Discussion of the Padian paper

As promised, a discussion on the paper, Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten-year study.

First, let’s backtrack a bit and see what’s already been said, lest I repeat myself. The little summary below can also catch anyone up who’s not up to wading through 250-odd comments. Those who’ve already done so can skip the quoted parts and scroll down…

[Note: I've uploaded a .pdf of the Padian paper for anyone to access Here.]

Hank Barnes said here about the paper:

1. It was the longest and largest epidemiological study of heterosexual tranmission of HIV (1986-1996);

2. For 10 years, it followed 175 discordant couples, who had a lotta sex. “Discordant” means for each couple, 1 person was HIV+, and one was not.

3. So, obviously, if you’re gonna have lots of sex with an HIV+ person, you’re gonna get the virus, get AIDS and die, right?

4. After 10 years, the scientists found NO seroconversions.

5. The couples who used condoms, did not transmit the virus
6. The couples who failed to use condoms, did not transmit the virus
7. The couples that exclusively engaged in vaginal intercourse did not transmit the virus;
8. In fact, 39% of the couple engaged in anal sex — they too did not transmit the virus.

The only logical, scientific conclusion from the Padian report is that AIDS is not a sexually transmitted disease.

Indeed, How can you have a sexually transmitted disease, that is not transmitted by sex?

If anyone here disputes any of the fact I’ve recited above re Padian, please feel free to read the paper and tell me where I’ve erred.

More importantly, assume my recitation of the paper is true. Then, what logical, scientific conclusion would YOU reach regarding HIV?

Dale then pointed out:

Hank is factually correct about some aspects of the Padian paper. No seroconversions occurred during the course of Padian’s study although some may have occurred prior to the study. Over 400 individuals in stable relationships were initially identified as potential participants in this study. When their partners were tested, 15% of the 400 couples were excluded at the outset because the partner was already HIV positive. There was no way to know whether the partners had acquired HIV from each other but neither was there any way to demonstrate that they hadn’t.

However, Hank is wrong about the duration of the study. Individuals were recruited over a ten year period. No couple was actually followed for anything even approaching ten years. 3000 couple months of follow-up for 175 serodiscordant couples – that’s an average of less than two years per couple.

Also there have been other studies of heterosexual transmission of HIV that do show apparent seroconversion in individuals with no known risk factors other than a seropositive spouse. The conclusion of heterosexual transmission is subject of course to all the caveats that apply to studies of human beings.

Enter Darin Brown in the rudely hijacked thread:

Unfortunately, what you say is completely wrong, assuming that the sexual encounters are identically and independently distributed, which would seem to be a fairly reasonable assumption in this case.

Have you heard of random variables? Expected value? The situation you’re describing is something studied in lower-division stats courses — it’s called the geometric distribution. You have a trial with 2 outcomes: success (probability p) and failure (probability q = 1 – p). The geometric distribution assigns to each positive integer n the probability of exactly n trials before success is reached. The situation you describe above is the case p = 1/1000.

Of course “3 seroconversions per hundred couple years doesn’t mean 1 serodiscordant couple can go at it in relative safety for 33 years; or to use your numbers, that an HIV negative individual can have 999 sexual encounters before running into a problem.” That’s not what is being claimed. What’s being claimed is a mathematical statement: that the expected number of sexual encounters before “success” is 1000 = 1/p. And, in fact, that is the case. A random variable with geometric distribution does indeed have mean equal to 1/p.

You are quite wrong with the lottery ticket analogy. It does not matter WHO buys the tickets, what matters is that the trials of buying a ticket to see if you win are identically and independently distributed. And this is true for lottery tickets, regardless of whether one person buys 1,000,000 tickets or 1,000,000 people each buy one ticket. The trials don’t give a hoot about who’s buying the tickets…why should they?

and Dale responds:

Darin, Your post in response to my post on the other hand demonstrates a lack of understanding (or a masterpiece of ignorance if you prefer that term) of biology.

In particular your statement “assuming that the sexual encounters are identically and independently distributed, which would seem to be a fairly reasonable assumption in this case.”

That might be a reasonable assumption to a mathematician but no biologist would ever make such an assumption, particular as applied to human beings.

Human beings are not a homogenous population, neither genetically nor with regard to the environments they live in. Some are more susceptible to HIV infection than others. Sexual encounters are not all the same,some incorporate more risk factors for transmission than others. The viruses themselves also vary genetically and that too will affect transmission rates.

The identification of any individuals in whom sexual transmission of the virus has occured says the virus can be transmitted sexually and a hundred or a thousand population studies such as Padians will not determine the true probability of transmission for any given individual at any given sexual encounter.

Hank Barnes impatiently returns:

1.The year is 1985 — one year after the supposed “cause” of AIDS has been discovered — a virus called HTLV-III (now called HIV).
2. The thought is HIV is sexually transmitted.
3. The thought is once acquired, within 2 years, you die.
4. Most of the folks dying of AIDS are gay males. But, this is a bit nonsensical, since viruses don’t discriminate. They are real dumb and real small.
5. The thought is an infectious disease will likely move into the general population and kill a lot of people.
6. So, a buncha brilliant epidemiologists from San Francisco set out test the hypothesis: Find HIV+ people and observe what happens to their partners when they have a lotta sex. Clean. Easy. Crisp science.
7. So, the a priori hypothesis is this: We expect the uninfected partners of HIV+ people to become infected at some rate. 100%? 50%? Who knows? Padian does not say (for good reason).
8. We get a lotta $$ from the gov’t to fund this study. It lasts 10 years. We test a lotta people for HIV. We follow them for years. They have a lotta sex. We keep re-testing them. So, How many got infected? The answer is:

Zero. Zip. Zed. Nada. Nil. Nothing. Nobody.

NOT ONE SINGLE PERSON (175 discordant couples), after unlimited, abundant, (dare I even say wild and kinky?) sexual acts over 10 years contracts HIV. Not one.

Buried in the paper on pg 354 (“We observed no seroconversions after entry into the study”).

Those are the facts. So, what is one to conclude?

My conclusion is that the connection between sex and AIDS has been proven false. Some folks don’t like that conclusion. The ostrich crowd has emotionally invested in the wrong paradigm, and are unwilling to change their beliefs, despite the evidence. Not very scientific, mind you.

Myself, I go with the facts. NO SEROCONVERSIONS. You cannot have a sexually transmitted disease, where sexual activity is abundant, yet sexual transmission is non-existent.

So, put that in your pipe and smoke it!

Some mostly off-topic comments (for the Padian paper analysis anyway), and then Hank asked for this:

Please provide a cite for a 10-year study (or less, if you like) where uninfected folks did in fact become infected from heterosexual transmission of HIV.

Chris Noble enters with this:

OK I’ll bite.

Rates of HIV-1 transmission per coital act, by stage of HIV-1 infection, in Rakai, Uganda.

The Rakai cohort studies began in 1994.

While the researchers did not have the genitalia of the couples under an electron microscope at the time of transmission they did do sequence analyses to confirm transmission.

Note the strong dependence on the stage of infection upon transmission risk. This confirms earlier studies showing a relationship between viral load and transmission risk. It is also common sense. The risk of transmission of HSV is not constant. It varies with viral load and the amount of viral shedding.

The HIV+ member in Padian’s serodiscordant couples had been infected for a period of time before the start of the study. None were in the initial infection stage.

The HIV dissidents may be surprised that this is exactly what Duesberg has been saying – that the transmission of HIV should be highest during the initial infection stage.

Hank then shifts the goalposts:

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.

Darin Brown adds:

Noble “ET AL” — You really must learn to read the body of scientific papers in addition to the abstracts, just like Hank has pointed out (n-times, n > 7). Because if you had read the body, you would know that overall transmission rate in the Rakai study was 1 in 856, over a whopping total of 6700 couple-months. That’s more than TWICE as many couple-months as Padian! They even admit in the discussion, “The overall rate of HIV transmission…is consistent with previous estimates from Rakai, Europe, and North America.” But since this would further confirm HIV can’t possibly cause a sexually transmitted disease, they had to hide this fact a few pages deep into the paper, and let all the lazy eyes glaze over “.0082/coital act within ~2.5 months after seroconversion” in the abstract, a ridiculous statement given the fact it’s only based on 10 couples who were only surveyed ONCE every TEN months…but wait, you would have to actually READ the paper to know that! Silly me.

and JP adds this study:

But this whole debate piqued my interest, and I ended up stumbling across this:

“Incidence of HIV Infection in Stable Sexual Partnerships: A Retrospective Cohort Study of 1802 Couples in Mwanza Region, Tanzania” (Hugonnet et al. 2002 JAIDS 30(1)73-80).

In the text (which I read this time), they show that, of the 42 discordant couples, there are 6 seroconversions in 2 years.

For comparison, there are 1742 couples where both partners are HIV- at the outset. After 2 years, there were 21 seroconversions. The difference between the two groups is significant.

I don’t think you have a strong argument that HIV isn’t sexually transmitted, no matter how you frame it.

A bit more off-topic discussion, followed by JP’s comment:

Darin Brown–

“6 transmissions out of 8400 coital acts is a transmission rate of 1 in 1400. Unless you’re misrepresenting the data.”

Sure. Here’s a comparison:

The transmission rate per sexual act for herpes simplex 2: 1/1200 (from “Effect of Condoms on Reducing the Transmission of Herpes Simplex Virus Type 2 From Men to Women JAMA 2001 285(3100-3106)”)

Herpes is considered to be sexually transmitted. Why not HIV?

[Adding from the conclusion of that paper: "Our study revealed several new findings about the frequency and prevention of transmission of HSV-2 infection to sexual partners. Among monogamous couples with 1 partner who had known symptomatic genital herpes and 1 who was susceptible, we showed that the rate of transmission from men to women is 8.9/10 000 sex acts. This rate is similar to that seen with sexually acquired HIV.--Tara]

followed by me logging on and getting pissed that y’all ruined my happy nephew news with more of this after I already noted I’d come back to it at a later date. Patience, anyone?

So, let me start my portion by summarizing my thoughts on the Padian paper. As others have noted, the paper had 2 parts–a retrospective analysis, and a prospective analysis. The retrospective portion showed findings similar to previous studies–anal sex, history of other STDs, injection drug use, and not using condoms increased the risk of transmission. Nothing too surprising here, and nothing that’s really been harped on by Hank or others. So, let’s get to the meat of the objections.

The prospective portion began in 1990. As noted, 175 couples were enrolled where one person was HIV+ and the other partner negative. However, there were only 282 couple-years of followup, they note that “attrition was severe,” and the longest duration of follow-up was 12 visits (6 years). Additionally, while “3384 couple-months of followup” was observed, note that there were only 2 visits per year. They also say on page 351 that “the couple was counseled together regarding safe sexual practices,” and the stats bear out that many of the couples got the message. Abstention increased from 0% at baseline to 14.5% in the final follow-up visit; consistent condom use increased from 32.3% to 74%, and any anal intercourse decreased from 37.9% to 8.1%. Obviously, these behavioral changes would severely decrease the ability to detect the transmission of *any* sexually-transmitted disease (borne out by the study on herpes cited above).

What’s missing from their paper is data on the distribution of follow-up of the couples. 282 couple-years of follow-up for 175 couples that are only seen every 6 months ain’t a lot. If all of the couples were followed for at least a year, that alone takes up 175 of the couple-years, and only 3 visits per couple (assuming a visit at enrollment, 6-month followup, and 12-month followup). They note that at least one couple made it the whole 6 year period, but it’s not clear from their paper how many couples had significant follow-up (and the risk factors associated with said couples). This also makes their discussion less impressive. As Hank notes, they say that “no transmission occurred among the 25 percent of couples who did not use condoms consistently at their last follow-up nor among the 47 couples who intermittently practiced unsafe sex during the entire duration of follow-up,” but was this duration 6 months? A year? More? How many sexual encounters occurred during this period? Obviously no one reports every single bit of data, but knowing even the average duration of follow-up would be helpful.

Continuing on, as noted in one of the exchanges above, they note they don’t have data on the incidence of the HIV+ partner’s infection–in other words, was the infected partner diagnosed a month before enrollment? A year? Longer? Other studies have shown that HIV is most infectious shortly after acquiring the virus, so that’s another piece of data that would have been nice to have. Additionally, they note in the discussion that there have been a number of host factors identified that have been associated with decreased susceptibility–and none of them were examined in this study. They also noted a low rate of other STI prevalence in the couples included in the retrospective study, but don’t specifically say what this was in the couples involved in the prospective portion. Was it similarly low? Concurrent STI is another risk factor for acquisition of HIV, and if that was essentially absent in the prospectively studied population, that’s another key data element missing.

Next, any study that uses volunteers brings in potential biases, the most obvious one being, “is this group representative of the general population?” Again, they’re lacking stats on a number of things epidemiologists usually look at when grappling with this issue–things like education and socio-economic status (they do provide race and age data). They don’t even mention, however, the total number of couples invited to particpate, or how they recruited couples, though they reference 2 older papers–not available online–and say “study protocol and data collection methods ahve been described in detail previously.” The abstract of one of those says “Participants were recruited from various HIV counseling and testing sites throughout California,” suggesting that they offered enrollment to a cohort of individuals–some accepted, likely many declined. This also brings bias into the study–why did those who declined, do so? Were those who accepted the invitation representative of the group? Why or why not? Again, this may have been addressed in the 1991 paper linked above, but IMO it’s also worth noting briefly in the new paper.

These criticisms may seem like I’m really down on the paper. I’m not, really–overall, it’s not bad, not great. Thing is, I find it rather strange that it’s being used to beat down the idea that HIV is a sexually-transmitted disease. For one, their first analysis clearly shows support for that hypothesis. Two, even the prospective portion of the study wasn’t designed to “catch” sexual transmission in the act. Their introduction notes the reason for the study:

…to address this shift in the epidemic toward heterosexually-acquired infection, a deeper understanding of risk factors for heterosexual transmission is imperative. We have been able to identify risk factors at the individual level that affect the likelihood of transmission between infected individuals and their heterosexual partners. Elimination or modification of these factors could result in reduced transmission of HIV. In addition, predictions about the epidemic might be refined by identification of such risk factors, because their prevalence signifies potential for future epidemic spread.

That’s why their analyses focused on the risk factors for transmission, and how they changed over time–including in the prospective cohort. Indeed, their prospective study design–even without the flaws I note above–is a pretty poor setup for detecting a transmission event. A better–but still far from perfect–design is this study, which collected not only blood but also vaginal swabs, so that the presence of other co-factors could be examined, and the HIV strain could be subtyped. Viral load was also measured, and data was collected regarding stage of infection. That’s data you want when you’re carrying out a study trying to witness transmission events.

Finally, there’s a lot of “this can’t happen” being thrown around by those who don’t accept that HIV causes AIDS. Again, this goes back to my question of why this virus/disease receives special treatment. JP already noted that similar rates of transmission have been found with herpes as are seen with HIV, so you can’t rightly say that HIV “can’t be” a STI without saying the same thing of herpes. (In the study referenced above, they had an even *lower* rate of condom use than the Padian study–so theoretically, with identical levels of condom use, herpes could be even less transmissible than HIV). Duesberg and others note that HIV “discriminates” by race and gender, yet rates of syphilis and gonorrhea are nearly 30 times higher in blacks than in whites. Do these also not cause the diseases they’ve long been associated with? Similarly with male-to-female ratios of the disease: we’ve seen the same thing during outbreaks of hepatitis A and shigella, among others. As I said before, this can easily be explained as a type of founder effect due to the original group HIV was introduced into in the US. The rest of the arguments are just more of the same–retroviruses “can’t” kill cells, or HIV “can’t” cause disease after antibodies are present (what about shingles?), or is too small or “simple”–it “can’t” cause AIDS (what about rabies, West Nile, polio, HPV, influenza–all with genomes of similar size? Or teeny-tiny Hepatitis B at only 3000 bp, going around and causing all that cancer? [Of course, Drs. Bialy and Duesberg don't think viruses cause cancer, either]). You get the point.

Last but not least, even though I may be young (though I’m not exactly a “recently minted” PhD–I finished grad school in 2002), even I’m not naive enough to say some microbe “can’t” do something–others have done it, and been proven wrong. If anything, studying all sorts of microbial life over the past decade-plus has made me aware of all the crazy things microbes can do. Hell, that’s one reason I started this site–there’s a never-ending stream of fascinating new discoveries in the microbial world to discuss. And this will further piss some people off, but again, I see a parallel here between creationists and many of y’all who rail against HIV. We don’t have all the answers yet, therefore, hey, let’s just throw in the towel. One of the oddest objections to me is that we don’t have a vaccine yet, “despite 20 years of searching.” Again, I’ll note that we don’t have vaccines against group A or B streptococci, even though group A has been studied for well over 100 years, and group B for 30 years now. Nor do we have vaccines for other pathogens that emerged ’round the same time as HIV, such as E. coli O157:H7. Like I said–special treatment. Mystifying.

Anyhoo, apologies for this being a bit long and rambly–I’m trying to get some answers to objections in that I think fit in with the Padian paper analysis. I’ve not overlooked other questions waiting for me, and have some other posts in the hopper, but I’d prefer to try to keep this a bit more focused. I think the material above provides a lot of fertile ground for discussion, but I’ll note a few things: 1) I ain’t at your beckoned call–I have a life, a family, and a grant due Tuesday, so if I can’t answer your right away, them’s the breaks; and 2) must you resort to name-calling? “Dumbass”? “Weenie?” If you’re going to fling insults, dear lord, at least do it at a junior high level. Graduate to “vagina blood fart” or something.

Okay, have at it.

Comments

  1. #1 Harvey Bialy
    February 23, 2006

    May I point out that a more instructive and readable (if I say so myself) account of the mini-marathon leading to this remarkable post by Dr. Smith is to be found at

    http://bialystocker.net/files/Pipedream.pdf

  2. #2 Tara
    February 23, 2006

    As I said before, have you nothing better to do than spam your site?

  3. #3 Hank Barnes
    February 23, 2006

    1. Is the Padian study, the longest and largest epidemiological study of the heterosexual transmission of HIV?

    2. In the prospective study (the one that mattered), How come not one uninfected partner who had sex with an HIV+ person contracted the virus?

    3. How come not one uninfected partner contracted the virus from anal sex?

    4. What was Padian’s a priori hypothesis before she embarked on the prospective study?

    5. Don’t the Padian results lend greater support to the hypothesis that HIV is a garden-variety endogenous retrovirus, rather than a sexually-transmitted pathogenic killer of t-cells?

    6. The scientific community declared that AIDS was a sexually-transmitted disease by the mid-1980′s. Upon what epidemiological study was this based?

    7. When did you first learn of the existence of the Padian study?

    Hank Barnes

  4. #4 Tara
    February 23, 2006

    Hank, did you even bother to read what I wrote? How about some of you answer *my* questions for a change?

  5. #5 Hank Barnes
    February 23, 2006

    Dr. Tara,

    Of course, I read what you wrote! It’s not bad.

    Anyhoo, apologies for this being a bit long and rambly

    I’m just “having at it” as you invited, cutting thru some of your ramble. You don’t have to answer immediately, though, I know you’re busy.

    Take your time.

    Hank Barnes (Doctor of Democracy)

  6. #6 Dale
    February 23, 2006

    Tara, Empirical observation from one of the longest (albeit unpublished) studies of the Internet behaviour of AIDS dissidents, suggests that most likely Hank will either continue to spout his “talking points” about Padian or attempt to change the subject by challenging you to address some other cherry picked piece of data from a published paper. The probability that he will actually engage in a discussion of the merits of your arguments is, unlike the probability of heterosexual transmission of HIV, truly vanishingly small. Not a single occurrence has yet been observed.

  7. #7 Tara
    February 23, 2006

    You still didn’t answer any of the questions I posed above, Hank. :) And I addressed most of your points in the post, and don’t see what others have to do with anything (for example, #7). I also addressed your question #6 in a previous comment.

  8. #8 Hank Barnes
    February 23, 2006

    Dale,

    No need to continually follow me around the internet. Particularly, when you have nothing of interest or substance to add. If you wanna answer those questions posed, feel free to.

    Tara,

    No, you haven’t answered the questions. You have given a “long and rambly” smorgasbord of this and that, ranging from Padian to shingella to e. coli to creationism to other stuff.

    If you don’t want to or can’t answer the questions, just say so. It seems a bit odd to me that a highly intelligent, Professor of Epidemiology would dodge such simple, straightforward questions — in the field of her own specialty, no less.

    But, hey, that’s life!

    Also, to be fair, feel free to ask me any questions on the topic.

    Cheerfully yours,

    Hank

  9. #9 Darin Brown
    February 23, 2006

    I ain’t at your beckoned call–I have a life, a family, and a grant due Tuesday, so if I can’t answer your right away, them’s the breaks.

    Fine, Tara. I also have a life, 4 classes to teach, and I’m job-hunting to boot. So, I totally understand. But there was no reason to close those threads. The name-calling was not beginning to threaten the discussion.

  10. #10 mgr
    February 23, 2006

    The way I understand Tara’s critique of the Padian study is to substitute chicken pox for HIV. I hope I do not have to elaborate, but the same problems arise with cross couple infection–unless the infected partner is in the early stage of chicken pox, no way the other partner is likely to get it from them. This problem stands regardless of the mode of transmission.

    Mike

  11. #11 Dale
    February 23, 2006

    Hank,
    re your questions, sure I’ll answer and I’ll be very brief.

    #1. It may have been at the time but there are now studies in the literature, like the one Chris Noble linked, that are larger.

    #2. There is no reason to believe the prospective study is any more important than the retrospective study and in fact one might argue it is less important since this and other studies suggest that awareness of HIV status modifies sexual behaviour in ways that will reduce the probability of viral transmission. As to why no seroconversions were observed in this study, ask Darin Brown to explain statistical inference to you.

    #3. See the answer to #2.

    #4. Her stated hypothesis was that there would be factors associated with increased probability of heterosexual viral transmission.

    #5. No they don’t because (1) they can’t be taken in isolation from other epidemiological studies and (2) epidemiological studies can’t be used to dismiss case reports demonstrating heterosexual transmission.

    #6. Based on case reports, contact tracing and data being compiled by the CDC. Also based on what was being learned about HIV.

    #7. I think I learned about it from you Hank.

  12. #12 Dave S.
    February 23, 2006

    Tara writes:

    Two, even the prospective portion of the study wasn’t designed to “catch” sexual transmission in the act.

    To me, this is the major flaw in the argument the AIDS deniers (sorry if y’all don’t care for that term) seem to be making here. This experiment cannot be used to support the hypothesis that the HIV cannot be sexually transmitted, because it was never designed to test that. At best, if you ignore the retrospective part of the experiment and all the other experiments linking HIV and heterosexual transmission, then that remains only a possible hypothesis to be tested with better designed experiments like the one to which you linked.

    Note: It seems the kind of study the AIDS deniers really want to see is one where humans volunteer to have unprotected sex with someone HIV-seropositive in a controlled setting without any efforts made to mitigate transmission. Such experiments are of course unethical and would not be published by any reputable journal if they were done (although AIDS deniers are welcome to try, using themselves as the guinea pigs).

    Such experiments have been done using animals, although that also raises ethical concerns in some. The result being that the animal versions of that virus (simian, feline, bovine) can be passed sexually. Although that is not the only mode of transmission in animals. In horses for instance the equine version of the virus can apparently be transmitted via horse-fly bites.

    Yes, I know these are not the human form.

    Note 2: What is the best paper that shows that cholera can be transmitted by contaminated water? What is the first paper to demonstrate positively the link between sneezing and influenza transmission? If we knew this, perhaps it would be easier to know what kind of evidence the AIDS deniers (they know who they are) would accept showing that HIV is transmitted sexually.

  13. #13 Darin Brown
    February 23, 2006

    The rest of the arguments are just more of the same–retroviruses “can’t” kill cells,

    Well…they can’t:

    “Since on average only 0.1% (1 out of 500 to 3000) of T-cells are ever infected by HIV in AIDS patients, but at least 3% of all T-cells are regenerated (Sprent, 1977; Guyton, 1987) during the two days it takes a retrovirus to infect a cell (Duesberg, 1989c), HIV could never kill enough T-cells to cause immunodeficiency. Thus even if HIV killed every infected T-cell (Section 3.5.10), it could deplete T-cells only at 1/30 of their normal rate of regeneration, let alone activated regeneration. The odds of HIV causing T-cell deficiency would be the same as those of a bicycle rider trying to catch up with a jet airplane.” (Duesberg, “AIDS Acquired by Drug Consumption and Other Noncontagious Risk Factors”)

    What part of the above paragraph is unclear?? Even if (*IF*) HIV killed T cells, it could never kill enough to overcome the body’s regeneration of T cells. The argument above seems clear and compelling to me. It’s astonishing to me how certain people just disregard the above argument.

    or HIV “can’t” cause disease after antibodies are present (what about shingles?),

    Gee, Tara, I’m really beginning to wonder if you’ve ever read *ANY* of “Infectious AIDS” or Duesberg’s papers, as you were so quick to claim earlier:

    “The virus would be a plausible cause of AIDS if it were reactivated after an asymptomatic latency, like herpes viruses. However, HIV remains inactive during AIDS.” (Duesberg, “HIV is Not the Cause of AIDS”)

    And this is the point: it’s not just the puzzling fact that HIV is supposed to cause AIDS after antibodies are present, it’s the fact that after the latency period, when HIV is supposedly causing AIDS, HIV is inactive. That’s why the word is called: “re-ACTIVation”. You can’t say something is “reactivated” if it’s inactive.

    From what I understand of shingles and reactivation of herpes viruses, this occurs when the immune system is compromised so much that reactivation is possible. This makes perfect sense to me. Reactivation should occur only in cases when there is some other reason for severe immunosuppression. But HIV is completely backwards in this regard — it’s supposed to be the CAUSE of the immunosuppression itself…but if it “reactives”, there must be something else suppressing the immune system? In other words, reactivation of HIV causes the immunosuppression, but at the same time, the reactivation wouldn’t be possible without that very immunosuppresion in the first place. So, yet another example of circular logic.

    or is too small or “simple”–it “can’t” cause AIDS (what about rabies, West Nile, polio, HPV, influenza–all with genomes of similar size? Or teeny-tiny Hepatitis B at only 3000 bp, going around and causing all that cancer? [Of course, Drs. Bialy and Duesberg don't think viruses cause cancer, either]). You get the point.

    Whoa, let’s slow down. First, you’re falling into the same erroneous argument I mentioned earlier of trying to compare “AIDS” with other traditional diseases that have specific, restricted clinical symptoms. I discussed this earlier in some depth in the previous threads.

