or had CD4+ counts less than 200. By comparison those not HIV positive did not progress to AIDS.

    Duesberg, Rasnick, and Bialy ignore this evidence apparently deliberately. It blows there claims out of the water. Incredibly they still accept the estimate of HIV prevalence in 1985 that was based on this data. How can anyone still be regarded as honest?

    Anyone with a glimmer of curiosity would also read the CDC reports that DRB use for the “flat” graph. In each of these reports the majority of the HIV prevalence is constrained to risk groups such as homosexual men and drug users. This is incompatible with Duesberg’s thesis that HIV is predominantly passed on from mother to child. It is completely illogical to simultaneously accept the CDC estimates of approximately 1 million (of which the majority are male) and claim that HIV is predominantly passed on from mother to child and that the prevalence of approximately 1 million can be extrapolated back 200 years.

    Can any “rethinker” explain that? For instance look at one of the data points in the DRB “flat” graph.

    http://www.cdc.gov/mmwr/preview/mmwrhtml/00014715.htm

    Estimates of HIV prevalence in the general population (from blood donors and military recruits) is approximately 0.043% this translates to a US nationwide figure of 64,000 which most mathematically able people would recognise as not being equal to 1 million. The estimate of 1 million specifically includes a non-random distribution of HIV with higher prevalences of around 10-70% in specific risk groups such as homosexual men and IVDUs. This is simply not compatible with Duesberg’s thesis that HIV is predominantly spread by mother to child transmission.

    Anyone with a femtogram of skepticism would see the breathtaking inconsistencies in the arguments put forward by “rethinkers” such as Duesberg, Rasnick and Bialy. This does not appear to include you.

    The very references that DRB give completely contradict their own argument. This is why virtually 100% of scientists ignore them.

  448. #448 Dale
    July 31, 2006

    Gene writes Subgroup seropositivity measurements are not the same as population-wide transmission-incidence data which doesn’t exist. So how can there be error bars?

    So if the flat line prevalence graph that you claim supports your ‘theory’ that HIV is an endogenous retrovirus is really nothing more than an ‘approximation’ based on data that you claim doesn’t exist … doesn’t that make support for your theory pretty flimsy?

  449. #449 Gene Semon
    August 2, 2006

    Okay, fine, Chris and Dale, everything you say is all well and good, putting your best case forward so to speak.

    Of course, the “real curve” is more likely a sharply-spiked sawtooth with a flatness approximation. You guys can huff and puff all you want about mathematical precision and a presumed necessity for me to prove “my theory” (if only it really WAS mine), but these are not relevant to the issues at hand.

    Ignoring the specificity problem of retrospective HIVAb seroprevalence measurements in subgroups like SFCCC, MTCT (yes, Duesberg did claim more “efficient” transmission as far as the general population goes), blood transfusions and vaccinations; these could all be sharp spikes of incidence-transmission and the closest thing we have to “data”. But let me submit, once again, the comments of DJ Bregman and AD Langmuir, which passed JAMA’s peer review and apply even more in trying to determine if such a thing as an exponential “HIV incidence” can actually be measured, “We have made no effort to calculate confidence limits for these projections. We humbly submit that we do NOT KNOW HOW TO ACCOUNT* for the error due to biases in the reporting system. Furthermore, we believe it would be futile and meaningless to place a 95% confidence interval based on random error about the projections that extend out for a decade. To do so would suggest a greater confidence in both the method used and the data available than is justified.” The authors conclude, “the use of the normal curve was chosen partly in respect to the Farr-Brownlee tradition but more practically because of the stark SIMPLICITY* of the method. Others have also discussed the complexity of modeling the infinite number of events, circumstances and relationships that have conspired to create the epidemic of AIDS. There is reluctance to accept simple explanations of complex phenomenon.” (1) *(emphasis added)

    Dale says he needs to be convinced that a flat “HIV” curve existed prior to 1983 (the first year Duesberg states a one million prevalence). Since the burden of proof is still on those who propose a unique, specific agent x, causing a singular disease y, I’m saying that Joshua Lederberg’s little joke is on them. But I will offer reasons why a Bayesian prior suggests flatness of horizontal human/primate retroviral incidence-transmission for millions of years.

    The first problem, as we all should know by now, is what to use as a gold standard; if we want to (and I maintain we don’t, for a multitude of socio-political reasons – at least in the current frame), say, measure human retroviral incidence-transmission. Again, let’s ignore the Perth Group’s standard and, accepting Duesberg’s definition of isolation consider the gold standard as set up by AIDS researchers in an AIDS journal; ie proviral DNA. First problem for YOUR theory, as pointed out at the beginning, is the falsification by Gallo himself of his putative unique, specific agent, HTLV IIIb, after it was announced to the world as THE AIDS virus (singular). I’ll give him this, he certainly was correct on the unique part, since it came out of Montagnier’s lab.