    Second, the comparison with these other diseases actually lends support against HIV/AIDS hypothesis. Because HIV *DOES* cause disease — namely, a small, mononucleosis-like disease that is quickly neutralised by antibodies within a few weeks or months after infection. And that agrees pretty well with the comparison to the other diseases you mention. “AIDS” does not agree well with the comparison.

  14. #14 Hank Barnes
    February 23, 2006

    Dave S,

    This experiment cannot be used to support the hypothesis that the HIV cannot be sexually transmitted, because it was never designed to test that.

    Huh?!!? Did you not read the title of the piece, we are discussing?

    The study is called, the “Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten-year study.”

    It was designed to study the rate of heterosexual transmission of HIV. The study found….”no seroconversions” after entry into the study (Padian, pg 354).

    Dave S, despite your name-calling, I’m not an “AIDS Denier”, and I generally hate to be rude to people, but, really, you are lost beyond hope.

    If you continue with ad hominem, you’re going to get it back harder and better from me. Please stop embarrasing yourself.

    Barnes, Hank

  15. #15 Tara
    February 23, 2006

    The study is called, the “Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten-year study.”

    Hank, wasn’t it you who chided folks for reading only the abstract on one of the earlier threads? As I mentioned in the post, the goal of the study was to examine *risk factors* that influenced transmission–both retrospectively and prospectively. One can examine risk factors without seeing any transmission if they are highly protective, as the ones in the study were found to be.

  16. #16 Tara
    February 23, 2006

    Darin, I’m beginning to wonder if you ever read anything *but* Duesberg.

    Let’s step away from HIV for a moment and look at another retrovirus, called the visna virus. It’s kind of an HIV cousin, and certainly can kill cells. Still want to say “retroviruses can’t kill cells?”

    From what I understand of shingles and reactivation of herpes viruses, this occurs when the immune system is compromised so much that reactivation is possible.

    Sometimes, yes. Other times, there’s no clear indication of immunocompromise. We don’t fully understand it for herpesviruses, which have been studied much longer than HIV–yet again, no groups out there rallying against varicella as a cause of shingles, just ’cause we don’t understand the whole clinical picture.

    Whoa, let’s slow down. First, you’re falling into the same erroneous argument I mentioned earlier of trying to compare “AIDS” with other traditional diseases that have specific, restricted clinical symptoms. I discussed this earlier in some depth in the previous threads.

    Because I don’t see the dichotomy. *NO* pathogen has “restricted” symptoms. Hell, group A strep can cause 25 different disease pathologies all by itself. You’re trying to make a division where there is none. Sure, strep has some “typical” symptoms–pharyngitis is, of course, a common manifestation, resulting in fever, achiness, sore throat. HIV also has a common manifestation–decreased T cell count, resulting in immunosuppression leading to secondary disease. (Y’know, influenza does this as well–most influenza deaths aren’t due primarily to the influenza virus, but to secondary bacterial infections that set into viral-damaged lungs: just like the secondary infections that result from HIV). But no one criticizes influenza simply because it’s associated with so many different species of secondary infections.

    Again, special treatment. That’s the heart o’ the matter.

    Isn’t anyone going to answer why herpes can’t be a STD, according to your criteria?

  17. #17 Dave S.
    February 23, 2006

    Hank Barnes –

    Please read more carefully. The paper was never designed to test the hypothesis that HIV was transmitted sexually, but to address risk factors in a particular small population. That no seroconversions took place in the prospective portion of the experiment does not mean that HIV cannot be transmitted sexually. That is only one possible hypothesis that someone might formulate, until that is they had seen the retrospective portion of that experiment or the hundreds of other experiments showing this link unequivocally. Then that hypothesis would be rightfully rejected (unless one has a pre-existing notion that would absolutely prevent such a conclusion).

    Another more reasonable hypothesis given this data might be that concilling and safer sex practices work.

  18. #18 Orac
    February 23, 2006

    Hank Barnes said:

    No, you haven’t answered the questions. You have given a “long and rambly” smorgasbord of this and that, ranging from Padian to shingella to e. coli to creationism to other stuff.

    Perhaps you could explain what aspect of your questions, specifically, Tara hasn’t answered, rather than just asserting that she hasn’t answered your questions and waltzing away.

  19. #19 Tara
    February 23, 2006

    Perhaps you could explain what aspect of your questions, specifically, Tara hasn’t answered, rather than just asserting that she hasn’t answered your questions and waltzing away.

    ‘Tis okay. I assume it’s a dance he learned from Harvey, who still hasn’t filled me in on all the mistakes I made in the Bethell post.

  20. #20 Hank Barnes
    February 23, 2006

    Dr. Smith wrote:

    As I mentioned in the post, the goal of the study was to examine *risk factors* that influenced transmission–both retrospectively and prospectively.

    Retrospectively, nobody can tell how or when or under what circumstance the HIV+ people contracted HIV. Every human being is born, every human being has sex. So, it’s fallacious to attribute –without evidence — HIV transmission to either of these 2 events.

    One can examine risk factors without seeing any transmission if they are highly protective, as the ones in the study were found to be.

    Not quite, Tara. Here’s Padian, pge 356.

    While lack of transmission in our prospective
    study may in part be due to such unidentified protective factors, we also observed significant behavior change over time…

    Ok, great.

    Nevertheless, the absence of seroincident infection over the course of the study cannot be entirely attributed to significant behavior change. No transmission occurred among the 25 percent of couples who did not use condoms consistently…..

    Translation:

    The folks who used condoms didn’t contract the virus! (Yea for condoms!)

    The folks who didn’t use condoms failed to contract the virus as well. (Darn, back to the drawing board.)

    Padian’s results — squarely, defiantly, unambiguously — support Duesberg’s hypothesis that AIDS ain’t a sexually-transmitted disease.

    Barnes

    p.s. Dale answered my questions above (I’ll comment on those after lunch). Why won’t you?

  21. #21 Dave S.
    February 23, 2006

    Barnes writes:

    Padian’s results — squarely, defiantly, unambiguously — support Duesberg’s hypothesis that AIDS ain’t a sexually-transmitted disease.

    Assertions don’t get more convincing with repetition. No matter how “defiant” you are.

    Is that all you got?

  22. #22 TonyL
    February 23, 2006

    I find it quite telling that after it was shown that Hank’s claim

    2. For 10 years, it followed 175 discordant couples, who had a lotta sex. “Discordant” means for each couple, 1 person was HIV+, and one was not.

    was a blatant misrepresentation of the paper, he deftly drops this claim and continues to argue as if none of his points have been adequately adressed.

    Hank: answer these 8 points
    multiple answers come in
    Hank: you still havent adressed these 7 modified points.

  23. #23 Tara
    February 23, 2006

    Retrospectively, nobody can tell how or when or under what circumstance the HIV+ people contracted HIV. Every human being is born, every human being has sex. So, it’s fallacious to attribute –without evidence — HIV transmission to either of these 2 events.

    Excellent. This, again, must then also be applied to every infectious disease known to man. All retrospective disease studies are out yonder window. That’ll ease my teaching burden immensely, thank ye kindly.

    Not quite, Tara. Here’s Padian, pge 356.

    While lack of transmission in our prospective
    study may in part be due to such unidentified protective factors, we also observed significant behavior change over time…

    Ok, great.

    Hank, perhaps you’re missing that it *is* those “significant behavior changes” that were exactly the risk factors under examination. Let me add in the part you quote-mined out of Padian’s paper that precedes that (the “unidentified protective factors” they’re discussing):

    As with studies of long-term survivors of HIV infection, an obvious area for future investigations is to focus on immunologic, genetic, and virologic risk factors among those individuals with multiple risk factors for whom transmission did not occur, compared with couples where transmission occurred in the absence of known risk factors.

    That doesn’t negate the fact that the risk factors they examined–condom use, anal sex, and any sexual activity–were indeed protective. They just aren’t the full story. I addressed that in my post:

    Additionally, they note in the discussion that there have been a number of host factors identified that have been associated with decreased susceptibility–and none of them were examined in this study.

    We know things like the CCR5 delta 32 mutation play a role in infection–this wasn’t examined in their study. You’re only further proving my case for me.

    Nevertheless, the absence of seroincident infection over the course of the study cannot be entirely attributed to significant behavior change. No transmission occurred among the 25 percent of couples who did not use condoms consistently…..

    Translation:

    The folks who used condoms didn’t contract the virus! (Yea for condoms!)

    The folks who didn’t use condoms failed to contract the virus as well. (Darn, back to the drawing board.)

    I already addressed this above as well. There’s no data on how long those couples didn’t use condoms consistently, or indeed, even what “consistently” meant. Did they miss one time? Rarely used condoms? Practically never? How many follow-up visits did they have? Hardly “back to the drawing board”–it just opens new areas for investigation.

    Padian’s results — squarely, defiantly, unambiguously — support Duesberg’s hypothesis that AIDS ain’t a sexually-transmitted disease.

    Then you’ll have no problem stating that herpes isn’t an STD either.

    p.s. Dale answered my questions above (I’ll comment on those after lunch). Why won’t you?

    Dale’s more generous than I am. Your questions are boring to me, and you’ve not answered any of mine. I’m selfish that way.

  24. #24 Dave S.
    February 23, 2006

    Barnes writes:

    The folks who didn’t use condoms failed to contract the virus as well. (Darn, back to the drawing board.)

    Why? Does the fact that many people who drive drunk don’t end up dying in a car wreck mean that it’s safe to drink and drive?

  25. #25 Dave S.
    February 23, 2006

    Barnes, Hank writes:

    The study is called, the “Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten-year study.”

    Reading beyond the title, all the way to the first sentence in the abstract you find …

    To examine rates of and risk factors for heterosexual transmission of human immunodeficiency virus (HIV)…

    Clearly the question of whether or not HIV can be transmitted by heterosexual sexual contact at all was not the issue.

  26. #26 Guitar Eddie
    February 23, 2006

    “The folks who didn’t use condoms failed to contract the virus as well. (Darn, back to the drawing board.)”

    Not so, Mr. Barnes. Remember the empirical universe operates probabalistically – if you do the “horizontal mambo” with an HIV+ person, you are more likely to get the virus. Your odds of winning increase if you do the dance without a condom.

    GE

  27. #27 Tara
    February 23, 2006

    One more thing:

    Every human being is born, every human being has sex.

    Well, now, that latter just ain’t true, now is it? What’s the rate of HIV infection in virgin priests and nuns? By your examples, it shouldn’t be any different than the population at large, if they acquired it at birth.

  28. #28 Darin Brown
    February 23, 2006

    (Y’know, influenza does this as well–most influenza deaths aren’t due primarily to the influenza virus, but to secondary bacterial infections that set into viral-damaged lungs: just like the secondary infections that result from HIV). But no one criticizes influenza simply because it’s associated with so many different species of secondary infections.

    Whoa, you’re pulling out influenza now. That’s kind of a stretch. MILLIONS of people in the US get influenza every year, and only a few thousand die from it. Most of these (not all, I know) occur in very young people, older people, or people with chronic medical conditions or pre-existing immunodeficiency. In other words, these people are generally ALREADY beat up or immunocompromised before the influenza, and they are people you would already suspect to be more at risk, unlike HIV, which is supposed to be able to strike “anyone”.

  29. #29 Darin Brown
    February 23, 2006

    Tara,

    You still haven’t answered how HIV kills T cells when it doesn’t even infect cells fast enough to cover regeneration. Nor how HIV causes clinical AIDS when it’s inactive.

  30. #30 Tara
    February 23, 2006

    Whoa, you’re pulling out influenza now. That’s kind of a stretch. MILLIONS of people in the US get influenza every year, and only a few thousand die from it. Most of these (not all, I know) occur in very young people, older people, or people with chronic medical conditions or pre-existing immunodeficiency. In other words, these people are generally ALREADY beat up or immunocompromised before the influenza, and they are people you would already suspect to be more at risk, unlike HIV, which is supposed to be able to strike “anyone”.

    First, you totally missed the point of my bringing up influenza. Y’see, very few people die from “influenza.” They die from the secondary bacterial infections that set in as a result of influenza-damaged cells in their lungs, just as HIV-infected individuals die from secondary infections resulting from an HIV-damaged immune system. And both of them can strike “anyone.” Look at the age-adjusted mortality curve for the 1918 influenza virus.

    Second, as I mentioned and you didn’t address, the idea that there’s some magical symptom restriction for specific pathogens is just bunk. Again, take influenza. Some cases of recent H5N1 infections haven’t even presented with influenza-like illness–they had severe diarrhea, fer crimeny’s sake. I’m sure you’re an excellent mathematician, Darin, but as I told you before, you really need to bone up more on infectious disease. It’s an immensely interesting subject once you break out of the “this virus can only do this, this bacterium can only do that” box.

    You still haven’t answered how HIV kills T cells when it doesn’t even infect cells fast enough to cover regeneration. Nor how HIV causes clinical AIDS when it’s inactive.

    Like I told Hank, I’m bored of answering your questions. You answer mine for a change. Just from my last post to you, you’ve still not touched:

    Still want to say “retroviruses can’t kill cells?”

    Why does HIV get special treatment?

    Isn’t anyone going to answer why herpes can’t be a STD, according to your criteria?

    Your move. Surprise me for a change.

  31. #31 Hank Barnes
    February 23, 2006

    Oh my! … it’s a mutating attack from all angles:) (Tara, Dale, Dave S, Orac, some dude name Tony L, Guitar Eddie)

    Or, I reckon, a swarm of gnats to be swatted.

    I’d like to single out Dale, though. In all seriousness, he has (without all this circumlocution, snark, obfuscation, and evasion) answered the questions, and for that, he deserves genuine credit.

    The best answer, of course, is No. 7:

    7. When did you first learn of the existence of the Padian study?

    I think I learned about it from you Hank.

    I might frame this — Hey, you take what you can get:)

    Gentlemen, Doctors, Scholars:

    Had Padian’s prospective study resulted in, say, 125/175 seroconversions (71%) or 100/175 (57%) or 42/175 (24%), you would be touting Padian as evidence that HIV was in fact heterosexually transmissible, and, hence, that AIDS is an infectious disease. (As would I).

    Padian, herself, starts out her paper with the following:

    As of June 1996, a total of 44,980 cases (8 percent) of AIDS among adults and adolescents have been reported to the CDC that were attributed to heterosexual contact with a high risk or infected partner.

    An honest scientist, conducting an honest study, in hopes of honestly trying to explain this phenomenom known as AIDS, in hopes of honestly helping and/or curing patients would — after obtaining zero seroconversions — pause (one would hope), reflect on this result, and seriously question the afore-mentioned 44,980 cases attributable to heterosexual contact. Perhaps, they would also question what they believe about AIDS and why they believe it. (As I did).

    They might also question how the infinitesimal risk of heterosexual transmission explains how 1 million people in US are infected with HIV, and, why Padian’s data doesn’t strongly suggest that these 1 million HIV+ were simply born with said retrovirus.

    We might go back and forth all day on this, but I can confidently state 4 things:

    1. Y’all were ignorant of the Padian study for 9 years.

    2. Y’all are furiously trying to disregard/reinterpret its findings so that it is harmonized with your pre-existing beliefs and biases.

    3. The one fellow who figured all this out well before any of you, is Dr. Peter Duesberg, National Academy of Science.

    4. And you hate Dr. Duesberg, because he exposed y’all as absolute poseurs and charlatans on this topic.

    To conclude: We know that Dr. Hwang Woo Suk of stem cell frame is a fraud. We also know that Dr Robert Gallo of AIDS fame is a fraud, too.

    Does that mean our scientific system is corrupted on the whole? I don’t know. But the question remains: Is there any more fraud we should know about?

    Hammerin’ Hank Barnes

  32. #32 Gene
    February 23, 2006

    Perhaps this is addressed in the paper, but I see a major issue with looking at seroconverion in discordant couples. Given that HIV transmission rates vary by individual (both for being infected and for infecting someone else). Then the discordant couples will be enriched for those where seroconversion is less likely than the general population, since couples were transmission is most likely are the couples most likely to have already experienced seroconversion before the study began and would thus be excluded. The greater the variance in individuals, the stronger would be this effect. And we know that some people are highly resistant to HIV infection.

    Only couples were both partners were HIV-negative before the study began, and one partner became infected during the study would be useful for gauging HIV-transmission rates within couples.

  33. #33 Tara
    February 23, 2006

    Gene,

    That’s a good point, and no, they don’t mention it.

    Only couples were both partners were HIV-negative before the study began, and one partner became infected during the study would be useful for gauging HIV-transmission rates within couples.

    You’d need a huge cohort, though. More realistic would be to enroll a couple as soon as one partner is found to seroconvert so that at least it’s known that it’s early in the infection, and go from there. Swabs could also be taken to *really* look at only transmission, since the Padian study is looking at transmission + seroconversion, two related but distinct processes.

  34. #34 Harvey Bialy
    February 23, 2006

    Now George Kaplan informs me that he cannot post to this thread, nor can Darwin nor Mr. Barnes.

    I trust this is only a glitch….cf. “fair debate” etc. above.

  35. #35 harvey Bialy
    February 23, 2006

    Glad it was only a temp. glitch. Carry on. Don’t mind me.

  36. #36 Hank Barnes
    February 23, 2006

    Well, I guess I have been un-banned. Sorry for the multiple posts.

    Barnes

  37. #37 Tara
    February 23, 2006

    You were never banned in the first place. Posts with multiple links get sent to the junk box, from which I have to move them. As I said, email me rather than assuming I banned anyone. Sheesh, if I’ve let all Harvey’s self-promotion posts stand, there’s no reason I’d ban someone I simply disagree with.

  38. #38 Hank Barnes
    February 23, 2006

    ..there’s no reason I’d ban someone I simply disagree with.

    Well, good. It’s all squared away then.

    Barnes, Hank

  39. #39 Tara
    February 23, 2006

    In the meantime, Hank, you gonna answer any questions, or just keep repeating the same ol’ schtick? At least Harvey’s interesting with his creative insults.

    To conclude: We know that Dr. Hwang Woo Suk of stem cell frame is a fraud. We also know that Dr Robert Gallo of AIDS fame is a fraud, too.

    Y’know, creationists claim Darwin was a fraud too. Even if all that’s true, does it disprove evolution?

  40. #40 Hank Barnes
    February 23, 2006

    In the meantime, Hank, you gonna answer any questions, or just keep repeating the same ol’ schtick?

    Sure, I’ll answer your questions. What are they? Or do I have to sift thru your smorgasborg and discern which ones are rhetorical?

    Ask away

    At least Harvey’s interesting with his creative insults

    I haven’t insulted a solitary person on this thread — except I did call Ivan a “dumbass”.

    Y’know, creationists claim Darwin was a fraud too. Even if all that’s true, does it disprove evolution?

    Well, I ain’t a creationist, and think Darwin was a great scientist, so the matter is moot.

    Darwin once said:

    If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case.

    Often, creationists or ID guys omit the last sentence, but I think Charles Darwin has it exactly right here: A falisifiable theory, that has not been falsified. Beautiful.

    Which reminds me:

    1. If you contend that HIV is the sole cause of AIDS, what evidence would falsify this causal connection?

    Hank “the Tank” Barnes

  41. #41 Tara
    February 23, 2006

    One quickie then I’m out for the evening–

    Sure, I’ll answer your questions. What are they? Or do I have to sift thru your smorgasborg and discern which ones are rhetorical?

    Ask away

    Any I posed above to Darin would be a fine starting point. Is herpes a STD, since it has a similar transmission rate as HIV? Why the special treatment for HIV in the first place? Do you realize by pushing the objections you do, that you’re denying not only HIV causation of AIDS, but essentially the entire germ theory of disease?

    I haven’t insulted a solitary person on this thread — except I did call Ivan a “dumbass”.

    And did I say you were Harvey?

    Well, I ain’t a creationist, and think Darwin was a great scientist, so the matter is moot.

    Um, no, it’s not. You miss my point. You’re trying to use Gallo’s sketchy image as a reason to dismiss HIV causation of AIDS, just as creationists use Darwin’s deconversion or other personal matters to dismiss evolution. Beautiful example of a classic ad hominem. I’d rate it a 8.5 since you botched the landing.

    Which reminds me:

    1. If you contend that HIV is the sole cause of AIDS, what evidence would falsify this causal connection?

    I already discussed this. Like I said, you’re boring me.

    Hopefully your dance team is back with some new material in the morning. (And please, if a comment doesn’t get published, don’t resubmit it a thousand times. I’ll approve it when I get in tomorrow morning).

    Ciao.

  42. #42 Tara
    February 23, 2006

    One last question–Hank, what would it take to get you to accept that HIV is the cause of AIDS?

    Okay, really out…

  43. #43 Hank Barnes
    February 23, 2006

    Tara’s Questions:

    1. Is herpes a STD, since it has a similar transmission rate as HIV?

    Yes, Herpes is an STD. I don’t know that it has similar transmission rate at HIV. Nobody dies from Herpes. The “anti-viral” given to Herpes patients, Acyclovir, is prescribed for 3 or 4 days, only during active infection. Not for life. Not when the person is asymptomatic. Not as a prophylactic. By the way, Gertrude Elion was very hot during her younger years.

    Why the special treatment for HIV in the first place?

    Huh? I don’t know the “special treatment” to which you refer. Medical treatment? Scientific treatment? Cultural treatment? What are you trying to say?

    Do you realize by pushing the objections you do, that you’re denying not only HIV causation of AIDS, but essentially the entire germ theory of disease?

    No, you are grossly wrong. The germ theory is alive and well. Small pox is caused by a germ, the variola virus. Said virus has been conquered by a vaccine.

    The hard part is discerning between a pathogenic germ and a passenger germ. There are millions of passenger germs infecting healthy people, that do absolutely nothing.

    Now, quit dodging and answer my questions:

    1. Is the Padian study, the longest and largest epidemiological study of the heterosexual transmission of HIV?

    2. In the prospective study (the one that mattered), How come not one uninfected partner who had sex with an HIV+ person contracted the virus?

    3. How come not one uninfected partner contracted the virus from anal sex?

    4. What was Padian’s a priori hypothesis before she embarked on the prospective study?

    5. Don’t the Padian results lend greater support to the hypothesis that HIV is a garden-variety endogenous retrovirus, rather than a sexually-transmitted pathogenic killer of t-cells?

    6. The scientific community declared that AIDS was a sexually-transmitted disease by the mid-1980′s. Upon what epidemiological study was this based?

    7. When did you first learn of the existence of the Padian study?

    Bonus Question:

    8. If you contend that HIV is the sole cause of AIDS, what evidence would falsify this causal connection?

  44. #44 Dale
    February 23, 2006

    HB,

    you asked 7 questions and I answered them. Your response to my answer :
    “And you hate Dr. Duesberg, because he exposed y’all as absolute poseurs and charlatans on this topic.”

    That doesn’t even really qualify as an ad hominem attack – it’s more of a non sequitur.
    Perhaps if you’d address my responses to your questions, Tara would be more inclined to answer your questions herself.

  45. #45 Dale
    February 23, 2006

    HB’s answer to Tara’s question “1. Is herpes a STD, since it has a similar transmission rate as HIV?
    Yes, Herpes is an STD. I don’t know that it has similar transmission rate at HIV. Nobody dies from Herpes. The “anti-viral” given to Herpes patients, Acyclovir, is prescribed for 3 or 4 days, only during active infection. Not for life. Not when the person is asymptomatic. Not as a prophylactic. By the way, Gertrude Elion was very hot during her younger years.”

    Neither the difference in mortality nor differences in treatment between HIV and herpes are relevant to the definition of an STD.

  46. #46 Hank Barnes
    February 23, 2006

    Dale,

    Hey, I singled you out for credit above– so I don’t place you in the “poseur” or “charlatan” group.

    Hank & Dale’s Q & A:

    1. Is the Padian study, the longest and largest epidemiological study of the heterosexual transmission of HIV?

    It may have been at the time but there are now studies in the literature, like the one Chris Noble linked, that are larger.

    Grade: B-. “may have been” is sketchy, better answer is “Yes”

    2. In the prospective study (the one that mattered), How come not one uninfected partner who had sex with an HIV+ person contracted the virus?

    There is no reason to believe the prospective study is any more important than the retrospective study and in fact one might argue it is less important since this and other studies suggest that awareness of HIV status modifies sexual behaviour in ways that will reduce the probability of viral transmission. As to why no seroconversions were observed in this study, ask Darin Brown to explain statistical inference to you.

    Grade: D+. The better answer is that HIV is probably an endogenous retrovirus, that is passed from mother-to-child at birth, and resides in the cell doing nothing. Remember, it is estimated that 8% of the human genome consists of viral DNA incorporated therein.

    3. How come not one uninfected partner contracted the virus from anal sex?

    See the answer to #2.

    Grade: F. Merely repeating an evasive non-answer. Surely, at least one of the 38% of folks who engaged in anal sex, should have seroconverted, no? (See, Padian, Table 3, page 355.)

    4. What was Padian’s a priori hypothesis before she embarked on the prospective study?

    Her stated hypothesis was that there would be factors associated with increased probability of heterosexual viral transmission.

    Grade: C-. The hypothesis was (or should have been) that: (1) Heterosexual intercourse between HIV+ and uninfected persons would result in the latter seroconverting at X%.

    5. Don’t the Padian results lend greater support to the hypothesis that HIV is a garden-variety endogenous retrovirus, rather than a sexually-transmitted pathogenic killer of t-cells?

    No they don’t because (1) they can’t be taken in isolation from other epidemiological studies and (2) epidemiological studies can’t be used to dismiss case reports demonstrating heterosexual transmission.

    Grade: F. Of course it does. At least 1 uninfected person should have seroconverted after 6-10 years, doncha think? If a large number had seroconverted, that would have supported the conventional theory, wouldn’t it?

    6. The scientific community declared that AIDS was a sexually-transmitted disease by the mid-1980′s. Upon what epidemiological study was this based?

    Based on case reports, contact tracing and data being compiled by the CDC. Also based on what was being learned about HIV.

    Grade: F. Epidemiology trumps case reports, which you failed to name anyway.

    7. When did you first learn of the existence of the Padian study?

    I think I learned about it from you Hank.

    Grade: A+ :)

    Bonus question to Dale:

    8. If you contend that HIV is the sole cause of AIDS, what evidence would falsify this causal connection?

    Barnes, Hank

  47. #47 Harvey Bialy
    February 23, 2006

    Tara,

    You asked above about Visna virus. I suggest you take another look at this from the 1989 PNAS review of Duesberg that you claim to have not only read but studied.

    “In an effort to rationalize the long intervals between infection and AIDS, HIV has been classified as a slow virus, or lentivirus (40), a type of retrovirus that is thought to cause disease only after long incubation periods (129). Yet there are no “slow” viruses. Since viral nucleic acids and proteins are synthesized by the cell, viruses must replicate as fast or faster than cells (i.e., within hours or days) to survive (86, 87).

    Nevertheless, as pathogens, viruses may be (i) fast in
    acute infections that involve many actively infected cells, (ii) slow in subacute infections that involve moderate numbers of actively infected cells, or (iii) asymptomatic and latent. Retroviruses provide examples of each different pathogenic role. Acute infections with the “slow” Visna/Maedi retrovirus of sheep, a lentivirus, rapidly cause pneumonia (131), and those with equine anemia lentivirus cause fever and anemia within days or weeks of infection (132). Such infections typically generate titers of 104 to 105 infectious units per milliliter or gram of tissue (132, 133). The caprine arthritis-encephalitis lentivirus is also pathogenic within 2 months of inoculation (134). Acute infections with other retroviruses also rapidly cause debilitating diseases or cancers (23). This includes retrovirus infections that are now considered to be animal models of AIDS, termed simian or feline AIDS (12, 23, 30, 111, 135). Unlike HIV in AIDS, these viruses are all very active when they cause diseases, and the respective diseases appear shortly after infection (23). In rare cases, when antiviral immunity fails to restrict Visna/Maedi or other retroviruses, they persist as subacute symptomatic infections (3, 86, 129, 133). Under these conditions,
    Visna/Maedi virus causes a slow, progressive pulmonary
    disease (129, 133, 136) by chronically infecting a
    moderate number of cells that produce moderate titers of
    102 to 105 virus particles per gram of tissue (136). However, in over 99% of all Visna/Maedi or caprine arthritisencephalitis virus infections, and in most equine anemia virus infections, the retrovirus is either eliminated or restricted to latency by immunity, and hence asymptomatic, exactly like almost all other retroviruses in mice, chickens, cats, and other animals (23). For instance, 30–50% of all healthy sheep in the U.S., Holland, and Germany have asymptomatic Visna/Maedi virus infections (129, 137, 138), and 80% of healthy goats in the U.S. have asymptomatic caprine arthritis-encephalitis virus infections (133) in the presence of antiviral immunity.”

    P.S. The *great* virologist Robert Gallo promised in the pages of the very same issue of the Proceedings to write a full refutation of all of Peter’s arguemnts. We are still waiting for the first installment.

  48. #48 Pharma Bawd
    February 23, 2006

    Hank,

    Valacyclovir, the L-valyl ester of acyclovir, is now prescribed for prevention of recurrent episodes of herpes. http://www.valtrex.com/hcp/suppression.html

    Famciclovir is also prescribed for suppression of herpes. Prior to these two drugs acyclovir was prescribed for suppression in some cases, however Valacyclovir and Famciclovir are far more efffective antivirals for suppressive therapy because of higher bioavailability, fewer daily doses, etc.

    Why the special treatment for HIV in the first place?

    She means, why deny that HIV/AIDS is an STD based on a low transmission rate, when that transmission rate is very similar to the rate found with genital herpes? This has come up several times now, it’s time to respond to this point.

    On a related vein, you do realize that decades of research has not yet produced an effective vaccine against HSV-1 or HSV-2? Is it your contention that any disease for which a vaccine has not been developed is not caused by a virus? Or does this “special treatment”, again, just apply to HIV/AIDS?

    Regarding your questions I’ll concur with Dale’s answers and add to number six:

    If HIV is a harmless passenger virus passed along at birth, why is there such a high degree of sequence similarity of the virus between donor/recipient pairs?
    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1376536&dopt=Abstract

    On #7 I also read your comment at Dean’s World. I have not read the Padian paper, if anyone can email me a PDF I would love to take a look at it. Otherwise it will be a week or two before I get to the library.

  49. #49 Karen Lynne Lambert
    February 23, 2006

    If HIV is not the cause of AIDS, then, what is?? Because HIV-Negative AIDS patients are not prescribed any toxic antiretroviral medications. Nobody even acknowledges our idiopathic illnesses, never mind to care enough to want to drug us…

    I believe that to systemically diagnosis my undiagnosed infectious pathogen — and millions of ailing, med-free, immunosuppressed CFS patients — will be to answer the next-most, sequentially-logical question: What is the cause of Chronic Fatigue Syndrome (CFS)?

    Orthodoxy: HIV/AIDS
    AIDS Myth: HIV?AIDS
    Proposal: CFS->AIDS

  50. #50 Chris Noble
    February 23, 2006

    Just a few more points.

    It is normal Denialist rhetoric to claim that Padian’s study was designed to test the hypothesis that HIV is sexually transmitted. It wasn’t.

    The cohort that Padian and others studied produced a number of papers not just one. If you bother to read these other papers it is obvious that Padian’s primary goal was to reduce transmission of HIV. She in fact attempted to stop all transmission of HIV by modification of behaviour – safe sex etc. This is completely the opposite strategy than tring to prove HIV is sexually transmitted.

    Part of her research was to try to ascertain risk factors for transmission and rough estimates for transmission risk. These are estimates. The study was not sufficiently well designed to obtain accurate measures. A study that was well designed to measure transmission risk would never get ethics approval.

    In case anybody has any misunderstandings monogamous couples do not create epidemics.

    I will quote Duesberg here: “In order to survive, a virus must infect new hosts, which it does most readily when it is at the highest titer (153). In the case of HIV, this would be before antiviral immunity, or 1 to 2 months after infection (69).”

    Anybody that does not attempt to understand the Padian study in the light of this comment and the study I posted is simply being dishonest.

    At this point I would also introduce the concept of reproduction number in epidemiology. Ronald Gray who has been studying the Rakai cohort has used the transmission risk values (that Denialists claim can’t possibly cause an epidemic) together with frequency of sexual intercourse and other factors to calculate a reproduction number for the Rakai cohort that is approximately 1.44. This value is consistent with the observed incidence of HIV in this cohort. Clearly the estimated transmission risks are consistent with an epidemic (R0 > 1).

    I’ll also restate one of my questions. Even if we accept the 1/3000 value for the prevalence of HIV in the US population (240,000,000 / 3000 = 80,000 which is a long way off the 1 million figure. All of the CDC reports since 1985 show that the majority of HIV infected are in high risk groups and are predominantly male) then simple mathematics tells us that for a 50% efficient perinatal transmission that the prevalence for the previous generation must be 2/3000. For the generation before that 4/3000. If we keep on going we can extrapolate back n generations to obtain a prevalence of (2^n)/3000. If we go back 12 generations then more than 100% of the population must have been carrying the “harmless passenger” virus.

    Denialist love asking questions yet none of them ever provide coherent answers to simple questions. How can a “harmless retrovirus” with a 50% efficient perinatal transmission rate survive by perinatal transmission?

    The answer to most people is that it can’t. Sexual transmission is a major factor. In the SFMHC where prevalence rose from 4% to 68% in a period of 6 years it is the obviously a very major factor. IVDU is also a likely factor. Perinatal transmission is not a major factor.

    The evidence is simply and clearly against Duesberg’s “harmless passenger virus” theory. Duesberg claims that the estimates put out by the CDC for the prevalence of HIV in the US demonstrate that HIV is a passenger virus with a constant and stable prevalence. What Duesberg does not mention is that the CDC estimates are broken down into risk categories and that right from 1985 the major risk groups are MSM and IVDUs. The virus has never been uniformly distributed throughout the population. Duesberg cannot have it both ways. He can’t claim on the one hand that HIV has had a constant prevalence of roughly 1 million since 1985 and simultaneously claim that HIV is equally distributed amongst the sexes.

    If Duesberg could come up with a consistent and coherent theory that did not conflict with mountains of data then people would take him seriously. He hasn’t and he isn’t.

  51. #51 Darin Brown
    February 23, 2006

    Isn’t anyone going to answer why herpes can’t be a STD, according to your criteria?

    Okay, I have the HSV-2 paper in front of me. The purpose of the study was to see how effective condoms were in preventing transmission of HSV-2. I don’t think the paper warrants a comparison to say suddently that HSV-2 isn’t sexually transmitted, though.

    First of all, the comparison to HIV doesn’t make sense at face value. Right in the first paragraph, the authors say, “Recent estimates indicate that 22% of persons who are older than 12 years in the US are infected with HSV-2. Except for rare perinatal acquisition, HSV-2 infections are acquired by contact with infected secretions during sexual encounters.” So, immediately one wonders how an infection can be present in 22% of persons older than 12 years, not be perinatally acquired, and only have 1/1200 sexual transmission rate? Something must be up. Pigs can’t fly.

    The first BIG thing that pops out for me is that the couples were counselled to avoid sex when the infected partner had lesions! “At each visit, clinicians counseled the participants to abstain from sex if the source partner had a genital herpes recurrence and to use condoms at all other times.” And also “Furthermore, the proportion of participants having sex when the source partner had genital lesions declined from 20% to 13% over the study period. While sex when lesions were present was rare, it was reported in the interval preceding acquisition of HSV-2 by 23% of the subjects who seroconverted.”

    In other words, they were specifically counselled not to go dancing when the infected partner had lesions, and they not only got the message and followed directions, they got the message even better as time went on.

    Also note, many of the infected partners were on acyclovir, which reduces transmission. And all couples were in long-term (> 6 months) relationships prior to entry, meaning that they had most likely already passed the stage when transmission is the most likely to occur!!

    Near the end of the study, the authors note, “Our study population differs from most HSV-2 discordant couples in several important aspects. First, in this clinical trial both partners knew that one had genital herpes and one was at risk. This knowledge of being at risk, and sufficient concern for transmission to enroll in a vaccine study, were likely to be associated with a lower risk of transmission. Second, eligibility for this study required that couples had been together for at least 6 months. A previous study has shown that the median duration of relationship prior to acquisition of genital herpes is 3 months. Thus, the period in a relationship of highest risk for transmission was not included in this study. Our finding that the rate of acquisition was highest in the first month of follow-up supports this observation.”

    And in the conclusion in the abstract, “Changes in sexual behaviour, correlated with counselling about avoiding sex when a partner has lesions, were associated with reduction in HSV-2 acquisition over time.”

    So, it seems to me the authors’ own comparison to HIV is negated by their own observations. Nice try, though.

  52. #52 TonyL
    February 23, 2006

    I’ll tell you what. Although I am not an epidemiologist, I can answer several of your questions based on the responses you seem to be ignoring. (Including Tara’s initial post)

    1. Is the Padian study, the longest and largest epidemiological study of the heterosexual transmission of HIV?

    No. It was a 175 couple 3000 couple month study. The Rakai paper was a 6700 couple month study and the Hugonnet study followed 1802 couples. So clearly, the Padian study is not the longest, nor largest study.

    2. In the prospective study (the one that mattered), How come not one uninfected partner who had sex with an HIV+ person contracted the virus?

    several possible reasons. Unlike your initial characterizations of the study, the participants were not having “unlimited, abundant, (dare I even say wild and kinky?) sexual acts over 10 years”. If you had bothered to read Tara’s post, you would have seen her point out that the paper claimed “Abstention increased from 0% at baseline to 14.5% in the final follow-up visit; consistent condom use increased from 32.3% to 74%, and any anal intercourse decreased from 37.9% to 8.1%”. Note that the condom rate is for “consistant condom use” meaning that the inconsistant condom rate could be much higher. So the majority of the couples were not engaging in particularly risky types of sex. Couple this with the fact that few of the couples were followed for more than a year and the null result is not particularly surprizing.

    3. How come not one uninfected partner contracted the virus from anal sex?

    Once again, you missed the part of the paper that pointed out “anal intercourse decreased from 37.9% to 8.1%”. Which means that the sample size was SMALL. Furthermore, it’s not clear that the 8.1% that had anal sex throughout their participation did not use condoms during anal sex. Finally, based on the short time for which any given couple was followed, that’s a pretty damn small study on the chances of transmitting HIV through anal sex. Basically, this data is insufficient to make the claim that anal sex does not transmit HIV.

    4. What was Padian’s a priori hypothesis before she embarked on the prospective study?

    Irrelevant. Unless you have evidence that this somehow caused her to misrepresent the data, or you have a good reason to claim that her conclusions don’t match the data.

    5. Don’t the Padian results lend greater support to the hypothesis that HIV is a garden-variety endogenous retrovirus, rather than a sexually-transmitted pathogenic killer of t-cells?

    No. There is not enough information in that paper to jump to such a conclusion. At best, you could say that it lends support to a low rate of transmission. But hey, I’m an experimentalist who doesn’t like to claim more than the data tells me.

    6. The scientific community declared that AIDS was a sexually-transmitted disease by the mid-1980′s. Upon what epidemiological study was this based?

    Well, this hasn’t been answered on this thread yet.

    7. When did you first learn of the existence of the Padian study?

    Well, since I don’t study HIV/AIDS, when I read this blog. But that question wasn’t really adressed to me. Either way, it’s pretty irrelevent, since the paper does not say what you initially claimed it said. 1. It did not follow 175 couples for 10 years. 2. It did not claim that the couples were having wild kinky sex. (quite the opposite) 3. It is not the largest epidemiological study of its kind. What else did you get wrong about the sudy?

  53. #53 Dale
    February 23, 2006

    HB,

    In response to your response

    HB:The better answer is that HIV is probably an endogenous retrovirus, that is passed from mother-to-child at birth, and resides in the cell doing nothing. Remember, it is estimated that 8% of the human genome consists of viral DNA incorporated therein.

    Dale: Based on the literature you are incorrect. There is no evidence that HIV is an endogenous retrovirus nor that the majority of seroconverted adults acquired it at birth. The presence of “viral DNA” in the human genome does not account for the presence of HIV sequences. Want to try again.

    HB: Merely repeating an evasive non-answer. Surely, at least one of the 38% of folks who engaged in anal sex, should have seroconverted, no? (See, Padian, Table 3, page 355.)”

    Dale: Wrong answer HB. For it to be correct we would have to have a p value for seroconversion rate per anal sex act and at least a crude estimate of the number of such acts engaged in by these 38% of folks.

    HB: The hypothesis was (or should have been) that: (1) Heterosexual intercourse between HIV+ and uninfected persons would result in the latter seroconverting at X%.

    Dale: You didn’t ask what the hypothesis should have been but what the hypothesis WAS. Wrong again HB.

    HB:Of course it does. At least 1 uninfected person should have seroconverted after 6-10 years, doncha think? If a large number had seroconverted, that would have supported the conventional theory, wouldn’t it?

    Dale: Wrong both on the facts and the expectation. The duration of the study was ~3000 couple months for 175 serodiscordant couples. The longest any couple was studied was 6 years. Whether one would expect at least one uninfected person to seroconvert would depend on the probability of hetersexual transmission which as ‘Darin Brown’, Ph.D. mathematician, has pointed out is about the same in this study as in others in the literature. The conventional theory doesn’t say anything about the rate of heterosexual transmission, only that it exists.

    HB: Epidemiology trumps case reports, which you failed to name anyway.

    Dale: You are partially correct on this one. I didn’t cite the literature describing case reports. But you are wrong that epidemiology trumps case reports. Epidemiology is used to estimate frequencies of heterosexual transmission; case reports and contact tracing verify its existence.

    Overall I’d have to give you a failing grade and suggest that you read the literature before attempting a make up test.

  54. #54 Darin Brown
    February 23, 2006

    One last question–Hank, what would it take to get you to accept that HIV is the cause of AIDS?

    I’ll take a quick bite.

    1. Show me that HIV infects enough T cells to cover their regeneration.

    2. Show me that HIV is active at the time of clinical progression to AIDS.

    3. Show me that degree of pathogenicity is proportional to the number of infected cells.

    4. Show me that HIV is always present in the affected (diseased) tissue at the time of clinical progression to AIDS.

    5. Show me that the HIV/AIDS hypothesis can predict what diseases a patient will get. (Note: recalling your comparison to strep…in that case, the type of symptom can be determined to some degree by the location of infection, e.g. That’s an example of what I’m asking for.)

    6. Show me that the HIV/AIDS hypothesis can explain epidemiological paradoxes, e.g. why Kaposi’s sarcoma is extremely common in homosexual AIDS patients but virtually non-existent in hemophiliacs, and other cases where the percent incidence of AIDS diseases are not equal across different risk groups.

    For starters.

  55. #55 Chris Noble
    February 23, 2006

    Denialists like to claim that retroviruses do not kill cells.

    This is not supported by the evidence.

    There are many papers that describe the effect of SHIV chimeras in macaques.

    There are highly pathogenic strains such as SHIV89.6p that reproducibly cause rapid CD4+ loss in macaques.

    Arthur C Clarke said “When an eminent but elderly scientist says something is possible, he is probably right, but when an eminent but elderly scientist says something is impossible, he is probably wrong.”

    When Duesberg or anyone else says that retroviruses cannot cause the loss of CD4+ cells he is more than just probably wrong he is definitely wrong. The evidence shows that they do.

  56. #56 Harvey Bialy
    February 23, 2006

    Two bialystockers worth. Before Dr. Smith or one of the other docs commenting here come with “viral loads” as somehow being the modern day equivalent of the infectious titres Duesberg reports above, let me remind you that these viral load measurments were made famous by Ho and Wei in the very famous Nature papers of 1996 that Tara cannot be expected to remember.

    On can decudece from their methodology that the PCR units they report are 60,000 times as sensitive as traditional measures of infectious virus. Even Dale can divide 100,000 (the highest viral oads reported in their landmark papers) and discover that these terrible viral loads correspond to 1.7 infectious particles per ml of serum. Seems like a potent chemical is just what the doctor ordered to eliminate this ferocious amount of t-cell eating virus.

  57. #57 Chris Noble
    February 23, 2006

    Darin Brown wrote:

    The first BIG thing that pops out for me is that the couples were counselled to avoid sex when the infected partner had lesions!

    Ahhh. Padian counselled members of her cohort to reduce high risk behaviour.

    Thanks for emphasising that Padian’s study cannot be used to argue that HIV is not sexually transmitted.

  58. #58 Pharma Bawd
    February 23, 2006

    Dr. Bialy,

    Tara brought up the visna virus to refute Darin’s claim that retroviruses cannot kill cells. Nothing you’ve quoted from Duesberg above addresses that point in any way.

    Well, I take that back. Duesberg himself refutes Darin?s claim when he mentions the examples of FIV and SIV, both of which are retroviruses able to induce cell death. This is not particularly interesting as Darin has already established himself as a better mathematician than biologist. The interesting thing is this:

    ? But, retroviruses do not kill cells because they depend on
    viable cells for the replication of their RNA from viral
    DNA integrated into cellular DNA (4, 25). Thus, T-cells
    infected in vitro thrive, and those patented to mass-produce
    HIV for the detection of HIV antibodies and diagnosis
    of AIDS are immortal (9?15)!”

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

    So which is it? Can a retrovirus trigger cell death? Yes or no?

    Then Regarding the Duesberg passage you quote:

    ?Since viral nucleic acids and proteins are synthesized by the cell, viruses must replicate as fast or faster than cells (i.e., within hours or days) to survive (86, 87).?

    An HIV pro-virus integrated into the genome will, by definition, replicate as fast as the cellular DNA will it not? Why is latency by HIV proviruses followed by reactivation at a later, even much later, time any more improbable/impossible for HIV than it is for herpes viruses?

    We know that VZV will emerge from very lengthy periods of latency to produce shingles late in life, even in the presence of protective antibodies. Why does Duesberg argue that HIV cannot do the same thing.

  59. #59 Dale
    February 23, 2006

    Darin Brown asks:
    1. Show me that HIV infects enough T cells to cover their regeneration.
    2. Show me that HIV is active at the time of clinical progression to AIDS.
    3. Show me that degree of pathogenicity is proportional to the number of infected cells.
    4. Show me that HIV is always present in the affected (diseased) tissue at the time of clinical progression to AIDS.
    5. Show me that the HIV/AIDS hypothesis can predict what diseases a patient will get. (Note: recalling your comparison to strep…in that case, the type of symptom can be determined to some degree by the location of infection, e.g. That’s an example of what I’m asking for.)
    6. Show me that the HIV/AIDS hypothesis can explain epidemiological paradoxes, e.g. why Kaposi’s sarcoma is extremely common in homosexual AIDS patients but virtually non-existent in hemophiliacs, and other cases where the percent incidence of AIDS diseases are not equal across different risk groups.

    1. HIV doesn’t have to infect enough T cells to cover their regeneration. The observation is that HIV infection leads to progressive immunosuppression characterized by loss of a particular class of T cells. Some of that appears to be direct and some appears to be indirect. From HIV infection to progressive loss of CD4+ T cells involves a complex interaction between virus and immune system.

    2. HIV is actively replicating throughout HIV infection, your statement makes no sense.

    3. Again the statement makes no sense in terms of what is known about the progression of the disease. Cllinical symptoms of AIDS are determined by opportunistic infections acquired in immunosuppressed individuals and by progressive loss of a subset of T cells.

    4. And once again the statement makes no sense in terms of what is known about HIV or AIDS. HIV infects cells of the immune system. By infecting cells of the immune system it leads to a chronic and progressive immunosuppression. The presence of HIV in peripheral T cells isn’t relevant – the number of peripheral T cells is what is important in determining that HIV infection has progressed to AIDS.

    5. The HIV/AIDS hypothesis says that an individual infected with HIV in whom CD4+ cells have been depleted will be susceptible to opportunistic secondary infections. That is determined by the infectious agents to which they are exposed and will vary with environment.

    6. See the answer to #5. The opportunistic infectious agents an individual is exposed to will vary with environment.

  60. #60 Moment of Science
    February 23, 2006

    Darin,

    Re: number 6, I suggest you start here:

    http://momentofscience.blogspot.com/2006/02/everybodys-talking-about-herpes.html#links

    The JAMA article here:

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11779265&itool=pubmed_Abstract

    is a very nice hypothesis. Queries regarding KSHV in pubmed will prvide you ample and convincing reading material. I acknowledge transmission routes and etc. are still somewhat up in the air but it’s pretty convincing that a “founder effect” of KS among homosexuals at the initiation of the AIDS epidemic in America has led to the disproportianate numbers of KS among male homosexuals with AIDS in the US.

  61. #61 Chris Noble
    February 23, 2006

    Hank Barnes wrote:

    Grade: D+. The better answer is that HIV is probably an endogenous retrovirus, that is passed from mother-to-child at birth, and resides in the cell doing nothing. Remember, it is estimated that 8% of the human genome consists of viral DNA incorporated therein.

    This is so silly that not even Duesberg would say it.

    If HIV were an endogenous virus then:

    • a) Every single human cell would have proviral HIV DNA.
    • b) Tests for proviral HIV DNA would find it in every single human
    • c) Viral burden measurements would not vary
    • d) Genome sequences of HIV would be very constant
    • e) ….
  62. #62 Chris Noble
    February 24, 2006

    Another comment on the retroviruses can’t kill cells dogma.

    Duesberg cites this paper as evidence that HIV exists: A molecular clone of HTLV-III with biological activity. Fisher AG, Collalti E, Ratner L, Gallo RC, Wong-Staal F. Nature. 1985 Jul 18-24;316(6025):262-5. in his reply to the “Perth Group” Duesberg Defends Challenges to the Existence of HIV: Article 1 of 2 for Continuum . (As an aside it is worth noting that the editors of Continuum Jodie Wells and Huw Christie died of PCP and KS)

    Duesberg is keen to emphasise the molecular clone part of the article. I gather he was worried that the “HIV does not exist” claims of the Perthies made him look like a crackpot by association. What Duesberg fails to mention is the with biological activity part.

    Fig 2 nicely shows HIV killing T-cells compared to controls using plasmids with HTLV-I sequences or no retroviral sequences.

  63. #63 Chris Noble
    February 24, 2006

    Pharma Bawd wrote:

    This is not particularly interesting as Darin has already established himself as a better mathematician than biologist.

    I don’t rate someone who simultaneously claims that 1 million Americans were infected with HIV in 1985 and that the prevalence rate was 1/3000 as being a particularly good mathematician.

    VZV has a latent phase where very little replication occurs. Despite the confusion created by people like Darin Brown HIV exists as a chronic infection. There is viral replication during all periods of infection.

  64. #64 Chris Noble
    February 24, 2006

    The paper in which Ronald Gray uses the estimates of transmission risk from the Rakai cohort to model the epidemic is found here.

    Stochastic simulation of the impact of antiretroviral therapy and HIV vaccines on HIV transmission; Rakai, Uganda.

    I suspect that people that claim that transmission rates like this are incompatible with a sexually transmitted disease have never bothered to do any calculations.

  65. #65 Shygetz
    February 24, 2006

    One point that seems to be underemphasized here is the fact that the Padian study, by its very nature, selected against highly likely infection events. The vast majority (>90%) of the discordant couples had been monagamous for over a year, and (if I remember correctly)all had been previously sexually active. If transmission of the virus were likely in their particular coupling (due to the transmissibility of the particular viral strain, the susceptibility of the uninfected partner to infection, etc.), then that couple would have ceased to be discordant and excluded from the sample selection in the study due to infection by HIV early in their relationship. However, this portion of the population was excluded by experimental design, making this study invalid for studying overall rates of heterosexual transmission. If you wanted to study the sexual transmissibility of HIV, you would need a population of discordant couples that were not yet in a sexually active relationship, and follow them through their sexual activity, controling for the time of infection of the HIV+ participant and other risk factors.

  66. #66 Tara
    February 24, 2006

    Thank you, Hank, for at least trying to answer (some) of my questions.

    Yes, Herpes is an STD. I don’t know that it has similar transmission rate at HIV. Nobody dies from Herpes. The “anti-viral” given to Herpes patients, Acyclovir, is prescribed for 3 or 4 days, only during active infection. Not for life. Not when the person is asymptomatic. Not as a prophylactic.

    So wrong, I’m not quite sure where to begin. First, as mentioned, it doesn’t matter that “no one dies from herpes.” The question on the table is, “is herpes an STD?” I cited a study (several times, in fact) that showed that herpes had the same transmission rate as HIV. In fact, let me quote once again from that study:

    Our study revealed several new findings about the frequency and prevention of transmission of HSV-2 infection to sexual partners. Among monogamous couples with 1 partner who had known symptomatic genital herpes and 1 who was susceptible, we showed that the rate of transmission from men to women is 8.9/10 000 sex acts. This rate is similar to that seen with sexually acquired HIV.

    Now, as Darin mentioned, these people were cautioned about risks of transmission for herpes virus. Darin says this means we can’t compare the study to the Padian study, but as was already mentioned, the Padian study did the same thing! So you in no way can discount the herpes study because of this, unless you discount the Padian one as well.

    Checkmate. Y’all have backed yourselves into a corner with that one–now I guess we’ll see who are really the “dogmatic” and “closed-minded” ones.