    Then came the proliferation of subtypes, which has resulted in the two moving targets hitting each other problem discussed above, which appears to make it a practical impossibility of ever obtaining transmission-incidence data that would necessitate mathematical treatment.

    So Dale, here’s why I think the default position should be flat model of endemic human/primate retroviral prevalence:

    1. All mammalian cells have latent genes which are “… units of DNA called retriviral-like transposable elements (that) play an important role in mediating regulatory changes that can result in the evolution of development … “(2)

    2. “We report here the detection of a 70S RNA and RNA-instructed DNA polymerase (reverse transcriptase)* in 87% of the Burkitt’s lymphomas examined. We further show that the enzyme and its RNA template are localized in a particle possessing the density characteristic of the RNA tumour viruses (retroviruses)*.” (3) *(parens added)

    4. The natural history-SIV(agm) research (I can provide ref, if you need.)

    5. The Huebner reference (PNAS, 1972) cited above.

    6. The DRB arguments that HIV is a harmless passenger.

    Chris and Dale, if I were you, I would be more concerned with the context-specific problems that you (and I don’t care how many other scientists) are ignoring in cobbling together the amalgams HIV and AIDS, than about the “strawman” mathematical precision. Consistent with above HERV posts, retroviral research of the 70’s and reference (3); in addition to KS, ALL lymphomas should each be in a specific set with meta-analyses using LTR retrotransposon/retroviral markers and toxicological epidemiology: the calculation of odds ratios, confidence intervals, etc. – applied to the data.

    (1) DJ Bregman and AD Langmuir, Farr’s Law Applied to AIDS Projections, JAMA, V263, 1522 (1996)

    (2) McDonald J, Macroevolution and Retroviral Elements, Bioscience, 40, 183-191 (1990); plus subsequent J McDonald papers (Genome Research) and HERV references posted above.

    (3) Kufe, Spiegleman, et al; Burkitt’s tumours contain particles encapsulating RNA-Instructed DNA polymerase and high molecular weight virus-related RNA. PNAS, V70, N3, 737-741, March 1973.

  450. #450 Dale
    August 2, 2006

    And once again Gene, we aren’t talking about retroviruses in general, we are talking about HIV. So while HIV genes share some similarity with endogenous latent retroviral genes they are different enough that their sequences can be easily identified. The latent retroviral gene sequences are found in all cells of the body and at similar frequencies in healthy individuals and AIDS patients while the HIV sequences are found in only a subset of body cells and are restricted to those who either have AIDS or have a high probability (90%) of going on to develop it. The existence of reverse transcriptase activity in Burkitt’s lymphoma is a non sequitor that once again attempts to imply that retroviruses are indistinguishable from one another. T cells of AIDS patients and Burkitt’s lymphoma cells may both have reverse transcriptase activity but only the former will synthesize HIV specific proteins or contain HIV specific DNA or RNA sequences. The natural history of SIV says that SIV has been in the agm population much longer than HIV has been in the human population. Why should you accept the one conclusion and deny the second when both are based on the same arguments? Huebner, writing 12 years before the discovery of HIV, is supposed to prove what? He clearly wasn’t writing with HIV in mind unless you are suggesting he was prescient? There is no evidence that HIV is a harmless passenger virus and plenty of evidence that it isn’t. I’m not going to list the evidence again because I’m sure I’ve done it at least once and probably more, in this thread alone. Duesberg’s ‘opinion’ is not evidence.

  451. #451 Chris Noble
    August 3, 2006

    Gene writes:

    Being Of course, the “real curve” is more likely a sharply-spiked sawtooth with a flatness approximation. You guys can huff and puff all you want about mathematical precision and a presumed necessity for me to prove “my theory” (if only it really WAS mine), but these are not relevant to the issues at hand.

    If you are going to claim or rather regurgitate Duesberg’s claim that HIV has had a constant prevalence of 1 million in the US population for the past 200 years then, yes, you should at least attempt to defend that claim.

    In typical “rethinker” fashion you attempt to avoid doing so.

    I repeat again: the very data Duesberg cites completely contradicts his own thesis.

    In early estimates of HIV prevalence the vast majority of infected people were homosexual men. This is clearly stated in the very references that Duesberg cites. It is completely illogical to a) round the figure off to exactly 1 million, b) extrapolate this prevalence back 200 years in time and c) claim that HIV is predominantly spread by perinatal transmission.