    As far as treatment, you’re also wrong there. For people with frequent outbreaks, there *is* a daily treatment that is prescribed and taken when the patient is asymptomatic–and indeed, for life, if they so choose.

    Huh? I don’t know the “special treatment” to which you refer. Medical treatment? Scientific treatment? Cultural treatment? What are you trying to say?

    Well, you quoted exactly what I was trying to say:

    Do you realize by pushing the objections you do, that you’re denying not only HIV causation of AIDS, but essentially the entire germ theory of disease?

    and answered with this:

    No, you are grossly wrong. The germ theory is alive and well. Small pox is caused by a germ, the variola virus. Said virus has been conquered by a vaccine.

    Now, Hank, realize here that I’m not trying to disprove the germ theory. I’m a microbiologist by training, an infectious disease epidemiologist by profession. Obviously, I think the germ theory of disease is as solid a theory as they come. But you and others who share your POV on AIDS apparently don’t realize that the objections you make apply equally to ALL infectious agents, not only HIV. I’ve shown this over and over, using influenza, strep, TB, etc. as examples.

    The hard part is discerning between a pathogenic germ and a passenger germ. There are millions of passenger germs infecting healthy people, that do absolutely nothing.

    Oh, indeed, there are millions of germs infecting all of us. But y’know what, what may be pathogenic in one person may be harmless in another. Just because a germ appears to be a “passenger” doesn’t mean it can’t cause disease. Hell, about a third of the population is colonized with Staphylococcus aureus, but we don’t all have crazy skin infections. Similarly with Streptococcus pneumoniae, but we rarely get pneumonia from it. But also, we don’t know the details of their pathogenic processes down to every single molecule or infected cell, as you demand we need to know for HIV.

    Again, there’s a parallel here with creationists. IDists like Michael Behe demand that evolutionary biologists figure out every single mutation that led to the development of the immune system, or the bacterial flagella. Obviously, this is absurd–it’s unlikely we’ll ever be able to do that, and certainly we can’t now. So he uses that to say evolution is wrong, or flawed. You use your arguments for HIV–things we don’t know yet or indeed, may never know–to say that the entire theory is flawed, yet no one puts those lofty demands on streptococcus, or helicobacter, or herpes. *That’s* what I’m referring to when I discuss special treatment, Hank (as I’ve explained many times now). If we applied your level of evidence to every single infectious agent, we couldn’t show that any of them cause the disease they’re associated with.

    With regard to this, and since you did answer some questions I posed, I’ll tell you what would falsify the HIV/AIDS hypothesis. In fact, I’ll start with an antecdote (get comfy, y’all). Clearly, it’s difficult to “un-ring” a bell, and HIV has satisfied Koch’s postulates (as I mentioned, as well as any other disease has–see my points above). However, there’s precedent here. Back at the beginning of the 20th century, there was a disease that was killing pigs, called “hog cholera.” Researchers who’d studied it believed it was due to a bacterium. Indeed, they fulfilled Koch’s postulates–the bacterium was found in sick hogs but infrequently in well hogs, healthy hogs became ill with the disease when inoculated, and the bacterium was recovered from them. (Even Koch and Pasteur agreed the cause of hog cholera had been found).

    But then something happened. A vaccine developed against the bacterium wasn’t protecting pigs from the disease. Scientists scratched their heads–was the vaccine just ineffective? A few scientists went back to the drawing board. Viruses were still pretty new at this time, so instead of just injecting the bacteria, they filtered the suspension (to remove the bacteria) and injected *that.* Lo and behold, the filtered solution still caused hog cholera. Now they knew they were dealing with a viral disease–the virus had been contaminating their bacterial solutions. It was subsequently isolated, a vaccine was made (a lengthy process–I’m summarizing about 40-50 years of work here) and swine cholera was largely under control by the end of the 1960s.

    So, like the hog cholera bacterium, HIV has fulfilled Koch’s postulates. Yet many still argue it’s a “passenger” virus, and that something else is really doing the dirty work. So find me the real culprit. Show me that something else is present in all these HIV+ people but largely absent in those who are HIV-, and that it causes the immunosuppression that leads to AIDS by itself. Then I’ll happily eat my words.

    Now, Hank, you still didn’t answer this one: what would it take to get you to accept that HIV is the cause of AIDS?

  67. #67 Karen Lynne Lambert
    February 24, 2006

    Personally, I think where most AIDS dissidents miss the boat is that they are so busy saying HIV is not the cause of AIDS (whether it is – or is not – a cause of immune deficiency I really do not know) pointing to drug toxicity, benzene, lifestyles, water supply, oxidative stress, etc. that they fail to see that other stealth pathogens (the result of a faulty HHV6 assay, for instance) are clearly causing immune dysfunction. Certainly, lifestyle, eating habits, and genetic predisposition are all secondary factors that can expedite one’s physical demise, but acquiring a nasty virus or bacteria can most definitely be the precipitating event.

    I think where most AIDS dissidents continue to miss the mark is that they are so busy saying HIV is not the cause of AIDS that they fail to see that there is a blazing heterosexual CFS epidemic sweeping across the developed world (http://lemonfoundation.blogspot.com/2005/12/do-i-have-aids-or-chronic-fatigue.html). In 3rd world countries, where HIV diagnostic tests do not exist (and/or are too expensive to conduct) CFS patients are labeled AIDS patients by sheer symptomatology alone. It is only in first and second world countries, where we over-complicate everything with questionably defective diagnostic tests and shoddy intellectual definitional platforms, where achieving the elite status of an AIDS diagnosis must be coupled with (or predestinated by) an HIV+ diagnostic test result. That’s right people…if I lived in Africa right now I would have an AIDS diagnosis in hand. Rather, because of geography, capitalism, and politics, I am both a CFS and an HIV-Negative AIDS patient instead (http://lemonfoundation.blogspot.com/2005/07/lets-redefine-aids.html).

    Can’t you see that I am living proof that we have our epidemics, and its causal pathogen, mixed up? Can’t you see, in the USA, AIDS patients are just more CFS patients, who only by coincidence, also have an HIV+ diagnosis? Can’t you see that I am living proof that we have it all backwards? Can’t you see that we coddle those with AIDS while neglecting those with CFS — even though they are the same exact illness? Can’t you see that all of the “AIDS” funding goes to just the tip of the iceberg? Can’t you see that cases like me represent the glimmer of hope that HIV+ individuals have been praying for (for decades)? Can’t you see that I have AIDS, but I don’t have HIV? What if HIV is not the cause of AIDS (and the real cause is the very same thing that is causing millions of undiagnosed CFS patients)?

    My case currently sits at the apex of three disparate paradigms: Chronic Fatigue Syndrome (clinical diagnosis: “CFS”), HIV/AIDS (clinical diagnosis: “viral syndrome of unknown etiology”), and AIDS Myth (clinical diagnosis: “idiopathic CD8 lymphocytopenia” – a.k.a. HIV-NEGATIVE AIDS) –> potentially representing over a billion ailing patients worldwide (and while I can not talk about everything, a few highlights of my plight are listed here: http://lemonfoundation.blogspot.com/2005/07/few-highlights-of-my-plight_12.html)

    We need to get our paradigms working together, if only for humanity’s sake. CFS patients are chronically suffering, destined to be ailing HIV-NEGATIVE AIDS patients although most of them refuse to acknowledge it. AIDS dissidents definitely have a valid point that HIV may not be a cause of AIDS, but they are suggesting the wrong non-viral and bacterial causes as alternatives. HIV+ individuals, the majority of whom are already part of socially-repressed classes (African Americans, homosexuals, the impoverish), are being falsely stigmatized/demoralized and in some cases criminalized, and possibly, and quite literally, drugged to death by an orthodoxy that may be questionably inaccurate. I really see no reason why there shouldn’t be an uprising, because each group has vested interest in the other (and billions of dollars of funding — i.e. our tax money — is currently fueling the entire monstrosity. It all just needs to stop!)

    I, unlike many, do not feel that I have the luxury of timelessly listening to stale ideologies. I know I must be doing and saying something right, because I am truly in awe at what I have accomplished — mentally, physically, academically, and politically — in just about two years. When was the last time you believed in something, put together a strategy and an action plan, and then communicated it, digging deeper inside of yourself than you ever knew anybody had the depths to dig, only to have the United Nations respond to your concept?

    It is clear to me that there is immeasurable passion, determination, and frustration amongst everyone involved, why not work harmoniously together by demanding our politicians to conduct a REAPPRAISAL OF AIDS?

  68. #68 Tara
    February 24, 2006

    Hi, Karen–

    If HIV is not the cause of AIDS, then, what is?? Because HIV-Negative AIDS patients are not prescribed any toxic antiretroviral medications. Nobody even acknowledges our idiopathic illnesses, never mind to care enough to want to drug us…

    I’m going to have a post on this next week (well, not on what’s the cause of “HIV-negative AIDS,” ’cause I wish I knew, but on the whole “HIV-negative AIDS” idea. Probably Wednesday–have a heavy teaching load and a grant due early in the week.

  69. #69 Pharma Bawd
    February 24, 2006

    Hank,

    In your response to Dale #2 above:

    “The better answer is that HIV is probably an endogenous retrovirus, that is passed from mother-to-child at birth, and resides in the cell doing nothing. Remember, it is estimated that 8% of the human genome consists of viral DNA incorporated therein.”

    Are you suggesting that HIV is transmitted from mother to child genetically? or infectiously?

    Because your link was to endogenous retroviruses which are part of the genome. I think you can see very easily that HIV is not transmitted in this way. Right?

  70. #70 Tara
    February 24, 2006

    Addendum: I uploaded a .pdf of the Padian paper for anyone without access here, so you can read for yourself and not take my word for it.

  71. #71 Hank Barnes
    February 24, 2006

    Wow. A lotta stuff. Today ain’t so hot for me, mebbe more later on.

    Tara,

    On falsifiability:

    So find me the real culprit. Show me that something else is present in all these HIV+ people but largely absent in those who are HIV-, and that it causes the immunosuppression that leads to AIDS by itself. Then I’ll happily eat my words.

    Excellent. That is a huge step in the right direction. Needs a little refinement, but I salute you.

    Now, Hank, you still didn’t answer this one: what would it take to get you to accept that HIV is the cause of AIDS?

    The scientific sine qua non of the HIV hypothesis is a 3-step assertion:

    1. HIV (formally called Human T-Cell Leukemia Virus-III) kills abundant numbers of T-Cells (aka CD4 cells).

    2. This depletion in T-Cells leads to immune dysfunction.

    3. The dysfunctional immune system leads to the proliferation of opportunistic secondary diseases (PCP, tuberculosis, dementia, yeast infection, etc, etc), which would ordinarily be contained by a properly functioning immune system.

    So, I would do a very, very simple experiment — a self-contained Koch’s Postulates assessment:

    1. Pick 10 people, HIV+ and clinically diagnosed with AIDS. (The Rock Hudson group)

    2. Pick 10 people, HIV+ but asymptomatic (The Magic Johnson Group)

    3. Pick 10 people, HIV- and clinically diagnosed with AIDS (the Idiopathic-Lymphocytopenia group)

    4. Pick 10 people, HIV- and healthy (The control group).

    5. Blood samples of each, randomized and blinded to various pathologists.

    6. Mission of pathologists:

    * Locate HIV.
    * Culture it.
    * Purify it.
    * Photograph it by electronmicroscope.

    Those doctors who obtained HIV — from the patient, mind you — are to inject said virus into rats. Measure T-cells of rats before and after injection. Follow their health, as compared to uninfected rats. See what happens.

    The conventional theory would predict that for Groups 1 & 2, HIV would be obtained, cultured, purified, photographed by electronmiscropy, given to rats, whose T-Cells would drop.

    The conventional theory would predict that none of that would occur for Groups 3 & 4.

    If those predictions came to pass, that would — in my view — be solid evidence of the causal connection between HIV and the destruction of T-cells, the critical component of current AIDS theory.

    If those predictions failed to appear, eg, the blinded pathologist could not even obtain purified HIV from AIDS patients, (or, somehow, were able to obtain HIV from groups 3& 4)then — in my view — that would strongly undermine the conventional hypothesis, and we should all go back to the drawing board.

    This experiment is inexpensive and quick. It wouldn’t take much to stamp out potential confounding factors. It would go a long way to resolving the debate one way or the other. In fact, the NIH should fund it, and have Gallo and Duesberg jointly administer it.

    Sure, I have simplified matters, and the screening process and protocals would need refinement and further elaboration. But, who could possibly object to this experiment?

    Barnes, Hank

    p.s. Dale, good discussion above! I think we’ve exhaused Padian — we’ll have to agree to disagree.

  72. #72 Tara
    February 24, 2006

    Hank,

    Your proposal wouldn’t help at all. First, it’s dependent on HIV having the same effect in rats as it does in humans. As far as I know (and I’ve not heavily researched this angle), there’s not a good rat model of HIV disease. You’d need to get that established first. Second, (again, as I’ve mentioned several times), there’s nothing to say that the idopathic T-cell lymphopenia folks (the “HIV-negative AIDS” group) can’t also be infected with a different agent that causes the same type of T-cell destruction. Third, there’s no reason to believe that even someone who’s infected–with *any* agent–will be viremic (have detectable virus in the blood) the entire course of their illness. So you may be able to isolate HIV at a particular time point, or you may not, but those types of negative studies prove very little. Just because one can’t isolate it at a particular point in time using a particular method doesn’t mean it’s not elsewhere in the body. Your study, as currently proposed, is a waste of time and money.

    I do hope you stop back by later to re-address the herpes issue, among other things.

  73. #73 Guitar Eddie
    February 24, 2006

    I really admire your patience, Tara.

    The Pope should canonize you.

    GE

  74. #74 harvey Bialy
    February 24, 2006

    GE,

    You mean Pope David I?

  75. #75 Hank Barnes
    February 24, 2006

    Tara,

    Sounds like you don’t like this study, because you fear no pathologist could obtain HIV, and no rats would be injured by said virus.

    Interesting.

    Barnes

    P.s. Critiquing my simple study is easy, Do you have a better one in mind?

  76. #76 Tara
    February 24, 2006

    Sure, Hank, those are potential outcomes. Not ones I “fear,” mind you, but possibilities. Again, though, those outcomes could happen with a similar study for any other virus that’s not in its acute phase and that doesn’t have a validated animal model.

    These aren’t minor issues. Researchers spend years and years developing appropriate animal models in which to study disease processes–and they still have their limitations. For example, again back to strep, for much of my dissertation research we used a mouse model of skin infection. This resulted in lesions and pathology that look somewhat like those in a human, but there are critical differences. For one, a mouse’s plasminogen is different enough from a human’s that some streptococcal virulence factors don’t recognize it on a molecular level. Long story short, this results in many differences when it’s looked at beyond the gross pathology. You can’t just throw a microbe into an untested animal and hope it causes the right kind of disease–there’s a lot of work that needs to be done first.

    So, even if your results were all negative, without a positively validated animal model and isolation protocol, all you’d show is that your study didn’t work. Could be because HIV doesn’t cause AIDS, could be because of technical issues, could be simple incompetence. Your study design doesn’t allow the researcher to sort out from among those possibilities. (See, this science stuff ain’t as easy as it looks!)

    As far as a better one, I’ve already said I don’t think one study proves much at all. I’m already aware of the vast amount of literature that comes from a variety of disciplines, and all converge to the same point: HIV causes AIDS. Please note that I never asked you for a study: I asked you “what would it take to get you to accept that HIV is the cause of AIDS?” I think to boil it down to results from a single study is beyond folly, personally.

  77. #77 Hank Barnes
    February 24, 2006

    Further:

    Just because one can’t isolate it at a particular point in time using a particular method doesn’t mean it’s not elsewhere in the body

    Then, take 12 blood samples: 1 per month. Surely, if HIV is killing T-cells, you oughta be able to isolate it at least 1 of these 12 times, if not all 12.

    It’s there, isn’t it?

    Barnes

  78. #78 Hank Barnes
    February 24, 2006

    Sure, Hank, those are potential outcomes. Not ones I “fear,” mind you, but possibilities.

    Well, then what would you conclude about HIV from these possible results?

    These aren’t minor issues. Researchers spend years and years developing appropriate animal models in which to study disease processes–and they still have their limitations.

    Yes, researchers will spend years and years of gov’t $$ on frogs, flies and yeast towards little or no particular end, as long as it adds to their collection of published papers, that nobody reads.

    How ’bout something new for a change?

    …Long story short, this results in many differences when it’s looked at beyond the gross pathology. You can’t just throw a microbe into an untested animal and hope it causes the right kind of disease–there’s a lot of work that needs to be done first.

    Right, but you can at least isolate the strep bacteria from the patient, no?

    So, even if your results were all negative, without a positively validated animal model and isolation protocol, all you’d show is that your study didn’t work.

    Or, that HIV didn’t do squat. But why prejudge the results, anyway? Mebbe you could isolate, purify, and photograph a whole lot of HIV, thus ending the debate forever. Doncha wanna try?

    I’m already aware of the vast amount of literature that comes from a variety of disciplines, and all converge to the same point: HIV causes AIDS.

    Ahh. The vast amount of phantom literature that nobody cites, and almost always starts from the presumption that HIV causes AIDS. You’ve heard of “confirmation bias”, right? Kinda like what happened with Bush’s weapons of mass destruction, when everybody knew there was a threat.

    Please note that I never asked you for a study: I asked you “what would it take to get you to accept that HIV is the cause of AIDS?”

    Right, and I told you what would be convincing evidence. Then, you ran off on another of your tangents trying to explain away, future, contingent results.

    If you don’t like my simple study, that’s cool. I’ll make it easy. Show me any 3 good papers from 1984-1986, that seek to discern whether or not HIV is a pathogenic virus or a passenger virus. I promise to read them, openly and honestly and I will join the club, if they simply demonstrate it, without all this static and distraction.

    I think to boil it down to results from a single study is beyond folly, personally.

    Single studies get prescription drugs approved by the FDA all the time. But, yes, more is better.

    Barnes

  79. #79 Tara
    February 24, 2006

    Sure it’s there, but is it there at that point in time, in that tissue of the body (blood), at a high enough level for culture of infectious virus? Maybe, maybe not. Again, your study doesn’t account for this.

    And don’t think I haven’t noticed that you only respond to about 5% of any given post. ;)

  80. #80 Hank Barnes
    February 24, 2006

    And don’t think I haven’t noticed that you only respond to about 5% of any given post. ;)

    I try to separate the pearls from the muck:)

    Barnes

  81. #81 Orac
    February 24, 2006

    f you don’t like my simple study, that’s cool. I’ll make it easy. Show me any 3 good papers from 1984-1986, that seek to discern whether or not HIV is a pathogenic virus or a passenger virus. I promise to read them, openly and honestly and I will join the club, if they simply demonstrate it, without all this static and distraction.

    Why restrict the studies between the years 1984-86?

  82. #82 Hank Barnes
    February 24, 2006

    Orac,

    Why restrict the studies between the years 1984-86?

    Because that is the era in which the purported “aetiology” of AIDS was first determined.

    Barnes

  83. #83 Shygetz
    February 24, 2006

    Barnes,

    Because that is the era in which the purported “aetiology” of AIDS was first determined.

    Who cares when it was first determined? What does that have to do with the current case for HIV causing AIDS? Unless you are just interested in trying to find some “gotcha” moment, where scientists based a conclusion on evidence you find unconvincing.

  84. #84 Tara
    February 24, 2006

    Hank wrote more while I was responding.

    Yes, researchers will spend years and years of gov’t $$ on frogs, flies and yeast towards little or no particular end, as long as it adds to their collection of published papers, that nobody reads.

    How ’bout something new for a change?

    Obviously, I disagree that “it’s to no particular end”–depends on what the study is addressing. As far as “something new,” again with strep, a zebrafish model of pathogenesis is being worked on (zebrafish are cheaper and easier than mice), but as I mentioned, it has to be validated and looked at from many different angles first.

    Additionally, many transgenic animals have been created in the past decade or so. These might be the best model for some diseases, but are very expensive as things currently stand. Anyhoo, regarding my strep example, you asked:

    Right, but you can at least isolate the strep bacteria from the patient, no?

    Depends on the stage of infection. You can’t always isolate it. Additionally, it’s generally easier to isolate bacteria than viruses, since they don’t (generally) need other cells to grow in.

    Ahh. The vast amount of phantom literature that nobody cites, and almost always starts from the presumption that HIV causes AIDS. You’ve heard of “confirmation bias”, right? Kinda like what happened with Bush’s weapons of mass destruction, when everybody knew there was a threat.

    I’ve avoided “literature bombing” because I find it almost universally gets ignored and therefore, wastes even more of my time than simple discussion does. Heck, you’ve still not gotten back to me on the herpes issue, above.

    Then, you ran off on another of your tangents trying to explain away, future, contingent results.

    Hank, I don’t know what you do for a living, but this “tangent” of mine that you’re dismissing is a critical part of the research plan. When anyone proposes a research study, they have to take these things into consideration. You can’t just throw an experiment together and hope everyhing works out the way you expect it will. In every grant application or other research proposal, you must address limitations of your methods, and alternative outcomes of the experiments. No one wants to throw away time or money on a research proposal that’s not going to have any solid results to show for it.

  85. #85 Harvey Bialy
    February 24, 2006

    Dr. Orac,

    Don’t you have anything substantive to say to this?

    http://www.lewrockwell.com/miller/miller18.html

    It is the number one emailed/saved/printed post on this very high profile *real* blog (unlike this, yours and my own of course, which is not even a blog).

  86. #86 Tara
    February 24, 2006

    See, Harvey, that’s what I mean by continually “pimping” your book. (see definition 6.2)

  87. #87 Hyperion
    February 24, 2006

    ” Tara: Sure, Hank, those are potential outcomes. Not ones I “fear,” mind you, but possibilities.

    Hank: Well, then what would you conclude about HIV from these possible results?”

    Ummm, leaving aside the fact that one cannot by definition draw conclusions from possible results, I think that her point was that your experiment as proposed would not generate outcomes that were conclusive. In other words, its scope was not narrow enough that any of the possible outcomes would indicate whether your hypothesis was true or false. The experiment would need to be narrowed so that a given result would verify or falsify the hypothesis, otherwise it’s rather pointless.

    “Yes, researchers will spend years and years of gov’t $$ on frogs, flies and yeast towards little or no particular end, as long as it adds to their collection of published papers, that nobody reads.”

    No particular end? When I had a respiratory staph infection, I was rather lucky to see an infectious disease specialist who was well read on which particular antibiotics would work best on that particular strain. Research saves lives, the fact that you seem not to grasp this is a little bit disconcerting.

    “Right, but you can at least isolate the strep bacteria from the patient, no?”

    Yes, and you can observe HIV in a patient too. Her point was that specifically in your proposed experiment, you may not be able to isolate HIV, because your specific experiment does not take into account important factors.

    “Or, that HIV didn’t do squat. But why prejudge the results, anyway? Mebbe you could isolate, purify, and photograph a whole lot of HIV, thus ending the debate forever. Doncha wanna try?”

    I am right now staring at several TEM micrographs of an HIV virus entering a human white blood cell, and then TEM micrographs of an HIV virus leaving a human white blood cell. It’s in Campbell’s Biology 5th Edition, an undergrad bio textbook. Your local university library ought to have a copy, I’d think. Now, granted, it’s not “a whole lot of HIV,” but it is a photograph of it, and I’d think that seeing it enter and exit a white blood cell would be even better than a photograph of it isolated.

    “Single studies get prescription drugs approved by the FDA all the time. But, yes, more is better.”

    Huh? There are four phases of testing for FDA approval. It is exceedingly rare for a drug to be approved based on one single study. In fact, I believe that it would violate federal law unless there were some extreme circumstance such as an epidemic that necessitated immediate use of an experimental drug. Occasionally, an already-approved drug may be approved for another use on the basis of one study, but this ignores the fact that such a drug will already have been exhaustively studied beforehand. I don’t know why you believe that drugs are approved based on one single study, but perhaps you misunderstand how drug or epidemiological studies work. This is essential for understanding why Dr. Smith felt that your proposed experiment would not be valid.

  88. #88 Harvey Bialy
    February 24, 2006

    For the benefit of those who have no idea to what Dr. Asst. Prof. Smith is referring, earlier today in response to my inquring if she were ever going to review my book, and that if she did she would actually have to read it, she replied that she was not going to help me “pimp” my book any more than she has.

    I replied in very vulgar Spanish, saying in essence that I was not a “chulo” nor was my book a “puta”, and that she could perform an unnatural act upon her mother.

    The review by Prof. Dr. Miller is quite substantive and addresses from a very profesional perspective all the issues that have been bandied about here.

    Surely Dr. Orac, the surgeon, has something to say to Dr. Miller, a Professor of Surgery at the University of Washington?

    Claro Dr. Smith?.

  89. #89 Tara
    February 24, 2006

    Si, pero let’s keep the record straight: you simply referred to me as a “puta” and told me to go **** my mother. You made no mention of your book in that message. Anyhoo, all of that is really neither here nor there as far as the HIV discussion goes.

  90. #90 Francis
    February 24, 2006

    I’ve been practicing law about 15 years now, and had to work with experts in all kinds of fields. One thing I learned early on is that the more your claim goes against conventional wisdom, the higher your burden of proof. Yet Harvey, Hank and Dean seem to believe (if they’re actually serious) that a single study — with proven weaknessess — can invalidate a theory with multiple strands of support.

    now, i’m willing to keep an open mind that the conventional wisdom is wrong. but before i’m going to start having serious doubts, the denialists are going to need to rebut some of the major threads of evidence found here. Personally, I find this evidence: “Before the appearance of HIV, AIDS-related diseases such as PCP, KS and MAC were rare in developed countries; today, they are common in HIV-infected individuals” and this evidence: “The availability of potent combinations of drugs that specifically block HIV replication has dramatically improved the prognosis for HIV-infected individuals” particularly compelling, along with the twins evidence and the blood donor evidence.

    Hank, Henry, Dean: any response?

  91. #91 Harvey Bialy
    February 24, 2006

    Mr. Francis,

    You mgiht try reading this:

    http://www.rethinkaids.info/documents/Specialist%20Literature/NIH%20Rebuttal.pdf

    Who is Henry?

    & Who is Pope David I?

  92. #92 Harvey Bialy
    February 24, 2006

    Mr. Francis,

    You might try reading this:

    http://www.rethinkaids.info/documents/Specialist%20Literature/NIH%20Rebuttal.pdf

    Who is Henry?

    & Who is Pope David I?

  93. #93 Harvey Bialy
    February 24, 2006

    FYIs

    The Alexa traffic rank for the Lew Rockwell site is 6,200, on a scale of 1 to 4,000,000, with the lowest number having the highest number of hits.

    What’s your’s Dr. Smith?

    BTW, the downloads for http://bialystocker.net/files/Pipedream.com are 1800+ as of last night at 7 PM EST.

  94. #94 Hank Barnes
    February 24, 2006

    Hyperion,

    Ummm, leaving aside the fact that one cannot by definition draw conclusions from possible results, I think that her point was that your experiment as proposed would not generate outcomes that were conclusive

    “conclusive” is your word, not mine. Yes, few studies conclusively establish or refute X. That doesn’t mean we don’t try to establish or refute X. We temper our conclusions — we don’t evade them as some are doing on this blog.

    But more importantly, To ascertain whether or not HIV was pathogenic or merely a passenger virus, Which experiment would you propose?

    Barnes

    p.s. Also, I have doubts that whatever textbook you’re looking at shows HIV. Retroviral particles band at a density gradient of 1.16 grams/ml. The first paper to try to publish proper electronmiscropy of HIV is: Gluschankof et al, 1997. It showed a whole buncha contaminants.

  95. #95 Hank Barnes
    February 24, 2006

    The greatest quote ever from one, Shygetz:

    O: “Why restrict the studies between the years 1984-86?”

    H: “Because that is the era in which the purported “aetiology” of AIDS was first determined.

    S: “Who cares when it was first determined? What does that have to do with the current case for HIV causing AIDS?”

    Cargo cult science at its best:)I love it!

    Barnes, Hank

  96. #96 Harvey Bialy
    February 24, 2006

    Where is George Kaplan when you need him?

    I meant, of course,

    http://bialystocker.net/files/Pipedream.pdf

  97. #97 Harvey Bialy
    February 24, 2006

    Tara,

    What scientific hypotheses do (nevermind theories) is make testable predictions.

    Here are some of the predictions of the virus-AIDS hypothesis of which “you” are so enamored.

    AIDS would explode into the general population.

    A vaccine would be produced in 5 years, then 10 years then 15 years …

    Drugs that targetted “HIV” with “exqusite specificity” would curtail the deadly progression from asymptomatic to dead.

    Plentiful HIV infectious particles would be shown to be in step with declining T-cells via experiment not imagination.

    I could go on…an on

  98. #98 Dale
    February 24, 2006

    HB,

    AIDS would explode into the general population was a prediction based on a “worst case” scenario. Padian and others showed that heterosexual transmission of HIV occurs at a relatively low frequency that can be further reduced by behaviour modification and condom usage.

    The lack of a vaccine speaks to the complexities of HIV’s interactions with the human immune system not the validity of the HIV/AIDS hypothesis. Develop a vaccine that prevents HIV transmission and show that heterosexual partners of HIV+ individuals still develop AIDS – that would certainly cause me to rethink the relationship.

    Drugs that targetted HIV with exquisite specificity would curtail the deadly progression. And they do albeit temporarily and imperfectly. Their inability to cure is explained by the biology of the virus and the presence of reservoirs of latent virus.

  99. #99 Harvey Bialy
    February 24, 2006

    Real “wears-his-uniform-to-bed” response Dale. I am beginning to think you are Tony again.

    But is this really the best *you* can do after two decades, 120,000+ peer-reviewed papers and 50 billion US?

    And I didn’t even ask anyone to defend this massive failure, you just jumped right in per usual, leaving out the last “hard” prediction (also as per usual).

  100. #100 Harvey Bialy
    February 24, 2006

    Dale,

    Your defense of virus-AIDS is a lot like the defense of virus-cancer.

    The NIH points to the fact that the US blood supply is screened for HTLV-I and therefore the American public is “safe” from ATL.

    They of course never say that prior to testing not a single case of transfusion-related ATL was ever reported.

  101. #101 Hank Barnes
    February 24, 2006

    Dale,

    The lack of a vaccine speaks to the complexities of HIV’s interactions with the human immune system not the validity of the HIV/AIDS hypothesis.

    No, you are confused here. The purpose of the vaccine is to stimulate the body’s immune system (the B-Cells) to produce anti-bodies to said antigen. So, detection of anti-bodies means, essentially, mission accomplished. Viral disease averted.

    Example:

    My kids get Hepatitis vaccine. Presumably, they develop anti-bodies to Hep, and, hopefully, never get Hep.

    With HIV, though, this long-standing principle is reversed– the detection of anti-bodies (via the HIV test) is the method by which an MD says, “You’re HIV positive, you’re gonna get AIDS and die, start your AZT immediately.”

    Do you see how the current paradigm has it backwards?

    That probably explains the ridiculous 10-year latency period or “slow virus” theory. That also explains the “long-term non progressors” –ie, HIV+ folks who are healthy because they take no AZT or other toxic anti-virals.

    The reason no vaccine for HIV has been developed (and will never be) is because anti-bodies are already present in each asymptomatic patient. It would be like putting a cast on somebody’s arm, after it was already healed.

    Develop a vaccine that prevents HIV transmission and show that heterosexual partners of HIV+ individuals still develop AIDS – that would certainly cause me to rethink the relationship.

    Hey, we’re approaching falsifiability here!!!! Alas, it is a bridge too far — there’s never gonna be an HIV vaccine. They’ve been working on it for 22 years now.

    Try again.

    Barnes, Hank

  102. #102 Harvey Bialy
    February 24, 2006

    & Dale,

    I strongly advise you not to start your usual palavar games with me here or I will refer the readers to a certain Dean Esmay discussion where you conclusively demonstrated (preserved for as long as the internet endures)that the orthodox virus-AIDS proponents are not above having the titles of papers in very prestigious journals fudged so as to be totally misrepresentative of the actual findings in the paper, and when Duesberg cites this paper as demonstrating “x”, and his vocal and powerful scientific critics look at the Pub Med abstract and facily say….Duesberg has once again misrepresented the literature he cites…they are dead wrong.

    The “Tool for the Truth” on the Rethinking Aids website (http://rethinkingaids.com) has all the data anyone who can read the literature needs to make up their own, independent minds as to which side of the debate “abuses” the literature.

  103. #103 Dale
    February 24, 2006

    Harvey,

    And your defense of HIV-does-not-cause-AIDS is a lot like the arguments put forward by IDers as proof of the “falsification” of the theory of evolution.

    But since that’s not what we were talking about, let me just add that according to the literature I’ve seen HIV viral loads do generally inversely correlate with CD4+ cell counts.

  104. #104 Harvey Bialy
    February 24, 2006

    Dale,

    Please read what I posted above in anticipation of just such a nonsensical reply.

    I will not link it. You will have to “search” the page for “viral load”.

  105. #105 Dale
    February 24, 2006

    Harvey, you are indeed the master of the non-sequitur. Where and when did this discussion become about Duesberg’s misrepresentation of the literature?

  106. #106 Harvey Bialy
    February 24, 2006

    Dale,

    You leave me no choice, since I am nothing if not a man of my word.

    http://bialystocker.net/files/The_Tony_Fauci_Hour,__A_Daily_Internet_Program_that_Educates_&_Entertains.pdf

  107. #107 Dale
    February 24, 2006

    Hank,

    I think you need to read up a bit on immunology and basic HIV biology. The presence of antibodies means the immune system has mounted a response – it doesn’t mean that a pathogen has been cleared from the body. See chickenpox or TB or malaria (if you want to consider non viral pathogens).

  108. #108 Dale
    February 24, 2006

    Harvey, This is something I’ve nevered posted on a serious discussion but you leave me no choice.

    ROTFLMAOTMEB!

  109. #109 Hank Barnes
    February 24, 2006

    Dale,

    Nice strawman and dodge. You are the Houdini of the internet:)

    The presence of antibodies means the immune system has mounted a response – it doesn’t mean that a pathogen has been cleared from the body.

    Yes, I know that. I did’t say the pathogen has been “cleared.”

    If anti-bodies are present, why would you need a vaccine?

    Hank

  110. #110 Dale
    February 24, 2006

    Because, Hank, all antibodies are not created equal as I’m sure you’ve already been told.

  111. #111 mgr
    February 24, 2006

    Hank:

    As anyone who works with stock animals knows, one gives tetanus vaccinations that give passive immunity as well as active immunity.

    Mike

  112. #112 Harvey Bialy
    February 24, 2006

    Dale,

    q.e.d.

  113. #113 Hank Barnes
    February 24, 2006

    No, I know all anti-bodies aren’t created equal. Tell me which ones y’all trying to stimulate — with grave futility– via the serendipitous HIV vaccine, nobody can produce.

    Hank

  114. #114 mgr
    February 24, 2006

    Hank:

    That would be an incorrect assumption, particularly as it applies to passive immunity. However, by your response it appears, that as I assumed, you are using the term vaccination in the loose sense (a shot), and do not know the difference between a vaccine and a treatment. I can see the concerns with a vaccination of killed virus (if one is fortunate to achieve 100% mortality to something that is borderline ‘live’)to give active immunity since that pathogen specifically targets elements of the immune response; and I can also see the pratfalls with obtaining a treatment employing antibodies derived from plasma or serum from those immune to the pathogen–it has both the pratfalls bringing HIV into the bloodstream, or stimulating an immune response against factors in the plasma or serum.

    Given these constraints, I can see why neither is available, and given human optimism in technology, why the breakthrough is always just around the corner. Just as I don’t fault the weatherman his predictions, nor would I fault the scientist’s.

    Ultimately, I think the issue with your position is that you confuse the heuristic with the practical.

    Mike

  115. #115 Hank Barnes
    February 24, 2006

    Mike,

    No, I completely understand the difference between “passive” and “active” immune system. Please spare me more subterfuge.

    The question is 2 part:

    Q: Since, the test for AIDS is “detection of antibodies to HIV,” the vaccine these keystone cops have been trying to develop for 22 years is a degraded form of HIV (weakened or dead) designed to ….do what?____________

    Is the answer, “stimulate more antibodies?” If not, what then?

  116. #116 Chris Noble
    February 24, 2006

    Could Hank Barnes either defend his assertion that HIV is an endogenous virus or admit that he was wrong before he makes a totally new set of false statements.

    All of the “rethinkers” have stopped addressing the issue of the Padian study once the errors in their arguments had been pointed out.

    They just move onto the next equally fallacious argument.

    In a year’s time a new set of “rethinkers” will again claim that Padian’s study proves that HIV is not sexually transmitted.

    Another set will argue that HIV has never been isolated.

    Another set will argue that all sexually transmitted diseases are equally distributed amongst the sexes.

    None of them will ever admit they are wrong.

  117. #117 Dale
    February 24, 2006

    Hank, a successful vaccine will stimulate antibodies or cellular response that inhibits replication of the virus. And it doesn’t even have to be a vaccine. Any treatment that successfully blocks, preferably infection but at least replication of the virus, but does not affect the development of clinical disease (ie. loss of CD4+ T cells, increase in opportunistic infections), in other words ‘cure’ HIV without affecting AIDS and I’ll rethink whether I still believe HIV causes AIDS.

  118. #118 Darin Brown
    February 24, 2006

    Dale –

    Regarding your response to my 6 things which would “get me to accept HIV is the cause of AIDS”, I am truly speechless. I’m not sure what to say, except, your response is ample evidence that you are a true and willing believer in “post-modern” biomedicine.

  119. #119 Darin Brown
    February 24, 2006

    (As an aside it is worth noting that the editors of Continuum Jodie Wells and Huw Christie died of PCP and KS)

    If this is an acceptable line of argument, then certainly I am entitled to call to the stand the tens of thousands of patients who believed the HIV theory and died on AZT monotherapy?? But, I don’t think that is either a good logical argument, nor in good taste, so I will refrain. I think such comments are very revealing about those who make them, though.

  120. #120 Dale
    February 24, 2006

    Darin, If I could render a few more dissidents “speechless”, I’d be a happy camper indeed.

  121. #121 Darin Brown
    February 24, 2006

    Shygetz said,

    Who cares when it was first determined? What does that have to do with the current case for HIV causing AIDS? Unless you are just interested in trying to find some “gotcha” moment, where scientists based a conclusion on evidence you find unconvincing.

    See my posts on the original Bethell thread on this, re: epidemiology justifying biology and biology justifying epidemiology. In 1982, HTLV-III was not known, and in 1985 almost everyone believed it caused AIDS. Within a couple years, HIV was part of the CDC definition. So, there should be some paper OR series of papers that warranted this enormous change of mind. Unless you want to quote “all papers published between 1982 and 1985″.

  122. #122 Darin Brown
    February 24, 2006

    Dale said,

    Darin, If I could render a few more dissidents “speechless”, I’d be a happy camper indeed.

    Be happy then, because you are quite good at it with me.

  123. #123 Richard
    February 24, 2006

    To weigh in on the immunology, I think it may be a bit of a mistake to even buy into the idea that the lack of a full understanding of HIV pathogenesis means that the virus can’t cause disease. That assumes we know enough about how the immune system works to understand every means by which it can be undermined, which we clearly do not. The same is actually true of vaccines, Hank is very credulous to think that antibodies=efficacy (although they’re often a good marker for it). The role of T cells in vaccine protection is only beginning to be uncovered because the tools for studying T cell responses were incredibly clumsy until the recent advent of technologies called ELISpot, intracellular cytokine staining (ICS) and tetramers. To quote from a review that just came out in Cell: “Despite the success of many vaccines, there is presently little knowledge of the immunological mechanisms that mediate their efficacy.”

    Given that T cells have been difficult to study, and that HIV primarily infects CD4 T cells, it is really not surprising that theories of HIV pathogenesis have not necessarily been that convincing. Darin raises some perfectly reasonable questions, but I think studies over the past few years are beginning to provide answers. To try and summarize some points:

    - the most important predictor of progression to AIDS is the level of immune activation, not peripheral blood CD4 counts or viral RNA copy counts
    - immune activation correlates with depletion of naive CD4 and CD8 T cell pools, depletion of which also predicts the onset of AIDS
    - in parallel with this process is a spreading dysfunction among memory CD4 and CD8 T cells involving increasing numbers of cells unable to perform a full spectrum of functions (e.g. IL-2 production) and declining functional T cell responses to opportunistic pathogens (eg MAC, candida)

    All of this is demonstrably occuring during that typically long period between infection and AIDS (loss of CD4 T cells from the blood is just a marker for this process, reflecting the naive T cell decline and redistribution of memory CD4 T cells to the lymphoid tissue).

    No study I know of has demonstrated equivalent immunological peturbations in the setting of malnourishment or chronic drug abuse, by the way.

    Because most activated T cells are automatically destined to die within a couple of days (activation induced cell death), the issue of whether HIV is cytopathic is essentially moot. The typical levels of immune activation in HIV infection are manyfold higher than the % of infected cells (and recent studies have also shown that they are many more infected cells in the gut than in the peripheral blood).

    There’s actually a recent mouse model that artificially creates persistent immune activation and it recapitulates these features of HIV pathogenesis very well.

    Antiretroviral therapy, for all it’s limitations, has the salutary effect of reducing immune activation, increasing naive T cell counts and causing a rebound of memory T cell responses to opportunistic pathogens (that can allow maintenance therapy to be stopped in people that have previously had an opportunistic infection).

    As to exactly why HIV drives persistent low level immune activation, it remains to be fully elucidated but the fact that the virus preferentially HIV-specific CD4 T cells – which are needed to drive the maturation of functional HIV-specific CD8 T cell and B cell and antibody responses – is probably a big clue. It also is the likely explanation as to why HIV-specific memory CD4 T cells generally show limited functionality (compared to CD4 T cells targeting CMV, for example) from the very earliest stages of HIV infection, and this has knock-on effects on HIV-specific CD8 T cells and B cells (neutralizing antibody responses lag several months behind the virus as a result). People actually slowly accumulate increasing numbers of dysfunctional HIV-specific T cell responses as disease progresses (up to ~50% of CD8 T cells have been shown to be HIV-specific in individuals with AIDS, and this is certainly an underestimate due to limitations in the ability of assays to capture all the responses to HIV antigens).

    Obviously this is all a bit incomprehensible if you’re not that familiar with the immunology literature, but I’m inclined to think that if you’re going make claims about what HIV may or may not do to the human immune system, it sort of behooves you to wade in there and become familiar. Citing a Jonathan Sprent article from 1977 is not really very useful in 2006.

    I’d be happy provide cites relating to this information on request (this is already a very long post I fear).

  124. #124 Hank Barnes
    February 25, 2006

    Well Chris Noble, one of the reasons I won’t engage you, is that you’ve lost all credibility with me for this asinine, arrogant statement:

    If Duesberg could come up with a consistent and coherent theory that did not conflict with mountains of data then people would take him seriously. He hasn’t and he isn’t.

    Really, who are you to talk down to Dr. Duesberg?

    1. He’s a tenured professor of molecular biology at University of California, Berkeley. Where are you tenured?

    2. He was personally recruited to UC Berkeley by Nobel Laureate, Dr. Wendell Stanley Who recruited you anywhere?

    3. He was elected to the National Academy of Science at age 49. When were you elected?

    4. He’s published more than 200 papers in the peer-reviewed literature, including, Science, Nature, PNAS, NEJM. Where are you published?

    5. The top journal, Science, writes articles about his work. Did Science or any journal ever write anything about you?

    6. Scientific American recognizes him as the one of the pre-eminent cancer researchers in the entire world. How ’bout you, chump?

    7. Dr. Bert Vogelstein of Johns-Hopkins –arguably the top cancer researcher of our time recently said this about Duesberg:

    I agree with him that aneuploidy is an essential part of cancer. Dr. Duesberg continues to have a major impact on this burgeoning area of research through his careful experimental observations as well as through his thoughtful reviews and critiques of the subject. There is no question that he is a world leader in this field of investigation.”
    –Harpers, March 2006.

    In sum, Chris, you aren’t fit to sniff Duesberg’s scientific jock-strap. You shouldn’t even mention his name, without a reverential prayer of respect. Sure, Duesberg may not have AIDS or cancer exactly right. But, he is provocative, perceptive, thoughtful and much more honest than some of the dolts on the other side. And, he is probably much closer to the truth than you are.

    Until you lose the attitude, I ain’t gonna waste further time in dialogue with you.

    Hank Barnes

  125. #125 Dean Esmay
    February 25, 2006

    I’ve been trying to stay out of this but since I was called out by name here by Francis, I’ll answer Francis:

    I’ve been practicing law about 15 years now, and had to work with experts in all kinds of fields. One thing I learned early on is that the more your claim goes against conventional wisdom, the higher your burden of proof. Yet Harvey, Hank and Dean seem to believe (if they’re actually serious) that a single study — with proven weaknessess — can invalidate a theory with multiple strands of support.

    First off, please be cautious with the generalizations. I came into this entire discussion because some years ago I read a few books on the subject, expressed some doubts in public a year or so ago, and got mocked and savaged and attacked, and my questions answered with arguments based primarily on ad hominem and/or appeals to authority. I became more skeptical of the HIV establishment as a result of that. A few times, I’ve lost my temper and been more strident than that, but I usually calm down and clarify my remarks when that happens. I’m a skeptic, not an advocate.

    Still, I got even more skeptical when some folks claiming to be scientists–some of them part of this discussion–said that there was simply no need to refute any of the papers Duesberg has published on HIV, because the evidence is so overwhelmingly against them they can simply be ignored. I know multiple scientists in multiple fields who’ll tell you that’s nonsense. Duesberg has published in some of the foremost journals in the world on this subject, usually because he was specifically asked to by the scientific editors to do so. The pretense here seems to be that somehow, he’s a crank who just churns out these papers and pesters people until they agree to publish him. That’s nonsense. That’s how you get published in pseudo-journals like Medical Hypotheses (look it up), not journals like Genetica or The Lancet or International Archives of Allergy and Immunology or J. Biosci–indeed, without being sarcastic I’d have to ask, just how many of these publications have Dale, Orac, Dr. Noble, Dr. Smith, etc. managed to get published in? Hmm? Indeed, if these papers are so easily and obviously rebutted and refuted, then why the HELL haven’t they been so rebutted and refuted in the very pages where they were published? Why do we need this ridiculous pretense that “well they aren’t serious so everyone ignores them?” Excuse me? You just indicted everyone associated with journals like the Proceedings of the National Academy of Sciences, The Lancet, Genetica, the International Archive of Allergy and Immunology, J. Biosci, and other world-class journals. Where the hell do you get off talking like that?

    Francis is right that extraordinary claims require extraordinary proof. Well in my view it is extraordinary to claim that multiple papers were BOTH solicited AND published in these journals, yet were so trivially meaningless that no one in the field felt the need to respond to them.

    Multiple scientists with substantial credentials and an impressive body of peer-reviewed papers in a number of disciplines have told me the same thing: if you get caught misrepresenting data and abusing the literature when submitting to these journals, you’ll be savaged in the peer review process and your paper will not get through to publication—and if you’re so caught out after publication because the peer review process broke down, it’s a huge embarrassment to that journal, and your career is likely over. Any one of the scientists here who really believes Duesberg does this should stop wasting time in these online discussions and simply sit down and write a paper which shows that Duesberg abuses the literature, and submit it for publication in one of the journals Duesberg’s appeared in (or to a competing journal). You don’t even have to refute all his points; just pick a few juicy and important ones. Do it successfully and you will probably advance your career to a considerable degree. Stop arguing with popular science writers like me, and go make your case in the pages of J. Biosci or The Lancet.

    Although you ought to be asking yourself why, if it’s so easy, those who actually study HIV for a living haven’t already done it. This alone is the most damning thing of all I see in the establishment’s position. That and the fact that instead of doing this, they rely on ad hominem attacks in the popular press instead (and on weblogs or the Usenet these days).

    As to whether a single study could be cited to throw out an entire hypothesis: I think a single well-done study can throw serious doubt on a widely-held hypothesis, yes, just like I think DNA evidence can prove that the entire legal system made up of judges, juries, and appeals courts convicted an innocent man of murder. But I also acknowledge that this isn’t usual. It often takes a great deal more than one piece of evidence to throw a conviction into doubt.

    Still, I think, for example, that the study which attempted to give chimpanzees AIDS by injecting them with HIV throws doubt on the establishment position, because chimps get most (all?) human diseases when infected with human viruses. Those chimps have gone a quarter century healthy as horses and are still sitting around in their cages. I also think the fact that even after a quarter century, AIDS is STILL TODAY overwhelmingly found in men (77%, see http://www.avert.org/statsum.htm )–despite the fact that we’ve been hearing since the early 1990s that it’s “spreading rapidly” in women and that it’s vastly easier for women to get it than men–is reason to give one pause. Conversely, and equally troubling, we’re told that it’s distributed evenly between the sexes in Africa, even though it’s still supposedly much easier for women to get it than men.

    I put it to you, Francis, that if you’re the prosecuting attorney that is indicting HIV, it’s your job to demonstrate that HIV is the murderer. The defense only needs to prove reasonable doubt. Well science isn’t a court room, and we may have to settle for less than “beyond a reasonable doubt,” but if there is reasonable doubt, it should be reasonable for there to be dissenters and skeptics, right?

    I further think that if a study, or series of studies, throws doubt on a hypothesis, it’s entirely normal for scientists to calmly say, “Well, it’s true that there are still big questions out there, although most of us in the community that study this issue are pretty sure that Hypothesis A is correct and that Hypothesis B is weak, but, we’re still all working on it.” Indeed, my personal experience is that this is exactly how the vast majority of scientists behave. What’s abnormal, on the other hand, is to simply trash the reputation of anyone who dares question hypothesis A–and to trash them not in the peer-reviewed literature, but in the popular press instead. That’s not science, that’s religion. Indeed, it’s what the so-called “Creation Scientists” and “Intelligent Design Theorists” spend most of their time doing.

    As for addressing the specific evidence that Francis brings up: Again, I am not one of a triad named “Hank, Harvey, and Dean.” I have my own opinions and my own perspectives. I also don’t pretend that I know everything or that I have an answer for every question. I fully acknowledge that my skepticism of the established wisdom on HIV may be mistaken; I merely find it telling that those on the other side rarely concede the same (i.e. admit that they might be mistaken), and instead rely primarily ad hominem slurs and appeals to authority to win their case. (Hi Chris Noble! Much love to you my brother! Hi Orac! You know I love you man, c’mere ya big lug and lemme give ya a big wet sloppy kiss! Oogie oogie, you guys are so cute!)

    I’ll close for Francis by noting what I find most disturbing of all: the HIV establishment has rigged the rules of the game. It’s illegal to study HIV without NIH approval. You can only get NIH approval if you get a grant from them. This has been true for nearly two decades now. Since the late 1980s, the only people who ever get such grants are people who accept the established theory. It does not take a rocket scientist to notice that this would not pass the smell test in any elementary text on good government or ethical business practice. Yet it’s the reality and has been for about two decades. And when asked about this, HIV’s defenders again say that the evidence is so overwhelming, we have *zero need* to bother funding any other hypotheses, or to even just *give permission to work with HIV* to someone who gets private funding. Wow, that’s pretty impressive: 1) Declare in the late 1980s that you’ve found the culprit, 2) Lock up all government funding, reserving it exclusively for those who accept this wisdom, 3) make it a felony for anyone to study it without permission, 4) only give permission to those who accept the common wisdom.

    Is that a conspiracy? Not really. You can find rational reasons for this stuff I’m sure. But the words “conflict of interest” should be brought up here. They should be brought up a lot. Especially when certain people who have been at the forefront of HIV research over the last 20 or so years have also made themselves multimillionaires based on their research. Does the fact that they’ve made money mean they’re venal and dishonest? No, no, no, no, no. I refer you again to the words “conflict of interest,” and point you to the fact that the establishment has literally made it *impossible* to work with HIV in a lab without risking going to jail if you don’t get their permission.

    I find it all troubling. And I do not hesitate to tell people, “there is reason to believe the scientific establishment may be wrong here… and here are the reasons that trouble me.”

    In closing, for Francis—who probably won’t read this, because it’s much too long—you seem to think I’m trying to convince people that HIV doesn’t cause AIDS. I’m not. The question is, why are others trying to convince us that it does? Is it purely because there’s no reason to doubt? Is anything in science, or the law, so utterly certain?

    (Note: I have a life and cannot devote it to discussing HIV and AIDS. I will likely not be back to this thread to see any responses unless someone emails me or otherwise lets me know there’s something they really feel I must see or respond to. I would rather be spending time on my own weblog, where I write about a thousand things besides AIDS, or playing with my sons, or spending time with my wife. Thanks.)