    Duesberg himself says that tests on military recruits and blood donors show only a prevalence of about 0.04%. This accounts for at most 100,000 of the magic 1 million. This leaves 900,000 that are mostly made up of homosexual men and IVDUs. How is it possible that this 900,000 were infected by perinatal transmission?

    In addition, in cases where we have blood samples of cohorts of homosexual men or IVDUs over the early part of the epidemic we see that seroprevalence was effectively zero in the early 70s, rises sharply in the late 70s/early 80s and then levels off again in the late 80s. Ie HIV incidence was highest in the late 70s/ early 80s. This is completely consistent with a peak in AIDS cases in the early 90s.

    This data is contained in the very references that Duesberg cites as evidence that HIV is a long established virus with a constant prevalence going back 200 or more years.

    Can you explain this?

  452. #452 Chris Noble
    August 3, 2006

    Dale writes:

    The latent retroviral gene sequences are found in all cells of the body and at similar frequencies in healthy individuals and AIDS patients …

    To the best of my knowledge all endogenous retroviral sequences in the human genome have been there for hundreds of thousands or even millions of years. As such they are common to all humans. It is conceivably possible that a retrovirus might have become endogenous in recent history (in the past 200 years) in which case a frequency of less than 100% would be possible. There is, however, no evidence for this. In addition, this would mean that the virus was until recently exogenous and is in all probability still replication competent and infectious in addtion to being endogenous.

    As you have previously stated if HIV were endogenous then you would not expect ARVs to have any effect whatsoever on MTCT. This is in contradiction to all experimental evidence.

  453. #453 Gene Semon
    August 4, 2006

    Dale,

    I appreciate what you are saying, but the heart of this argument is that with all the subtypes, there are no HIV specific proteins! Nor am I going to repeat the arguments in previous posts and of the Perth Group’s which can still be deployed re non-specific proteins consistent with Duesberg’s definition of isolation which was made for 20 or so subtypes. I understand there are dozens more on file at Los Alamos. How many more “isolated” since in addition to those on file and how many more “potentially”; do you know? Some HIV/AIDS researchers have speculated that isolation of new subtypes may just go on and on, consistent with the varieties of retroelements in the human genome (last part me). And what about the ever growing number of HIVAb sero-negative but proviral and/or RNA positive cases? What does that do to your specificity?
    And let’s not leave out Dr Urnovitz’ matching a subtype (O?) env gene to a chromosal locus.

    The point of bringing up Huebner is that he PREDICTS HIVs'”discovery” from “experimental manipulations”. Since lympadenopathy precedes lymphoma, Burkitt’s lymphoma “retrovirus-like” phenomena is a re-frame for Dr Fauci’s famous “reservoir” based on “in-situ hybridization” of genome fragments, which of course increase the sensitivity of the assay at great sacrifice to the specificity.

  454. #454 Gene Semon
    August 4, 2006

    Chris,

    “round the figure off to exactly 1 million” This is not Duesberg, but CDC. Duesberg’s style, clear from reading his papers is to accept (black box, so to speak) and use the estimates, experimental findings, conclusions, etc. of the HIV?AIDS biomedical institutions, HHS included, and “unpack” the assumptions, which pose as data-derived, that have led to the conclusions you defend. He also draws an ascending curve for Africa! This is not my style.

    I have “explained” those numbers you cite but the shorthand, consistent with the different slant from Duesberg re the gold standard is that he accepts seroprevalence (again black-boxing) as identification of at least a primary transmission (e.g. MTCT) wheras I’m saying we don’t know the real numbers and, yes, Duesberg’s SIMPLIFICATION can appear contradictory if you want to say that retrospective HIVAb prevalence measurements can be extrapolated to incidence numbers.

    As far as the rest, thanks to you and Dale, I will not avoid but plunge into a preliminary defense of a best-curve model based on non-pandemic horizontal retroviral transmission. I speculate on the sawtooth shape based on “primary” transmission limited to cohorts like SFCCC, a “bottoms-up” model so-to-speak with a one in 5 million risk of tertiary transmission from a a healthy bisexual secondary. Also reasons given above in GIGO post to Viji.

  455. #455 Dale
    August 6, 2006

    Gene, of course there are HIV specific proteins, subtypes notwithstanding. Short stretches of sequence similarity as Urnovitz describes may account for some indeterminate results on Western blots(indeterminate as opposed to positive Western blot results) but that is why Western blots alone are not used to diagnose HIV infection. And it’s clear that most HIV transmission is NOT through mother to child. If it were, the only adults who would ever seroconvert would be those who had proviral DNA sequences from birth. Where is the evidence?