  126. #126 Shygetz
    February 25, 2006

    Hank said:

    Cargo cult science at its best:)I love it!

    and Darin said:

    See my posts on the original Bethell thread on this, re: epidemiology justifying biology and biology justifying epidemiology. In 1982, HTLV-III was not known, and in 1985 almost everyone believed it caused AIDS. Within a couple years, HIV was part of the CDC definition. So, there should be some paper OR series of papers that warranted this enormous change of mind. Unless you want to quote “all papers published between 1982 and 1985″.

    Hank, coming from you, that’s a complement (way to dodge my point and rely on ridicule). Even though you don’t deserve it, since Darin actually addressed the comment in an appropriate manner, you can share in my response to him.

    If the only epidemiological studies were done between 82 and 85, you might have a point (although with the weight of the research that has been done into the biology of HIV since then, we could probably predict it as a pathogen without having epidemiological evidence). However, as many others have pointed out, many valid epidemiological studies have been performed since 85, none of which relied upon the earlier studies to be valid. Therefore, the only valid motivation for limiting studies to this timeframe (as opposed to simply limiting them to epidemiological studies in general) would be to state that scientists jumped the gun in endorsing the HIV-AIDS theory back then; it still would not address the question of the current epidemiological support for the theory.

    Dean said:

    Still, I got even more skeptical when some folks claiming to be scientists–some of them part of this discussion–said that there was simply no need to refute any of the papers Duesberg has published on HIV, because the evidence is so overwhelmingly against them they can simply be ignored.

    Are you blind, man, or merely a selective reader? Just PubMed “Duesberg HIV” and you will find numerous refutations of his postulates that refer to him by name. If you investigate the literature more deeply, looking for manuscripts that cite Duesberg’s skeptic publications, you will find even more.

    I have no problem with skepticism or dissenting scientific opinion; what I have a problem with is the manner in which people are trying to circumvent the scientific process and take their untested hypothesis directly to the public via popular literature and mass communication. Stop sniping from the scientific sidelines–collect your own epidemiological evidence (which doesn’t require NIH approval) and publish it in peer reviewed journals. If you have sufficient evidence on your side, you will not be ignored forever. Or, alternatively, you could do the striking single-subject study proposed earlier to refute the HIV-causation of AIDS. You must admit, it would be a very dramatic public gesture, putting your metaphorical money where your mouth is. While I do not recommend it, it would certainly prove that you have the courage of your convictions.

    Or, you could continue to bitch in blogs. That’ll show ‘em.

  127. #127 Richard
    February 25, 2006

    The epidemiology of HIV infection was predicted fairly well by the epimiology of hepatitis B, that epidemiological work was done in the 60s and 70s by, among others, Wolf Szmusness. A key difference is that HIV replicates much better in activated T cells (a consequence of the virus’s replicative machinery, which works best in transcriptionally active cells from which it can crib nucleotides), so things that increase immune activation – i.e. STDs – are typically associated with an increased risk of HIV infection. T cell activation also upregulates expression of CCR5, the major cooreceptor for viral entry into CD4 T cells. Also, geography influences background immune activation: Africa, being the seat of life, has the greatest pathogen diversity. Regardless of where you’re from, if you live in Africa your immune system will be more activated (with more CCR5-expressing T cells) on an ongoing basis than if you live in Italy, for example. This was nicely shown by a study that compared immune activation in Italians and Ugandans living in Rome to immune activation in Italians and Ugandans living in Uganda. There is a strong likelhihood that this explains the differential transmission rates that have caused so much controversy. I sometimes think that people love to obsess about sexual practices so much that they forget that, because HIV is a disease of the immune system, the answers to most of the questions people have are going to lie in human immunology.

  128. #128 George
    February 25, 2006

    So Harper’s has just disgraced itself completely, rendering its otherwise intelligent article on impeaching Bush to the trash bin of being utterly discredited. That is depressing.

    Why? Because in the same edition, they published a lengthy bit of drivel by that idiot, Celia Farber. Apparently, Harper’s has absolutely no fact checkers at all.

    Celia hasn’t any more brains than Gina Kolata. Two peas in a pod of nihilistic emptiness.

    HIV exists. It is the proximate cause of AIDS. And the denialists who are HIV+ generally find that out the hard way. Like David Pasquarelli, they wind up with opportunistic infections and then die.

    Like so many millions of men, women and children around the world, denied access to care through a heady and sickening mixture of political weakness, genocidal greed on the part of the pharmaceutical industry, religious intolerance, lack of public health infrastructure and–to a certain degree–buying the codswallop of morons like Mr. Bialy and others.

    It is truly, deeply profoundly depressing and pathetic.

    Worst, in terms of basic science issues, is how this idiotic debate subsumes the far more critically important question of HOW does HIV cause AIDS? A more rigorous examination of this question can have pertinent and important therapeutic implications, from micronutrient interventions and protecting gut function to actually developing a vaccine that could be effective.

    Carry on. To my dear friends who are trying to persuade these fucking nutjobs–I say good luck. I’ll contribute from time to time here too….but we all know full well that most of the hardcore denialists have their brains stuck where not even the best proctologist could find them.

    (The one exception being Robert Root-Bernstein, who says he now realizes HIV causes AIDS but caveats that it may require a co-factor. Closer and more intelligent but probably not true.)

  129. #129 Karen Lynne Lambert
    February 25, 2006

    Any discussion of AIDS without mentioning CFS (and/or HIV-Negative AIDS) as a major epidemiological issue is absurd.
    http://www.lemonfoundation.blogspot.com

  130. #130 George
    February 25, 2006

    I swear, some of these guys just make crap up.

    **
    Thormar H. Maedi-visna virus and its relationship to human immunodeficiency virus. AIDS Rev. 2005 Oct-Dec;7(4):233-45.

    University of Iceland, Institute of Biology, Sturlugata 7, 101 Reykjavik, Iceland. halldort@hi.is

    Maedi-visna is a slow virus infection of sheep leading to a progressing lymphoproliferative disease which is invariably fatal. It affects multiple organs, but primarily the lungs where it causes interstitial pneumonia (maedi). Infection of the central nervous system was commonly observed in Icelandic sheep (visna), infection of mammary glands (hard udder) in sheep in Europe and the USA, and infection of the joints in sheep in the USA. The name ovine progressive pneumonia (OPP) is commonly used in the USA and ovine lentivirus (OvLV) infection is also a name used for maedi-visna. A related infection of goats, caprine arthritis-encephalitis (CAE), is common in Europe and the USA. The natural transmission of maedi-visna is mostly by the respiratory route, but also to newborn lambs by colostrum and milk. Intrauterine transmission seems to be rare and venereal transmission is not well documented. Macrophages are the major target cells of maedi-visna virus (MVV), but viral replication is greatly restricted in the animal host, apparently due to a posttranscriptional block. The low-grade viral production in infected tissues can explain the slow course of the disease in sheep. The lesions in maedi-visna consist of infiltrates of lymphocytes, plasma cells, and macrophages, and are detectable shortly after experimental transmission. Several studies indicate that the lesions are immune mediated and that cytotoxic T-lymphocytes may be important effector cells. The persistence of the MVV infection is explained by a reservoir of latently infected blood and bone marrow monocytes, which migrate into the target organs and mature into macrophages with proviral DNA transcription, but limited replication of virus. The MVV particles are morphologically similar to those of other retroviruses and the mode of replication follows the same general pattern. The genome organization and gene regulation resembles that of other lentiviruses. In addition to gag, pol and env, MVV has three auxiliary genes (tat, rev and vif), which seem to have similar functions as in other lentiviruses, with a possible exception of the tat gene. A determination of the 9200 nucleotide sequence of the MVV genome shows a close relationship to CAE virus, but limited sequence homology with other lentiviruses, and only in certain conserved domains of the reverse transcriptase and possibly in the surface protein. MVV infection in sheep and HIV-1 infection in humans have a number of features in common such as a long preclinical period following transmission, and a slow development of multiorgan disease with fatal outcome. A brief early acute phase, which is terminated by the immune response, is also an interesting common feature. Like HIV-1, MVV is macrophage tropic and the early stages of the HIV-1 infection which affect the central nervous system and the lungs are in many ways comparable to maedi-visna. In contrast to HIV-1, MVV does not infect T-lymphocytes and does not cause T-cell depletion and immunodeficiency. This is responsible for the difference in the late stages of the HIV-1 and MVV infections and the final clinical outcome. Despite limited sequence homology, certain proteins of MVV and HIV-1 show structural and functional similarities. Studies of MVV may therefore help in the search for new drugs against lentiviruses, including HIV-1.

  131. #131 M. L. Green
    February 25, 2006

    Denial is an interesting thing, now isn’t it? One damned study isn’t the final word kids. Further, if the nasty little wee beastie *isn’t* transmitted sexually, then how the hell do you think it’s being transmitted? By ghosts, elves, and….(no, even I won’t sink that low)???? Come on now, pull yer heads out people.

  132. #132 haliaeetus
    February 25, 2006

    I don’t understand why these HIV-deniers are so emotionally wrapped up in the issue. It’s like HIV is evolution, to their AIDS god.

  133. #133 Richard
    February 25, 2006

    Darin Brown wrote:

    “From what I understand of shingles and reactivation of herpes viruses, this occurs when the immune system is compromised so much that reactivation is possible. This makes perfect sense to me. Reactivation should occur only in cases when there is some other reason for severe immunosuppression. But HIV is completely backwards in this regard — it’s supposed to be the CAUSE of the immunosuppression itself…but if it “reactives”, there must be something else suppressing the immune system? In other words, reactivation of HIV causes the immunosuppression, but at the same time, the reactivation wouldn’t be possible without that very immunosuppresion in the first place. So, yet another example of circular logic.”

    Funnily enough, this is actually a pretty good description of what is currently understood to be going on: HIV is preferentially suppressing the immune response to itself. This may sound a bit magical, but it really is not very surprising. HIV replicates best in activated CD4 T cells, and the majority of activated CD4 T cells that the virus is going to encounter are going to be those CD4 T cells that are becoming activated by HIV antigens (HIV-specific CD4 T cells). HIV’s ability to attach to dendritic cells – whose job it is to travel to lymph nodes and present HIV antigens to T cells – is likely a big part of the problem.

    And if the virus infects and compromises only a small % of HIV-specific CD4 T cells, that is sufficient to have knock-on effects on HIV-specific CD8 and B cells and thus allows the virus to escape immune surveillance enough to continue replicating, which in turn causes the activation of more HIV-specific CD4 T cells, which are in turn susceptible to infection and compromise…round and round it goes, circular indeed. The question of how this eventually depletes memory T cells specific for other pathogens is an interesting one that I won’t get into here (I think I’ve already started repeating myself as it is).

    And the shingles example is a very good one, since the question is: can a virus cause disease in the presence of antibodies? And since herpes zoster causes shingles in the presence of herpes zoster antibodies, the answer is yes. You’re right in that this is thought to be related to compromised T cell immunity to herpes zoster but again T cell immunity to HIV is also demonstrably compromised from the very earliest timepoints after infection, making the shingles analogy perfectly reasonable. Of course, there are also other viruses that can cause disease despite the presence of antibodies e.g. hepatitis B & C, herpes simplex, dengue (where the presence of antibodies can actually enhance disease).

  134. #134 Hank Barnes
    February 25, 2006

    Tara,

    I tried posting something last night, but it’s been blocked. It did have 3 or 4 links, so maybe that’s the cause.

    George,

    You seem a little unhinged.

    So Harper’s has just disgraced itself completely,..

    How so?

    Why? Because in the same edition, they published a lengthy bit of drivel by that idiot, Celia Farber.

    What in particular did you find unpleasant about the article? I’d like to read it, myself.

    Apparently, Harper’s has absolutely no fact checkers at all.

    I tend to doubt this. Is this hyperbole?

    Celia hasn’t any more brains than Gina Kolata. Two peas in a pod of nihilistic emptiness.

    So far, you’ve exhibited precious little brain-wave activity yourself.

    HIV exists.

    Yes, it probably does.

    It is the proximate cause of AIDS.

    Do you have a peer-review publication that you can cite to support this? I’m hoping for something in the 1984-1986 range.

    Also, outta curiousity, What evidence would falsify the presumed causal connection between HIV and AIDS?

    Like so many millions of men, women and children around the world, denied access to care through a heady and sickening mixture of political weakness, genocidal greed on the part of the pharmaceutical industry, religious intolerance, lack of public health infrastructure …

    I tend to agree with you here, George!

    “Codswallop”–I like that! Colorful use of language. “Morons like Dr. Bialy” would be more accurate, though.

    It is truly, deeply profoundly depressing and pathetic.

    Which part? (1)The pharmaceutical greed, (2) the corruption of governmentally directed science, or the irritating persistence of those who question both (1) and (2)?

    Worst, in terms of basic science issues, is how this idiotic debate subsumes the far more critically important question of HOW does HIV cause AIDS?

    No, the better question is, Does HIV cause AIDS?

    A more rigorous examination of this question can have pertinent and important therapeutic implications, from micronutrient interventions and protecting gut function to actually developing a vaccine that could be effective.

    I got nothing against micronutrient interventions or developing a vaccine. As to the latter, we have only 22 years of failure to show for it. Mebbe, folks have been barking up the wrong tree.

    Carry on. To my dear friends who are trying to persuade these fucking nutjobs–I say good luck.

    I dunno if I qualify as a FNJ, but good luck to you too George! Your vast understanding of science, medicine and logic has been quite illuminating.

    I’ll contribute from time to time here too….

    To continue this “idiotic debate”?

    but we all know full well that most of the hardcore denialists have their brains stuck where not even the best proctologist could find them.

    Funny! Are you an english lit type of fellow?

    (The one exception being Robert Root-Bernstein, who says he now realizes HIV causes AIDS but caveats that it may require a co-factor. Closer and more intelligent but probably not true.)

    Dr. Root-Bernstein wrote a great book, “Rethinking AIDS” I just got it from Amazon. Well-written and well-cited.

    Hank Barnes

  135. #135 Pharma Bawd
    February 25, 2006

    Hank,

    I just read the Padian paper (Thanks for posting it Tara!).

    And I have to say, you are way off base.

    Looking just at the prospective study 14.5% of the couples are abstaining from sex at their last follow up and 74% are consistently using condoms. That’s 88.5% of 175 couples who have removed themselves from your group of people having:

    “…unlimited, abundant, (dare I even say wild and kinky?) sexual acts over 10 years contracts HIV. Not one.”

    Then, the fact that 282 couple years divided by 175 couples comes out to 1.6 years per couple, not ten years.

    How confident are you that HIV is not sexually transmissible between heterosexuals if the study you are citing really only observed about 20 couples at risk of trasmission for only about 1.6 years?

  136. #136 Richard
    February 25, 2006

    Hank Barnes wrote:

    “No, the better question is, Does HIV cause AIDS?”

    If you really want to try and have an informed opinion about this question, you need to try and develop at least a passing understanding of human immunology. Unfortunately, your earlier comments about how vaccines work demonstrate that you do not. Until you do, I can’t see why anyone would feel it necessary to take a word of what you say seriously.

  137. #137 Mr. Bialy
    February 25, 2006

    from The Dusenberger

    “Today the San Francisco Chronicle reports the discovery of the prostate cancer virus by the Varmus clones and subclones Ganem and DeRisi at UCSF. DeRisi is also the hero who discovered the SARS virus 2 years ago and has since received a “genius award”!

    The new prostate cancer virus is tentatively called XMRV. The researchers acknowledge “It will take more studies …”

    This makes it 4 new pandemic viruses in 4 days, according to the SF Chronicle: 1) Wednesday, Bird Flu, 2) Thursday, Rotavirus, 3) Friday, West Nile virus, 4) Saturday morning, Prostate Cancer virus.

    I will let you know, what happens tomorrow, hopefully in time for you to take precautions in your daily risk behaviors.

    Cheerfully,

    Peter”

    Just thought I’d share.

  138. #138 Mr. Bialy
    February 25, 2006

    Richard,

    I’m just an ordinary moron, but it seems to me that 20+ years without a working vaccine means it is “you” guys that need to learn some immunology.

  139. #139 Mr. Bialy
    February 25, 2006

    And Richard, just think about. All you smart guy “virologists, tuned into the complexities of the immune system” (Fauci’s words) are outwitted for 20 years by a wee little beastie with a genetic complexity of 9000.

  140. #140 bialy
    February 25, 2006

    Richard, are you perhaps this Richard Miller who visited my “bllog” about one year ago?
    ————

    Richard Miller (mail):
    So? Is your posted assurance that “all questions will be cheerfully answered” another example of smoke, no mirrors? Eccles’s question has been twisting slowly, slowly in the void for more than 24 hours now ? do you intend to answer it?
    4.15.2005 12:00pm
    (link)bialy:
    richard,

    i am not so crazy as to begin internet discussions with eccles the cosmic idiot, no matter what.

    however, since it is you who are asking (presumably you are not eccles in cyberguise), allow me to provide a cheerful, experimental answer of exactly the same sort i once provided a ny highway patrol officer who had pulled over my 83 saab 900 for a defective tail-light and inquired about the nature of the handrolled cigaros on the dash.

    in this case though, you will need to print it before you smoke it to find out.
    4.15.2005 12:21pm
    (link)bialy:
    but richard,

    may i inquire as to what you might be fumigating, since according to the time signatures i just noticed on these posts, it will not have been 24 hours for a while.

    or maybe your horological devices are set for jupiter time as well?
    4.15.2005 12:26pm
    (link)Richard Miller (mail):
    I find you not the least bit humorous Dr. Bialy, anymore than I found your “falsification” of HIV/AIDS that received, and continues to receive so much attention on the blog thanks to the popular but misguided Dean Esmay, the least bit convincing.

    In any event, I shall not be returning, as I also find your so-called “art work” as intellectually empty as Duesberg’s “theories” about HIV.

    Richard Miller, Ph.D.
    4.15.2005 5:06pm
    (link)bialy:
    dick

    as the old jewish man on the subway said to the wall street investment banker who was telling his friend that he couldn’t wait for the taxi strike to be over so he wouldn’t have to ride with the riff raff….

    ‘vill miss you’
    4.15.2005 5:13pm

  141. #141 Richard
    February 25, 2006

    No, my name is Richard Jefferys, although it is rather hard not to sympathize with Mr. Miller. Am I to assume you haven’t got anything to say about the points raised above regarding immunology and HIV pathogenesis because you’re “just an ordinary moron.”? Thanks for sharing the Duesberg email, by the way, that comment about risk behaviors is so telling.

  142. #142 Wheatdogg
    February 25, 2006

    At the risk of being featured again in another of Bialy’s literary efforts, I am going to comment again, as an interested (indeed, curious) non-expert.

    Tara said:

    You use your arguments for HIV–things we don’t know yet or indeed, may never know–to say that the entire theory is flawed, yet no one puts those lofty demands on streptococcus, or helicobacter, or herpes.

    To which I would add our current model(s) of gravitation and the theory of the Big Bang.

    We do not know (yet, if ever) why objects have inertia. We observe that they do, and proceed from that point. Newton could not explain how two masses could act on each other across space, but yet developed a very effective model of gravitation without getting bogged down by explaining “action-at-a-distance.” Some of his contemporaries took him to task for that omission, implying he was invoking magical processes.

    We have not yet detected the gravitational waves that GR predicts, not the gravitons the Standard Model assumes must exist. Yet General Relativity is an accepted theory of physics, taught in some fashion to even first-year physics students.

    Big Bang theory cannot offer an explanation why there was a BB. The physics we have now only works to a point 10^-43 seconds after the BB. It does a stupendous job after that point.

    Forgive my using physics examples, but I am drawing parallels. From my non-biologist POV, the current HIV/AIDS model of transmission seems to be very effective in designing both preventive measures and treatment, regardless of any 100% positive causal link between the virus and the syndrome.

    To my knowledge, and I admit it’s very limited at this point, the Duesberg model does not offer any preventive measures or treatments.
    Perhaps someone from the dissenting POV could fill me in.

    During the Bethell fracas, I asked a question that has yet to be answered. So I will ask it again: why are there much lower rates of AIDS incidence in Muslim countries in sub-Saharan Africa than in non-Muslim nations? Could there be some correlation with sexual practices, dietary restrictions, etc.?

    From my perusal of the comments here and in the Bethell post, I am as yet unconvinced by the arguments of Duesberg, et alia, and judge that the majority opinion has won this debate.

    I am trying to be open-minded here, so please Bialy, Barnes and compadres, do not blast me with references to websites I will visit on my own or to book reviews, or use gutter Spanish in e-mails. (Si, hablo espanol bastante bien, gracias.) I am willing to explore and study. I am not willing to be bullied, insulted or condescended to.

    In addition, Dr. Bialy, please do not invoke my on-line persona in any more of your literary endeavours. That kind of publicity I can live without.

  143. #143 Hank Barnes
    February 25, 2006

    Pharma Bawd,

    Perhaps, you read Padian, but did you understand it?

    What part of “we found no seroconversions” (pg 354) is difficult to comprehend?

    Richard,

    I know that the AIDS vaccine has been an abysmal failure. I know the immune system is so complicated that even brainiacs like you can’t fully understand it.

    However, I do know that a virtually undetectable virus, that cannot even be cultured probably ain’t the cause of a defective immune system.

    Barnes

    Barnes

  144. #144 Richard
    February 25, 2006

    In trying to squeeze some semblance of meaning from your other posts, bialy, the best I can come up with is that, because I am one of the many people that believe HIV causes AIDS, I should be apologetic or embarrassed over the fact that there is no vaccine yet and because pathogenesis is not yet fully understood. I do not really understand why you think this. TB has done a pretty excellent job of outwitting scientists since the time of the Egyptians. Is there a rule that says, if the pathogen is made of RNA and has nine genes or less, you must be able to develop a vaccine in X years and understand pathogenesis in Y? Or rather, I suppose you are insinuating that an RNA organism with nine genes can’t possibly cause disease. You’re entitled to your opinion, I guess, although the dimwitted efforts of you and your colleagues to foist that opinion on others are regrettable.

  145. #145 Richard
    February 25, 2006

    Hank Barner wrote:

    “However, I do know that a virtually undetectable virus, that cannot even be cultured probably ain’t the cause of a defective immune system.”

    Virtually, probably. Nice use of qualifiers. It definitely causes immune activation, and that’s what correlates with progression to immune deficiency.

  146. #146 Harvey Bialy
    February 25, 2006

    Richard,

    Thank you for informing us that you are this Richard Jefferys.

    http://www.thebody.com/tag/tagix.html

    Your British use of “Mr.” is now also explained.

    Here are two links that give the lie to all your lies.

    http://www.rethinkaids.info/documents/Africa/Shisana.pdf

    http://www.tig.org.za/

    (These, and other “real deal” information packets are available on the “Africa” page of http://rethinkingaids.com

  147. #147 harvey Bialy
    February 25, 2006

    Richard,

    Thank you for informing us that you are this Richard Jefferys.

    http://www.thebody.com/tag/tagix.html

    Your British use of “Mr.” is now also explained.

    Here are two links that give the lie to all your lies.

    http://www.rethinkaids.info/documents/Africa/Shisana.pdf

    http://www.tig.org.za/

    (These, and other “real deal” information packets are available on the “Africa” page of http://rethinkingaids.com

  148. #148 Pharma Bawd
    February 25, 2006

    Hank,

    Yeah, I got that part.

    What part of: 288/175 = 1.6 years, not 10 years. are you unable to understand?

    Then the fact that 1/3 of the study participants were using condoms consistently before entering the study. So our sample size of 175 couples is really only about 115 and most of those stopped having unprotected sex which dramatically reduced the chance for a transmission. So we have a much smaller, drastically shorter study than the one you proffered as evidence that heterosexual transmission of HIV is not possible. Add to that the other studies indicating heterosexual transmission, the genetic similarities between virus isolated from donor/recipient pairs, the fact that HIV cannot be an endogenous retrovirus as you suggested,…

    If Padian publishes a paper saying someone from her study has seroconverted, will you stop flogging her work? Or will you say it’s due to IV drug use or some other non-sex route of transmission?

  149. #149 George Kaplan
    February 25, 2006

    from Dr. Bialy,

    Richard,

    Thank you for informing us that you are this Richard Jefferys.

    http://www.thebody.com/tag/tagix.html

    Your British use of “Mr.” is now also explained.

    Here are two links that give the lie to all your lies.

    http://www.rethinkaids.info/documents/Africa/Shisana.pdf

    http://www.tig.org.za/

    (These, and other “real deal” information packets are available on the “Africa” page of http://rethinkingaids.com)

    thanks

  150. #150 Harvey Bialy
    February 25, 2006

    Richard,

    Thank you for informing us that you are this Richard Jefferys.

    http://www.thebody.com/tag/tagix.html

    Your British use of “Mr.” is now also explained.

    Here is a link that gives the lies to your lies.

    http://www.tig.org.za/

  151. #151 Harvey Bialy
    February 25, 2006

    Richard,

    Thank you for informing us that you are this Richard Jefferys.

    http://www.thebody.com/tag/tagix.html

    Your British use of “Mr.” is now also explained.

    Here is a link that gives the truth to your lies.

    http://www.tig.org.za/

  152. #152 David Lowenfels
    February 25, 2006

    To me this thread is ridiculous banter amongst fairly intelligent people. Focusing on sexual transmission is misguided, as it is only one small avenue for oxidative stress. Sexually-acquired does not necessarily equate to sexually transmissible.

    Antibodies are not proof of infection, especially given that there is no gold standard of isolation!

    ( The following is going a little beyond the subject of Padian, but I’m not sure where else to post it… )

    It is a well elaborated fact that the “HIV antibodies” are actually autoantibodies to cellular actin, myosin, and their oligomers, not to mention anti-mitchondrial and anti-carbohydrate antibodies. See the work of The Perth Group (“Does the Western Blot prove HIV infection?”)

    It is a proven fact that everyone tests positive if their blood is not diluted 200 times (see the work of Dr. Rob Giraldo, “Everyone Tests Positive”)

    That greedy bastard Gallo just cooked up the test to find an arbitrary threshold that made most PCP/AIDS patients positive.
    He used circular lab trickery to fish out antibodies to oxidized cells. See quote below from Kremer, as well as details in the HIVgate paper.

    Tara: If you are unfamiliar with the details of the Gallo fraud, please read the article “HIVgate” by Janine Roberts at http://www.sparks-of-light.org/HIVGATE%20-%20review%20copy.pdf which outlines the sheer deception that Gallo premedititated in his “seminal” publications.. as convicted by a congressional investigation into outright scientific fraud. Not only did he steal the cell culture and EM photograph from the Montagnier, but he also lied about his methods (pooling supernatants from scores of patients in order to get RT activity, as well as spiking the cultures with hydrocortisone.) No one ever got a real EM picture of the so-called “isolate” until 1997, when they showed it was mostly cellular debris and not virus! http://aliveandwellsf.org/library#microvesicle
    Sure, it’s 20 years old, but it is the “seminal” papers for the HIV theory.. a house of cards.