  456. #456 Chris Noble
    August 6, 2006

    Genw writes:

    “round the figure off to exactly 1 million” This is not Duesberg, but CDC. Duesberg’s style, clear from reading his papers is to accept (black box, so to speak) and use the estimates, experimental findings, conclusions, etc. of the HIV?AIDS biomedical institutions, HHS included, and “unpack” the assumptions, which pose as data-derived, that have led to the conclusions you defend. He also draws an ascending curve for Africa! This is not my style.

    Either you have not bother to check the references he gives or you are lying it is that simple.

    Here is a list of some of the references that Duesberg, Bialy and Rasnick provide.

    1985 0.5-1.0 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=2994217&query_hl=3&itool=pubmed_DocSum
    1986 1.0-1.5 http://www.nap.edu/books/0309036992/html
    1987 0.945-1.4 http://www.nap.edu/catalog/771.html
    1988 1.0-1.5 http://www.cdc.gov/mmwr/preview/mmwrhtml/00001274.htm
    1989 1.0-1.5 http://www.cdc.gov/mmwr/preview/mmwrhtml/00001477.htm
    1990 0.8-1.2 http://www.aegis.com/pubs/mmwr/1990/MM3907-110.html
    1992 0.65-0.9 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8656504&query_hl=9&itool=pubmed_docsum
    1993 0.63-0.897 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7481828&dopt=Abstract
    1996 0.65-1.25 http://hab.hrsa.gov/reports/rp14.htm ???
    1998 0.8-0.9 http://ww3.aegis.org/pubs/mmwr/1999/RR4813A1.html
    2000 0.85-0.95 http://www.retroconference.org/2002/abstract/13996.htm
    2003 0.925-1.185 http://www.aegis.com/conferences/NHIVPC/2005/T1-B1101.html

    In particular the one and only reference that DRB provides for 1985 gives a range of 0.5-1.0 million. DRB magically round it down to 1 million. Later estimates for 1986 have a range of 1-1.5 million. DRB magically rounds it down to 1 million. If you actually plot the data as reported by the CDC with error bars it looks nothing like the DRB graph.

    If you bothered to read some of these references you would see that the CDC does not believe that 1 million people in the US were infected with HIV in 1985 (let alone 1984 which Duesberg has on one version of the graph). It is just plain dishonest to display the DRB flat graph and claim that it is supported by the CDC. It is also an incredibly stupid lie because it is so easy to check the references. It seems that Duesberg supporters never check his references or else they have well developed cognitive dissonance filters.

  457. #457 Gene Semon
    August 7, 2006

    “And it’s clear that most HIV transmission is NOT through mother to child.”

    Dale, I’m really rooting for you on this one. As I said, I don’t know.

    But the problems of specificity and cross reactions with HERVS won’t go away simply by repeating the mantra, “there is no evidence”. I didn’t even mention HRES, HIAP (matches, as you know, LTR retrotransposon genes), or HTLV I with its (different?) p24; but I read from a 1988 paper that antibodies in the Western Blot to “HIV core proteins” are false positives when they are found in blood donors(1). Why should that be if they are specific?

    The author’s also state, “Patients with cutaneous T-cell lymphoma or its prodromes have been found to have antibodies crossreacting with the core proteins of HTLV-I (55%) or HIV-1 (HTLV-IIIb isolate)(24%). In randomly selected dermatologic patients, such antibodies were found in a few cases with generalized warts without underlying systemic disease and in some cases with autoimmune connective tissue disease (HTLV-I, 3/55; HIV-1, 7/55) … (W)e found crossreacting antibodies to the core of HTLV-I but also to HIV-1 in patients with multiple sclerosis (HTLV-I, 2/17; HIV-1, 7/17).” (1)

    This to me is more historical evidence that this whole thing was cobbled together on the fly, a solid structure at first glance, but built on quicksand.

    1. Ranki et al, NEJM, 318, 448 (1988)

  458. #458 Chris Noble
    August 8, 2006

    Gene, what exactly is your theory. It is clear that you do not believe that HIV causes AIDS but apart from that it is impossible to ascertain any coherent train of thought in your writings. At different times you use arguments from Duesberg, the Perth Group and Urnovitz.

    Is there anyone that actually understands what your theory is? Can they explain it because you aren’t doing a very good job.

  459. #459 Gene Semon
    August 14, 2006

    Chris,

    My theory is that I’ve been dealing with two guys who resemble the walking dead of the Bush Administrarion who cannot help but utter their programmed talking points, endlessly, and can’t be persuaded by rational arguments.

    How can I explain what the sun is to blind men? When will you SEE the fundamentalism that has engulfed you. Stop being like the other robots and technicians posing as scientists, read all my posts and references and maybe, just maybe you’ll understand what I’m saying.

    If you want something more specific, read the Padian thread at Barnesworld and we can discuss that.

    Best regards,
    Gene