    In my educated opinion, “HIV-antibody” seropositivity is nothing more than oxidative-stress induced autoimmune hypergammaglobulinema, mediated by glutathione deficiency overactivating the Th2 humoral immune system. The pathophysiology of AIDS is well explained by the Th1/Th2 shift (evolved program for downregulation of nitric oxide defense as protective to life-threatening inflammation in the organism)

    Tara, you asked if there was other work that you should be aware of. Please check out the work of Dr. Heinrich Kremer, who was inspired by the late Dr. Alfred Hässig. He is a man who actually knows what is going on here, and doesn’t need to postulate fictitious viral entities who can only be found by laboratory footprints.
    I recommend that you read his articles (iatrogenic death syndrome, answers to mbeki, did gallo manipulate the AIDS test to order, perversions of AIDS medicine, etc) They are most illuminating, and I have not yet been able to find holes in any of his logic.

    http://aliveandwellsf.org/kremer/

    “Because the falsely interpreted ‘anti-HIV-antibodies’ are not a defense mechanism against an infectious agent, a virus, but are autoimmune antibodies, all AIDS research at present and the resulting treatments are totally wrong. In earlier work I have described why a new retrovirus is not needed to explain the clinical picture called AIDS.” from interview with A. Hässig
    http://www.virusmyth.net/aids/data/mbhassig.htm

    To quote from Heinrich Kremer’s article, Acquired Iatrogenic Death
    Syndrome:

    http://www.virusmyth.net/aids/data/hkpneumo.htm

    “Dr. Gallo and his colleagues brewed their test soup from already
    overstimulated CD4 lymphocytes obtained mainly from the serum of PCP
    patients as well as from cells of a particularly division-prone
    leukaemia cell line, spiced this with powerful oxidising agents,
    called mitogens, added a generous dash of hydrocortisone, and
    incubated it thoroughly. They then fished out of this brew a mixture
    of proteins which they ascribed to a hypothetical retrovirus, HIV. It
    follows that these proteins (antigens), released under the oxidative
    stress in the test-tube, will necessarily bind to their complementary
    proteins (antibodies) from the serum of patients who had themselves,
    due to pathophysiological processes, formed proteins analogous to the
    test antigens from Gallo’s brew. Antibodies found in HIV-positives
    are therefore to be seen as nothing other than increased levels of
    auto-antibodies against endogenous proteins which have been produced
    as a result of highly increased cell-turnover under chronic oxidative
    stress.”

  153. #153 Chris Noble
    February 25, 2006

    Dean Esmay writes:

    I also think the fact that even after a quarter century, AIDS is STILL TODAY overwhelmingly found in men (77%, see http://www.avert.org/statsum.htm )–despite the fact that we’ve been hearing since the early 1990s that it’s “spreading rapidly” in women and that it’s vastly easier for women to get it than men–is reason to give one pause.

    What Dean neglects to mention is that the HIV statistics on the same webpage that the majority of people with HIV in the US are also male. If Dean bothered to read the CDC reports since 1985 he would find that the estimates of HIV infection show a distinct male/female bias that has gradually decreased over the 20 or so years. At this point 73% of new HIV infections are still male. None of this is consistent with a passenger virus spread by perinatal transmission.

    When Peter Duesberg says “Now, if we wanted to distinguish between infectious and not, here are the hallmarks of infectious diseases versus non-infectious diseases: All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes” is it really necessary to publish a refutation in a peer reviewed journal? Or is it sufficient to point to current statistics for dieseases like syphilis in the US?

    So far not one Duesberg supporter has attempted to either defend this assertion or admit he was wrong.

    This is just one example of the Duesbergian arguments that if we accept them to be valid we must also accept that syphilis is not a sexually transmitted disease.

    Why can a single Duesberg supporter not address this issue?

    PS. This post is 100% ad hominem free.

  154. #154 Dale
    February 25, 2006

    It seems to me that Duesberg has made a number of pronouncements that are simply untrue.

  155. #155 Bialy
    February 25, 2006

    Richard,

    Thank you for informing us that you are this Richard Jefferys.

    http://www.thebody.com/tag/tagix.html

    Your British use of “Mr.” is now also explained.

    Here is a link that gives the truth to your lies.

    http://www.tig.org.za/

    (

  156. #156 bialy
    February 25, 2006

    Richard Miller, PhD is an invention of the poet Mikhail Horowitz btw.

  157. #157 Chris Noble
    February 25, 2006

    It’s worth providing an example of the way that Duesberg deals with questions regarding his theory.

    Daf9/Dale wrote:

    Dean,

    If the offer of forwarding questions to Dr. Duesberg is open to anyone I have one for him.

    How does your hypothesis that HIV is not sexually transmitted explain the apparent HIV cluster found in upstate NY in 1997-1998 in which 13 of 42 identified sexual contacts of one hiv positive person became hiv positive. The majority of these contacts had no other known risk factors for hiv transmission and sequencing analysis from 10 of these individuals indicated that the hiv recovered was related.
    Robbins et al. (2002) AIDS Res Hum Retroviruses. 18,1157-61.

    Duesberg replied:

    “One swallow doesn’t make a summer ….”

    But, in order to “explain” an exception, more info is necessary:

    1) What, besides sex, was going on between ” one hiv positive person” and his/her (?) 13 positive “contacts”?

    2)Was this homo or hetero-sex?

    3) What other sexual contacts did the 13 have? What was their ethnicity? />
    4) How many of the 13 had AIDS, and if so which AIDS-defining disease??

    5) Did the “hiv positive person” have AIDS, and if so which disease??

    6) What “other known risk factors” did the minority of the 13 have? Did the “hiv positive” have another known risk factor”?

    7) How many sexual contacts did the 13 have with the “hiv person”? Or how long a relationship did the “hiv person” and his/her positive 13 recipients have?

    Can the person, who asked supply a pdf of the Robbins paper?

    The replies from Duesberg indicate that he hadn’t read the abstract let alone the paper. They also indicate a series of ad hoc excuses for ignoring or, dare I say, denying evidence that contradicts his theory.

  158. #158 Bialy
    February 25, 2006

    Richard

    If you really wish to discuss anything with me seriously, I make you the following offer I have made to a few.

    Write a review of my very highly acclaimed biogrpahy of Peter Duesberg and post it on your website. I will discuss it with you, one on one, until the last cow comes home.

  159. #159 Chris Noble
    February 25, 2006

    If Harvey Bialy wants to direct us to South Africa can he explain what David Rasnick is up to?

    He is listed as being scientifically responsible for this illegal trial

    Matthias Rath is a vitamin salesman that makes completely unsubstantiated claims about the efficacy of his products in curing cancer and heart disease. He also claims vitamin c is effective aginst HIV. People who want to find out what sort of person Matthias Rath is should google for “dominik feld”.

    Rath also has a habit of suing anyone who makes true but critical statements about him.

    He started processes against a number of media agencies for writing about the above “trial” but later withdrew the lawsuits.

    Isn’t it ironic. The Denialists like to make allegations about drug trials being fraudulent but when people find examples of fraud in their own pseudo-studies they slap lawsuits on them.

  160. #160 Richard
    February 25, 2006

    Bialy, Matthias Rath’s thinly disguised vitamin potion sales pitch website has nothing to say about any of the HIV immunology discussed above. Your generous offer that I write a review your “highly acclaimed” book is so tacky as to beggar belief. Free publicity for your book in exchange for ripostes like those above is just not a fair deal I’m afraid. It’s a shame you’re not willing to discuss how immunology impacts your theories without making such daft demands.

  161. #161 Bialy
    February 25, 2006

    No Noble, I can’t. Why don’t you write him and ask him yourself? I have always found Dr. Rasnick to be quite forthcoming in his responses to questions from whatever quarter.

    I would have thought it was pretty plain by now that “I” speak for me, myself and “i”, and no one else, ever.

  162. #162 Chris Noble
    February 25, 2006

    Harvey Bialy wrote:

    Richard
    If you really wish to discuss anything with me seriously, I make you the following offer I have made to a few.
    Write a review of my very highly acclaimed biogrpahy of Peter Duesberg and post it on your website. I will discuss it with you, one on one, until the last cow comes home.

    Why on earth is getting intelligent answers from you contingent upon writing a review of your book?

    You are consistently rude and abusive and repeatedly avoid any questions directed at you.

    You and Hank Barnes are the ones that brought up the Padian study. Now that people have given you clear reasons why this study cannot be used to argue that HIV is not sexually transmitted you make no comment on it. The title of this thread is “Discussion of the Padian paper” yet you have avoided anything related to the paper.

    You brought it up. Are you prepared to debate it? Will you just send more abusive emails?

  163. #163 Richard
    February 25, 2006

    Rath just dropped some of those intimidation law suits:

    http://www.guardian.co.uk/southafrica/story/0,,1716782,00.html

  164. #164 Bialy
    February 25, 2006

    Noble,

    I will actually address the substance of your queery.

    Because I spent 4 years writing the book, and in the academic circles in which I grew up, it was considered the ultimate admission of idiocy to refuse to read something whose subject you wish its author to discuss with you.

    And in this case, that so many very distinguished, non-AIDS denier scientists, physicians and others of generally very high intelligence have written about it so glowingly should make you as a highly intelligent skeptic of the skeptics dying to read it too, just like Richard from the RSA.

    I hope this is sufficiently clear to penetrate even your thick skull. And when have I ever written an abusive email to you? My abusive emails to Dr. Smith are found at http://bialystocker.net/files/Pipedream.pdf

  165. #165 Chris Noble
    February 25, 2006

    Harvey Bialy wrote:

    Noble,
    I will actually address the substance of your queery.

    Because I spent 4 years writing the book, and in the academic circles in which I grew up, it was considered the ultimate admission of idiocy to refuse to read something whose subject you wish its author to discuss with you.

    And in this case, that so many very distinguished, non-AIDS denier scientists, physicians and others of generally very high intelligence have written about it so glowingly should make you as a highly intelligent skeptic of the skeptics dying to read it too, just like Richard from the RSA.

    I hope this is sufficiently clear to penetrate even your thick skull. And when have I ever written an abusive email to you? My abusive emails to Dr. Smith are found at http://bialystocker.net/files/Pipedream.pdf

    I never claimed you had sent me any abusive emails. You have, however, sent abusive emails to a number of other people. You have sent more abusive emails than you have answered questions.

    I have read the papers that Duesberg has published on HIV/AIDS. Does your book have anything new in it?

    Are you willing to defend Duesberg’s claim “Now, if we wanted to distinguish between infectious and not, here are the hallmarks of infectious diseases versus non-infectious diseases: All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes”?

    Are you going to defend the assertion that Padian’s study demonstrates that HIV is not sexually transmitted?

    Are you going to provide a list of the “numerous innacuracies” in Tara’s post on Bethell?

    Will you descend into one of your multiple personalities?

  166. #166 Chris Noble
    February 25, 2006

    Harvey Bialy wrote

    No Noble, I can’t. Why don’t you write him and ask him yourself? I have always found Dr. Rasnick to be quite forthcoming in his responses to questions from whatever quarter.

    Where do I send my email/letter. c/o Matthias Rath Health Foundation???

    I would have thought it was pretty plain by now that “I” speak for me, myself and “i”, and no one else, ever.

    Except when you are championing Duesberg.

  167. #167 Dean Esmay
    February 25, 2006

    Bwahahahaha! Chris Noble says:

    “What Dean neglects to mention is that…”

    and this:

    If Dean bothered to read the CDC reports since 1985…

    …and ends with this:

    “PS. This post is 100% ad hominem free.”

    Hilarious! Just look up what ad hominem means in an elementary logic text. Noble presumes to speak of my motives, or what I know or don’t know, or what I have or have not bothered to read, in a clear attempt to discredit not my logic but my person. Otherwise, he’d have said “Yes Dean, but what about this, or this?” Then we’d be having a discussion, and there might even have been the possiblity of my changing my mind.

    Chris, as you’ve made so abundantly clear so many times in the past, you aren’t interested in anything but bashing and attacking. Which hurt my feelings back when I thought you were a decent person, but only makes me laugh now that I know you’re just a blustering clown with oversized shoes and a bright bulbous nose that squeaks when squeezed.

    You know as well as I do that the pages of the peer reviewed journals are where these arguments should be taking place, Chris. My conclusion is that you’re either far too cowardly to try, or, that you know perfectly well you’d be shown up as a phony and a fraud if you did. So you restrict yourself to endless hours of internet discussions where you can spout whatever insulting drivel you like about your fellow scientists without anyone calling you out on your crap. (Oh, and by the way, every bit of this is ad hominem, in direct response to the floppy-shoed clown who chose to turn this conversation in that direction.)

    Please Chris, don’t ever change. You’re just so precious exactly the way you are. Squeek squeek!

  168. #168 Bialy
    February 25, 2006

    Noble you nitwit

    “Except when you are championing Duesberg.”

    When I am “championing Duesberg”, whatever that might mean, it is *I* who speaks for me, myself and “i”. Peter has no trouble speaking for himself.

    Now bugger off little boy.

  169. #169 Chris Noble
    February 26, 2006

    Harvey just to prove that I do read Duesberg’s articles I’ll quote from The Chemical Bases Of The Various AIDS Epidemics

    “Prediction” 11 AIDS spreads by infection of HIV.

    “Fact” 11 But, contrary to the spread of AIDS, there is no spread of HIV in the US. In the US HIV infections have remained constant at 1 million from 1985 (29) until now (30), (see also The Durban Declaration and figure 1b). By contrast, AIDS has increased from 1981 until 1992 and has declined ever since (figure 1a).

    The first thing an enquiring mind would ask is how it was that 1 million people were tested for HIV in 1985. The simple answer is they weren’t.

    Reference 29. the data point for 1985 is The epidemiology of AIDS: current status and future prospects.

    The first thing that is noteworthy is that the estimate is 0.5-1 million. For some reason Duesberg takes only the high end of the range and gives absolutely no clue about the uncertainty in the estimate.

    The basis of the estimate comes from the San Francisco CDC cohort study with a total of 6875 subjects. In this cohort the seropositivity was found to have increased from 4% in 1978 to 68% in 1984.

    In this group HIV prevalence increased from 4% to 68% in six years. Duesberg uses this study as evidence that “there is no spread of HIV in the US”.

    Can Harvey explain how someone can use a paper that presents a rapid increase of HIV prevalence in order to show that “there is no spread of HIV in the US”?

    Why does Duesberg round the estimate of 0.5-1.0 million up to 1 million?

    I first asked these questions over a year ago.

    There have been no answers.

  170. #170 Dean Esmay
    February 26, 2006

    Yes your questions were answered a year ago, Chris. So not only do you engage in ad hominem, but you also lie, as usual, and prove yourself unworthy of taking seriously. (There’s that ad hominem thing again. I’m happy to use it against people who start with it.)

    By the way, could someone please explain “viral load” to the audience?

  171. #171 Chris Noble
    February 26, 2006

    Dean Esmay writes:

    Bwahahahaha! Chris Noble says:
    “What Dean neglects to mention is that…”
    and this:
    If Dean bothered to read the CDC reports since 1985…
    …and ends with this:
    “PS. This post is 100% ad hominem free.”
    Hilarious! Just look up what ad hominem means in an elementary logic text. Noble presumes to speak of my motives, or what I know or don’t know, or what I have or have not bothered to read, in a clear attempt to discredit not my logic but my person. Otherwise, he’d have said “Yes Dean, but what about this, or this?” Then we’d be having a discussion, and there might even have been the possiblity of my changing my mind.

    Dean, you are the one who needs to understand what an ad hominem fallacy is.

    I directed my attention to your argument. You did neglect to mention that the estimates of HIV prevalence from the CDC since 1985 have shown that that by far the majority are in high risk groups and that there is a much greater number of men infected with HIV than women. This is clearly incompatible with the idea that anything more than a small percentage < 8% are infected by the perinatal route.

    You also constantly refer to the male-to-female ratio of AIDS as being some sort of paradox. I referred you to the statistics for syphilis which have a higher male-to-female ratio.

    Instead of addressing these points you have chosen to attack my character. Wait a minute. Isn't that an ad hominem attack

    Chris, as you’ve made so abundantly clear so many times in the past, you aren’t interested in anything but bashing and attacking. Which hurt my feelings back when I thought you were a decent person, but only makes me laugh now that I know you’re just a blustering clown with oversized shoes and a bright bulbous nose that squeaks when squeezed.

    Obviously a rebuttal of my points?

    You know as well as I do that the pages of the peer reviewed journals are where these arguments should be taking place, Chris. My conclusion is that you’re either far too cowardly to try, or, that you know perfectly well you’d be shown up as a phony and a fraud if you did. So you restrict yourself to endless hours of internet discussions where you can spout whatever insulting drivel you like about your fellow scientists without anyone calling you out on your crap. (Oh, and by the way, every bit of this is ad hominem, in direct response to the floppy-shoed clown who chose to turn this conversation in that direction.)

    Dean, Duesberg does not have any support in the scientific field on this issue. If I was vaguely worried that scientists working in the area would take Duesberg seriously then it would be worthwhile publishing a rebuttal.

    The major support Duesberg receives is from lay audiences many of which are HIV positive and are desperate enough to believe that HIV does not cause AIDS.

    You are willing to champion Duesberg and his theories but are unwilling to answer any criticisms of these theories. You are the coward. I asked you to explain a number of problems with Duesberg’s theory that HIV is just a harmless passenger virus passed on by perinatal transmission. You admitted you could not answer them. If you can’t answer these questions then you are not in a position to champion his theories.

    Please Chris, don’t ever change. You’re just so precious exactly the way you are. Squeek squeek!

    Well that’s a nice change from calling me a fascist and promising to punch me in the face if you ever saw me.

  172. #172 Chris Noble
    February 26, 2006

    Dean Esmay writes:

    Yes your questions were answered a year ago, Chris. So not only do you engage in ad hominem, but you also lie, as usual, and prove yourself unworthy of taking seriously. (There’s that ad hominem thing again. I’m happy to use it against people who start with it.)

    Then you can point out exactly where they were answered rather than just accusing me of lying.

    Are you denying that Duesberg cites this paper The epidemiology of AIDS: current status and future prospects. as the source of his 1 million prevalence for 1985?

    Are you denying that the estimate of 0.5-1 million is based on the SF CDC cohort where HIV prevalence rose from 4% in 1978 to 68% in 1984?

    Are you denying that this is inconsistent with there being no spread of HIV in the US?

    By the way, could someone please explain “viral load” to the audience?

    HIV Viral Load Assays

  173. #173 Chris Noble
    February 26, 2006

    Dean Esmay writes:

    You know as well as I do that the pages of the peer reviewed journals are where these arguments should be taking place, Chris.

    If Dean is implying that such a debate has not taken place he is wrong. Here is a list of some of the papers in peer reviewed journals that have directly responded to Duesberg. It does not include the many more papers that have results that refute his arguments.


    WEISS RA
    HOW DOES HIV CAUSE AIDS
    SCIENCE 260 (5112): 1273-1279 MAY 28 1993

    LIFSON JD, PIATAK M, SAAG MS, et al.
    HIV AND AIDS – RESPONSE
    SCIENCE 260 (5115): 1705-1706 JUN 18 1993

    Sabin CA, Pasi KJ, Phillips AN, et al.
    Comparison of immunodeficiency and AIDS defining conditions in HIV negative and HIV positive men with haemophilia A
    BRITISH MEDICAL JOURNAL 312 (7025): 207-210 JAN 27

    OBrien SJ, Goedert JJ
    HIV causes AIDS: Koch’s postulates fulfilled
    CURRENT OPINION IN IMMUNOLOGY 8 (5): 613-618 OCT 1996

    SULLIVAN JS, LEARMONT J, LUMLEY T, et al.
    A DIRECT ASSOCIATION BETWEEN HIV AND AIDS IN BLOOD-TRANSFUSION DONORS AND RECIPIENTS AIDS RESEARCH AND HUMAN RETROVIRUSES 11 (10): 1147-1148 OCT 1995

    ASCHER MS, SHEPPARD HW, WINKELSTEIN W, et al.
    DOES DRUG-USE CAUSE AIDS
    NATURE 362 (6416): 103-104 MAR 11 1993

    HOFFMANN GW
    A RESPONSE TO DUESBERG,P.H. WITH REFERENCE TO AN IDIOTYPIC NETWORK MODEL OF AIDS IMMUNOPATHOGENESIS RESEARCH IN IMMUNOLOGY 141 (8): 701-709 OCT 1990

    KURTH R
    DOES HIV CAUSE AIDS – AN UPDATED RESPONSE TO DUESBERG THEORIES INTERVIROLOGY 31 (6): 301-314 NOV-DEC 1990

    WEISS RA, JAFFE HW
    DUESBERG, HIV AND AIDS
    NATURE 345 (6277): 659-660 JUN 21 1

    JACKSON JB, KWOK SY, SNINSKY JJ, et al.
    HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 DETECTED IN ALL SEROPOSITIVE SYMPTOMATIC AND ASYMPTOMATIC INDIVIDUALS
    JOURNAL OF CLINICAL MICROBIOLOGY 28 (1): 16-19 JAN 1990

    ASCHER MS, SHEPPARD HW
    AIDS AS IMMUNE-SYSTEM ACTIVATION – A MODEL FOR PATHOGENESIS
    CLINICAL AND EXPERIMENTAL IMMUNOLOGY 73 (2): 165-167 AUG 1988

    OBrien TR, Blattner WA, Waters D, et al.
    Serum HIV-1 RNA levels and time to development of AIDS in the multicenter hemophilia cohort study
    JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION 276 (2): 105-110 JUL 10 1996

    ASCHER MS, SHEPPARD HW, WINKELSTEIN W
    AIDS DATA – RESPONSE
    SCIENCE 268 (5209): 351-352 APR 21 1995

    HORTON R
    WILL DUESBERG NOW CONCEDE DEFEAT
    LANCET 346 (8976): 656-656 SEP 9 1995

    FOX CH, HOOVER S, CURRALL VR, et al.
    HIV IN INFECTED LYMPH-NODES
    NATURE 370 (6487): 256-256 JUL 28 1994

    HORTON R
    DO DRUGS CAUSE AIDS
    LANCET 341 (8846): 686-686 MAR 13 1993

    MADDOX J
    HAS DUESBERG A RIGHT OF REPLY
    NATURE 363 (6425): 109-109 MAY 13 1993

    Sabin CA, Phillips AN, Lee CA
    Arguments contradict the ”foreign protein-zidovudine” hypothesis – Response
    BRITISH MEDICAL JOURNAL 312 (7025): 211-212 JAN 27 199

    SCHECHTER MT, CRAIB KJP, GELMON KA, et al.
    HIV-1 AND THE ETIOLOGY OF AIDS
    LANCET 341 (8846): 658-659 MAR 13 1993

    BAGASRA O, HAUPTMAN SP, LISCHNER HW, et al.
    DETECTION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROVIRUS IN MONONUCLEAR-CELLS BY INSITU POLYMERASE CHAIN-REACTION
    NEW ENGLAND JOURNAL OF MEDICINE 326 (21): 1385-1391 MAY 21 1992

    Sarid R, Olsen SJ, Moore PS
    Kaposi’s sarcoma-associated herpesvirus: Epidemiology, virology, and molecular biology
    ADVANCES IN VIRUS RESEARCH 52: 139-232 1999

    EIGEN M
    THE AIDS DEBATE
    NATURWISSENSCHAFTEN 76 (8): 341-350 AUG 1989

    MOSS AR, OSMOND D, BACCHETTI P
    THE CAUSE OF AIDS
    SCIENCE 242 (4881): 997-997 NOV 18 1988

    Denialists have built a fantasy world where they can sit back and say “Nobody has ever refuted Duesberg”.

    It is true that nobody has managed to convince Duesberg that he is wrong. This is not the way that science works. There will always be contrarians that stubbornly cling to their own ideas till the deathbed. What is important is that the vast majority of scientists have been convinced through the scientific process that HIV exists and causes AIDS.

    Having lost in the normal scientific process Duesberg has resorted to writing books for lay audiences and reaching people through the internet. He has been vastly more successful in attracting a lay audience than he has in the normal scientific process.

  174. #174 Bialy
    February 26, 2006

    May I ask all of you evolutionary biologists out there if one or another of you would care to express an opinion on the work, and intellectual calibre etc of Lynn Margulis?

  175. #175 George
    February 26, 2006

    Hank: I notice that in your response, you carefully elided the bit about David Pasquarelli. He’s not the only one who have literally died because they bought the nonsense of people like you.

    For you, the “better” question is, Does HIV cause AIDS. Answer: Yes, it does.

    Your desire for the proof in a narrow time period show your utter, abject disingenuousness.

  176. #176 Bialy
    February 26, 2006

    In case I be accused, yet again, of “pandering” my book on this weblog, I point to a free pdf of the page proofs of Chapter 3, which not only gives a complete, correct and comprehensible explanation of “viral loads”, but also answers the intriguing question on the back cover.

    http://bialystocker.net/files/Chapter_3.pdf

  177. #177 Dave S.
    February 26, 2006

    Bialy asks:

    May I ask all of you evolutionary biologists out there if one or another of you would care to express an opinion on the work, and intellectual calibre etc of Lynn Margulis?

    I think her earlier work on endosymbiotic theory was brilliant (and for a time highly controversial), and her more recent work on a more general symbiotic theory less convincing but still intriguing. As far as her intellectual calibre, she’s one of the great original thinkers of our time in my opinion.

    Why you ask?

  178. #178 Bialy
    February 26, 2006

    Because last night I received an email from a mutual friend that contained the following from Prof. Margulis:

    “The Bialy book to which your review sent us changed our lives: Duesberg reconsidered, etc.”

    So I was wondering if she was an ID nutjob too? Na mas.

  179. #179 Richard
    February 26, 2006

    Bialy wrote:

    “I will actually address the substance of your queery.”

    I have to confess I’m surprised you’re willing to make your prejudices so transparent. This and Duesberg’s little quip that you so kindly shared with us say more about your agenda than a Gibbons-length multi-volume tome. And of course, because of your agenda, facts are the last thing you’re really interested in. What you are peddling is propaganda. Now, why would you and friends – who I think we can safely assume share your retrograde prejudices – be trying to stop people with HIV from receiving treatment?

  180. #180 Dave S.
    February 26, 2006

    Bialy says:

    “The Bialy book to which your review sent us changed our lives: Duesberg reconsidered, etc.”

    Man, you are really pimping your book and website to the max.

    Who is “us”? Why the plual? “Changed our lives” … How?

  181. #181 Tara
    February 26, 2006

    I’ll note that many of Harvey’s and others’ comments still focus on things that I already mentioned, and again, would invalidate the germ theory altogether if applied universally.

    One word on the vaccine–the point of that would be to prevent infection on the first place. Neutralizing antibodies can prevent the establishment of viral infection when first exposed, even in cases where an immune response may not be able to clear an established infection. Again, group A strep provide a good parallel. 1) We have no vaccine, despite many decades of searching. 2) Bacteria can hide intracellularly (particularly in cells of the tonsils), preventing total clearance by the immune system. 3) Vaccine would be targeted to prevent acquisition of the infection in the first place, so bacteria can’t establish an intracellular reservior to later re-infect the host.

  182. #182 Karen Lynne Lambert
    February 26, 2006

    Over the last two years, I have read piles of medical research literature. HIV Negative AIDS (a.k.a. Idiopathic CD4 Lymphocytopenia, ICL) cases percolate throughout numerous HIV/AIDS research documents. I first stumbled across them in Johns Hopkins “2003 Medical Management of HIV Infection” guide (J. Barlett, J. Gallant – Chapter 2, Page 21) (http://www.hopkins-aids.edu/publications/book/03MMHIV1to3.pdf ). Interestingly, ICL cases also weave their way through the CFS literature (http://www.ncf-net.org/forum/presidentsMsg0402.html).

    HIV-NEGATIVE AIDS cases are the bridge that connects the CFS and AIDS paradigms. I wonder: if “AIDS” had been called a “low natural killer cell syndrome”, rather than having it’s present day man-made definitional construct, would the true nature of the relationship between AIDS and CFS been seen two decades ago?

    Interestingly, there are very strong coreelations between HHV6, AIDS and CFS (http://hhv6.blogspot.com). Also, interestingly: “Research conducted at Tulane University Medical Center suggests that Non-HIV AIDS is associated with a retroviral particle called Human Intracisternal A-Type Particle-Type II, or HIAP-II.” “Non-HIV AIDS patients may comprise perhaps one percent of all AIDS patients.” (http://www.autoimmune.com/Non-HIVAIDSGen.html).

    Statistically speaking, if there is an undiagnosed pathogen in my NON-RISK group body, it is not rare! Thus, I can only conclude that the 1% is grossly understated, and that there are probably MILLIONS of undiagnosed infectious patients in that are defaulted into the mysterious miscelleneous CFS category just waiting to be systemically diagnosed(http://www.cdc.gov/ncidod/diseases/cfs/publications/causes.htm#6),

    All I suggest, as AIDS reappraisors, is that you please: 1) open your eyes to a 3 dimensional discussion (HIV/AIDS, AIDS Myth:HIV-Negative AIDS, and CFS), 2) stop debating based on passion and 3) start debating CFS fact!!

  183. #183 Bialy
    February 26, 2006

    More shameless pandering:

    Prof. Miller just sent me this:

    Donald Miller
    to me
    3:18 pm

    Harvey,

    That’s great. I am familiar with Lynn Margulis’ work. She is a solid thinker and investiagor. She is a maverick who does not suffer fools. Two of her best books are Mystery Dance: On the Evolution of Human Sexuality (1991) and Microcosmos: Four Billion Years of Evolution from Our Microbial Ancestors (1997). I have not read her most recent one, Acquiring Genomes: The Theory of the Origins of the Species (2003).

    Your email has spurred me to order it. Check out the first reader’s review of it on Amazon. It would appear to be an aneuploidy view of evolution, as opposed to the genetic mutation dogma the neo-Darwinists espouse.

    I cite Lynn Margulis in the Postscript of my book Heart in Hand (the complete text of which is on my website–and is also sold by Amazon), in this paragraph:

    In carrying out this project I was struck by how close a biological connection we humans have with other living things. Just how tight this connection is was not well appreciated when I attended medical school more than thirty-five years ago. It turns out that a human being—all 100 trillion cells of one—can be viewed, in essence, as a highly evolved bacterial community with a multibillion-year history. We are, in a sense, “walking communities of bacteria,” as the microbiologist Lynn Margulis and science writer (her son) Dorion Sagan put it. Before some of them combined to form a more complex eukaryotic cell, bacteria were part of a stable and enduring living system that has blanketed the planet and survived for billions of years. Left alone, as we have seen, bacteria, having no nucleus, simply clone themselves. Our bacteria derived eukaryotic cells are evolutionarily designed to reproduce themselves through sex. And, as we have also seen, the biologic price of sex, and individuation, is death.

  184. #184 Dave S.
    February 26, 2006

    Margulis had positive evidence to back up her assertions.

  185. #185 Bialy
    February 26, 2006

    According to sources who should know, The Gay Men’s Health Crisis Center estimates the following chances for gay men to contract HIV via bathhouse (chemically-faciliated) sexual activity.

    About 1 in 50 if you are a bottom, and 1 in 500 if a top.

    This is the same ratio as Padian found for heterosexual transmission), so she must have gotten something right.

  186. #186 Dean Esmay
    February 26, 2006

    I was going to just give up on this conversation but then I got a note from Duesberg in response to this:

    “When Peter Duesberg says ‘Now, if we wanted to distinguish between infectious and not, here are the hallmarks of infectious diseases versus non-infectious diseases: All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes’ is it really necessary to
    publish a refutation in a peer reviewed journal? Or is it sufficient to point to current statistics for dieseases like syphilis in the US?”

    I forwarded it to Professor Duesberg, who responded:

    Dean,

    Please ask him to identify the refrence that he puts in quotes.

    Peter

  187. #187 McKiernan
    February 26, 2006

    Duesberg Lecture, Cal Alumni 1993

    (http://www.duesberg.com/about/pdlecture.html)

    “Now, if we wanted to distinguish between infectious and not, here are the hallmarks of infectious diseases versus non-infectious diseases: All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes. Of course, if you look at a narrow enough group, if you look at a monastery, that is male or female, which is what they do in cohort research, you’ll find it all of the sudden infecting only the boys or the girls. But if you averag e it out over 250,000,000 Americans, 200,000,000 Europeans, or a billion Africans, you will always find it equally distributed between the sexes. No exceptions.”

  188. #188 Pharma Bawd
    February 26, 2006

    Dean,

    Try this:

    Talk By Peter Duesberg
    CAL Alumni Day 6 March 1993

    http://www.duesberg.com/about/pdlecture.html

    It also contains this:

    ” There is no infectious disease that is ever so unevenly distributed. Virtually all of them are 50%. So it is very difficult to find a common cause.”…
    “But if you averag e it out over 250,000,000 Americans, 200,000,000 Europeans, or a billion Africans, you will always find it equally distributed between the sexes. No exceptions.”

  189. #189 Pharma Bawd
    February 26, 2006

    I don’t want to call the man’s honesty into question, but…

    since this begins to look more and more like a Creationist denying the facts of evolution, could someone save a screenshot of that page?

  190. #190 Pharma Bawd
    February 26, 2006

    Just out of curiosity gentlemen,…

    When was your last vaginal yeast infection?

  191. #191 McKiernan
    February 26, 2006

    I seem to have found an echo chamber. Must be too many bombing missions by my friend Yossarian.

    Catch 22

  192. #192 Chris Noble
    February 26, 2006

    Dean I have already cited the source here February 20, 2006 04:19 AM

    You seemed to have been to busy attacking the character of Tara and everybody else to bother reading it.

    The comment comes from a talk Peter gave in 1993. I read it on his own website.

    You might say that was over 10 years ago he doesn’t say anything that wild now.

    Well he does.

    Viral AIDS – like all viral/microbial epidemics in the past (41 43) should spread randomly in a population. (emphasis mine)

    Just go to the CDC webpage and read it.

    You’ll find that gonorrhea infects African Americans at 19 times the rate per population of whites. You’ll find that syphilis infects men at 6 times the rate of women.

    Are gonorrhea and syphilis sexually transmitted diseases? The male-to-female ratio for syphilis is higher than that for HIV! If we accept Duesberg’s “reasons” for doubting that HIV is sexually transmitted we have to also apply them to syphilis, gonorrhea, herpes simplex etc.

  193. #193 Chris Noble
    February 26, 2006

    My response has been put in the queue. Must have put too many links in it.

    Others have already shown that neither Dean nor Peter appear to be able to use google.

    In case people think that this was a one-off then here is another quote.

    Viral AIDS – like all viral/microbial epidemics in the past (41 43) should spread randomly in a population. (emphasis mine)

    Again simply go to the CDC website and you’ll find that gonorrhea infects African Americans at 19 times the rate of whites and syphilis infects men at 6 times the rate of women.

  194. #194 jonny
    February 26, 2006

    Harvey’s now citing the numbers I cited on Dean’s blog a few days ago. 1 in 50 chance if you’re a bottom. 1 in 500 chance if you’re a top. And that’s only–read this closely now–if your partner is HIV+. So imagine how many partners it would likely take to become infected.

    These numbers, which I suspect would surprise many people, might still account for the explosion of HIV/AIDS in urban gay men, where a culture of promiscuous and unprotected sex once reigned supreme. It cannot, however, explain a similar “explosion” in Africa.

    All of this debate over whether HIV can be transmitted sexually has obscured what to me is the more interesting question: how can Padian’s numbers, or the numbers of the other studies cited, explain an explosion, an “epidemic,” or a “pandemic,” as HIV/AIDS has been called.

    Even if Hank Barnes and Duesberg are wrong, and I suspect they are, Tara et al. aren’t necessarily off the hook.

  195. #195 Chris Noble
    February 26, 2006

    Jonny I have addressed that point here February 24, 2006 06:18 AM

    Gray took the estimates of transmission risk from his cohort and used them together with number of sexual partners, frequency of intercourse, viral load simulated the epidemic.

    What is important is if we take a population with X HIV+ people will the number of infected people go up or down. It comes down to on average how many people one person infects. If it is less than one the prevalence will decrease exponentially. If it is more than one then the prevalence will increase exponentially.

    It is important to note that there is not a linear relationship between the reproduction number (and the risk factors) and the observed prevalence rates. It is a non-linear process.

    It is also worthwhile emphasising that epidemics of sexually transmitted diseases are not spread by monogamous couples.

  196. #196 Dean Esmay
    February 26, 2006

    Heh. Mr. Noble the “I don’t do ad hominem attacks” once again takes a perfectly rational request–”where exactly are you quoting that from?”–and turns it into an ad hominem, while his vicious cronies read even more into the request. It just keeps getting funnier.

    Anyway, thanks for the response kids. You keep having your fun now. Do let us know if you ever figure out how to use a word processor to submit something to a peer-reviewed publication now…

  197. #197 Pharma Bawd
    February 26, 2006

    Dean,

    Please do ask your readers to explain to you what an ad hominem attack is. You’re obviously too stupid to understand the definition.

    Hint: The above was not an ad hominem. ;)

  198. #198 jonny
    February 26, 2006

    Chris: Since I lack access to the entirety of the study you’re citing, I can’t respond. Dr. Bialy: Care to respond in my place?

  199. #199 Dale
    February 26, 2006

    It would seem to me it comes down to, inequal distribution or not, does the distribution of the clinical disease, i.e. AIDS, follow the distribution of the virus, HIV? The literature convinces me that it does.

  200. #200 Chris Noble
    February 26, 2006

    Dean,
    It is a relatively simple process to cut and paste put of the citation into google and the relevant link pops up.

    I admit to not being particularly nice to you. That doesn’t make my arguments ad hominem.

    My argument is simple. Duesberg has repeatedly over the past two decades asserted that all infectious diseases are equally distributed between sexes and that they spread non-randomly.

    All I have to do is point you to the CDC website to demonstrate that this is not true. If you think that this is the first time that this has been pointed out to Duesberg you are wrong. People have been telling him this for years but he simply does not listen.

    You stubbornly refuse to deal with the issue and instead attack my character.

    You have accused me of lying but have not provided evidence. That is cowardly.

  201. #201 Dean Esmay
    February 26, 2006

    Okay Chris, perhaps you and I have merely misunderstood one another. I would like to think that–honestly, genuinely, I would like to think so. But just for the record, I DID put the whole thing into Google well before I asked. I came up with several things, some of which were close to what you quoted, none of which came from peer-reviewed papers. All of it seemed to come from remarks he made in public speaking engagements. So I would just ask Chris Noble on that score: would you honestly like to be quoted on every off-the-cuff remark you ever made in public? I wouldn’t.

    But I forwarded it all to Peter, and I just asked, “what do you have to say to this?” (Fair warning: at this point I do consider him a moderate friend, if not a close one). Peter asked a simple question: “What exactly did this come from?”

    Blunt observation about Duesberg: he is not, and never has been, particularly internet-savvy, and is certainly not a veteran of flame-wars. He’s just not. He’s an elderly and accomplished scientist who turns 70 this year. You can snear and you can mock, but honestly, how many of you are members of the National Academy of Sciences, or can boast of accomplishments of his caliber? This question DOES NOT mean he is right about anything in particular, but PLEASE, it’s something I’ve been asking all along: where’s the basic respect the man is deserved?

    So come now: Peter says, “uh, where is this coming from?” Can you not give this man the basic respect that says, “Professor Duesberg, you said X on Y occasion, can you defend it?”

    And this does get to my basic bone of contention with Chris and several others: god DAMN it, you don’t have to respect me. Why should you? I’m a fucking B.S. undergraduate for God’s sake. I don’t mean sh*t. But this man’s email address is a matter of public record. He’s a member of the National Academy of Sciences, which in America is second only to being a Nobel laureate. The entire field of retrovirology owes its existence in part due to this man. As crazy as you think he is, can you NOT do him the basic courtesy of saying, “Dr. Duesberg, you claim X. Can you please justify this for me?”

    Indeed, why the hell do you need ME to relay any of this crap? HIS EMAIL ADDRESS IS A MATTER OF PUBLIC RECORD. HE TEACHES AT BERKELEY FOR GOD’S SAKE. CAN YOU NOT FORMULATE AN EMAIL TO HIM??

  202. #202 Chris Noble
    February 26, 2006

    Dean Esmay writes:

    I came up with several things, some of which were close to what you quoted, none of which came from peer-reviewed papers. All of it seemed to come from remarks he made in public speaking engagements.

    So it’s okay to use this false rhetoric with lay audiences? I’m afraid that this just emphasises my point. Duesberg deliberately targets lay audiences. This particular piece of rhetoric from Duesberg has been particularly successful. I have been confronted numerous times with people saying that all infectious diseases are equally spread between the sexes and therefore AIDS is not infectious.

    Dean,
    you must remember that you are the one that promised a Single Damning Demonstration that would show that HIV cannot cause AIDS on your weblog.

    You are the one that said:

    Mark my words: this story is going to blow wide open sooner or later. My gut says that by the end of this year, no one will be talking about AIDS the same way again. It’s not going to be pretty. There’s going to be screaming and yelling and finger pointing and denial. Congress may even get involved.
    But HIV cannot be the cause of the AIDS epidemic.

    At the time you felt you were qualified to issue such a bold statement.

    Why don’t you feel qualified to answer my questions?

    If you are going to go on record on the internet making statements like that then you should be prepared to back them up.

    You are a coward.

    I saw the quality of the response that Duesberg gave to Dale’s question. It was pathetic and lazy. He didn’t even bother to read the abstract of the paper. He simply dismissed it sight unseen.

    I don’t care whether Duesberg is a member of the National Academy of Sciences if he can’t answer simple questions. I don’t argue from authority but from the evidence.

    If Duesberg says “All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes” it means nothing if the evidence shows otherwise.

    Here is another quote:

    All infectious diseases strike within weeks, days, or at the most, months of infection. There are no slow viruses or slow microbes. There are slow virologists, but no slow viruses. (Laughter)

    It seems that Duesberg is quite happy to insult his colleagues. Remember it is the Denialists that imply that everyone else is either stupid or lying.

  203. #203 Chris Noble
    February 26, 2006

    Dean wrote:

    But just for the record, I DID put the whole thing into Google well before I asked.

    OK, the snide comment I made was unnecessary. I apologise. I assumed that you were accusing me of lying again.

    I do find it personally insulting to be accused of lying. I find it cowardly that you don’t even attempt to support your accusation.

  204. #204 Bialy
    February 26, 2006

    Smith, Noble, Dale, Dave, Richard et al

    Reality street time.

    Not one of you miserable, illiterate morons is fit to lick Duesberg’s scientific dirty socks.

  205. #205 Chris Noble
    February 26, 2006

    Bialy wrote:

    Smith, Noble, Dale, Dave, Richard et al
    Reality street time.
    Not one of you miserable, illiterate morons is fit to lick Duesberg’s scientific dirty socks.

    Hmmm. The ad hominem fallacy and Appeal to Authority in the one sentence.

    Perhaps you want to comment on the current CDC statistics for gonorrhea and syphilis in the US and decide whether they are sexually transmitted diseases based on exactly the same criteria that Duesberg uses to claim that HIV is not sexually transmitted.

    Is it too much to admit that just perhaps Duesberg may have been wrong?

    You do have open minds. Don’t you?

  206. #206 Richard
    February 26, 2006

    Against my better judgement, I took a quick look at Bialy’s chapter three. In addition to articulating a doe-eyed affection for the ideas of Dr. Duesberg, the author makes specious arguments that are directed at literature that’s ten or more years old. In fact, out of 60+ cites (the numbering system is a mess for some reason), I count only 9 that are post-1990 and many of these are news reports or books. It is deeply ironic to me that, in order to imagine that a lack of cytopathicity would undermine the idea HIV causes AIDS – the main focus here – the denialists actually have to buy into the flawed premise of the virologists they are criticizing: HIV “must” be cytopathic to cause disease. But the fact that HIV is replicating primarily in activated CD4 T cells renders the point moot; these cells live no longer than a couple of days anyway. It is the persistent activation that is the problem, not cytopathicity.

    No immunologists that I am aware of still buy the David Ho tap and drain model of pathogenesis, few ever did. Witness the letters from people like Jonathan Sprent and Don Mosier that appeared in Nature in response to Ho’s paper. This does actually come up a bit at the end of the chapter but it is presented in such a bizarre way; it is a “distastrous admission” that Ho’s theory was shown to be incorrect and that we still don’t have a complete explanation of pathogenesis. Is it a “disastrous admission” to say that we still don’t fully understand how the human immune system works? Because that is the root of the problem when it comes to understanding HIV pathogenesis. Not too suprisingly, the scientific understanding of HIV pathogenesis is advancing in parallel with the understanding of human T cell immunology.

  207. #207 Dean Esmay
    February 27, 2006

    Well Chris, let me say this about you: anyone would be a fool to suggest that you are intellectually lazy. Either you’re just frikkin’ evil, or, you honestly believe the position you’re coming from. If you’ll grant me the same, we can talk to each other. Let us talk to each other, which is, honest to God, all I’ve ever wanted.

    We may have had a bunch of initial misunderstandings. Not least of which, when we first corresponded with each other, I swear, I thought you were another guy I knew named Chris Noble. The first 3-4 weeks where we were butting heads, I thought I was butting heads with someone I already knew, and was bewildered by the hostility. We should honestly write those first 3-4 weeks off, because a big part of my brain was saying, “Why is Chris being so angry with me? I don’t get it?!? RAAAARRH!”

    But now I get it. I screwed up. You’re not the same guy. Not the same guy at all. Whoops.

    Okay, let’s set ALL of that aside. Let’s start from square one:

    Why do you think Duesberg thinks what he does? Do you think it’s honestly because he wants black people and homosexuals to suffer? Do you think that’s a fair analysis? Come on man, is that a realistic interpretation of the man’s career? Do you think he’s that much the sadist? I know him, I’ve corresponded with him. He’s not like that.

    Do you think skeptics like me just express our skepticism because we revel in being rebels? I confess to being human, and thus a result of all such forces. But come on man, it’s not that simple. Is it?

  208. #208 Hank Barnes
    February 27, 2006

    Gentlemen:

    I know this is off-topic, but I have located my all-time favorite AIDS paper, from the esteemed pages of Cancer Research:

    Sandstrom et al. .Studies with canine sera that contains antibodies which recognize human immunodeficiency virus structural proteins. Cancer Res (1990).

    Short version: They gave HIV tests to dogs and — 50%, for crying out loud, turned out HIV+!

    Can we expect some major funding towards to the new “Doggy Vaccine” division of NAIDS to prevent future generations of our pooches from getting AIDS?

    In the meantime, can Lassie spare me some AZT?

    Barnes

  209. #209 Dean Esmay
    February 27, 2006

    Oh and by the way: that is as real and as raw and as truthful as I could possibly be.

    You can either choose to mock it or to accept it: it’s who I am.

  210. #210 Stein
    February 27, 2006

    Ricard you nitwit,

    Perhaps if you had applied a few neurons you might have figured out the following, which is made explicit in the notes to the first chapter of Bialy’s book.

    “10. Duesberg, P. H. 1983. Retroviral transforming genes in normal cells? Nature 304:219–225. [The convention used throughout this book for references within quotations is they will be presented in the order in which they occur in the text of the quotation, and in the format of
    the journal in which the article appeared.]”

    But then again somebody with their head so far up their ass and steeped in the crap of post-modern immunology cannot really be expected to do any better.

  211. #211 Richard
    February 27, 2006

    Not only do I not have access to the first chapter, I have no intention of ever reading it. And the referencing system still seems like a mess to me, however foolish that may be.

  212. #212 McKiernan
    February 27, 2006

    The pixelated brickbats seem to have cleared so he who has no dog in the fight would like to clarify the link re: Duesberg’s comment regarding his statement:

    “Now, if we wanted to distinguish between infectious and not, here are the hallmarks of infectious diseases versus non-infectious diseases: All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes….”

    The good news is yes, the quotation by Dr. Duesberg is in fact taken from a public speaking engagement and not a peer-reviewed article. The bad news it is a quotation that comes directly from:

    http: http://www.duesberg.com/about/pdlecture.html

    This would tend to suggest the remark is more than an off-the-cuff comment which the www. duesberg/com website wishes to expose for public scrutiny.

    Its amazing how the sudden interest to change directions on multiple levels on a a thread that up to Dale’s last statement:

    “It would seem to me it comes down to, inequal distribution or not, does the distribution of the clinical disease, i.e. AIDS, follow the distribution of the virus, HIV? The literature convinces me that it does.”

    would clearly indicate the side that has spent twenty years trying to jettison the HIV hypothesis got there arguments handed to them on a platter.

    Not to worry though as the bard has said,

    The quality of mercy is not strained,
    It is twice blessed, both on the paradigm that giveth,
    and the paradigm that taketh away.

  213. #213 Stein
    February 27, 2006

    McK,

    Are you an idiot too?

    Do you not see that the proposition you are so enamored of is nothing more than a restatement of the tautological definition of AIDS?

    “does the distribution of the clinical disease, i.e. AIDS, follow the distribution of the virus, HIV? The literature convinces me that it does.”

  214. #214 Chris Noble
    February 27, 2006

    Dean, let me be absolutely clear.

    I do not think that Peter Duesberg has anything other than honourable intentions. I do not think that he is homophobic. I think he truly believes what he claims. He has also made a far greater contribution to science than I have or probably ever will. He is quite possibly a nicer and better person than myself. By all accounts both from “rethinkers” and others he is a very likable person. None of this means that he is right about AIDS.

    I also respect Linus Pauling. He made enormous contributions both to science and society for which he was awarded two Nobel prizes. None of that will make me believe that megadoses of vitamin C can cure cancer without the evidence.

    I am afraid that when Duesberg says all infectious diseases are equally distributed bewteen the sexes and reality says otherwise I chose reality.

    You talk about reasonable doubt. I have spent a great amount of time looking at the precise reasons why people like Duesberg claim that HIV does not cause AIDS. So many of them are like this previous one.

    All infectious diseases cause disease straight away or not at all.

    All infectious diseases follow Farr’s Law

    All infectious diseases fulfil Koch’s Postulates

    The presence of antibodies indicates all active virus has been eliminated from the body.

    If we take any one of these then we are forced to conclude that syphilis, gonorrhea, chlamydia, Hepatitis B, typhus, TB, herpes simplex, adenoviruses, rhinoviruses, poliovirus do not cause disease.

    Put simply Duesberg’s reasons are not reasonable. The vast majority of scientists do not find them to be reasonable. This is not because they are too sheepish to challenge authority or think for themselves as you asserted in your Skeptican definition.

    I am sick of being told to just read Duesberg’s papers and that I’ll then see the light and stop believing that HIV causes AIDS (I had no fixed opinion when I started reading about this). Your Single Damning Demonstration that was supposed to falsify HIV/AIDS was dare I say arrogant. You insult the intelligence of a large number of scientists. Harvey Bialy offered nothing but condescension and derision. He is still in form and has not offered anything factual to support his claims.

    You are perfectly correct that my tone was hostile and at times rude. I called you a Denialist. This was after I had repeatedly informed you that Duesberg and Rasnick had cited this paper:

    The epidemiology of AIDS: current status and future prospects.

    for the claim that 1 million people were infected with HIV in 1985.

    This was not some supplemental reference. It was the only reference ever cited by Duesberg for 1985. He has cited it in 5 of his other papers.

    Duesberg, P.H. (1995) Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV
    (Genetica 95: 51-70)

    Duesberg, P. H. (1992) AIDS acquired by drug consumption and other noncontagious risk factors
    (Pharmac. Ther. 55: 201-277), and a searchable textfile.

    Duesberg, P. H. (1991) AIDS epidemiology: inconsistencies with human immunodeficiency virus and with infectious disease
    (Proc Natl Acad Sci USA 88: 1575-1579)

    Duesberg, P. H. (1989) Human immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation
    (Proc Natl Acad Sci USA 86: 755-764)

    Duesberg, P.H. (1987) Retroviruses as Carcinogens and Pathogens: Expectations and Reality
    (Cancer Research 47: 1199-1220)

    The paper by Curran et al gives an estimate of 0.5-1 million. No matter how many times I have been insulted or accused of lying nobody has managed to justify why Duesberg rounds it up to 1 million.

    Still worse than that is that the estimate was based on observations of the SF CDC cohort where HIV prevalence was seen to rise from 4% in 1978 to 68% in 1984. This is simply inconsistent with Duesberg’s assertion that HIV did not spread in the US. I think it is insulting to ask people to accept the estimate of 0.5-1 million rounded off to 1 million but to ignore the very data that the estimate is based on.

    The SF CDC cohort clearly shows a rising HIV prevalence over time followed by a rising incidence of AIDS. This is the same pattern that is seen repeatedly in sub-populations around the world.

    I even emailed you the Curran et al paper so you could read it yourself. You proceeded to ignore everything I said. This is when I called you a Denialist.

    All I have ever asked you to do is to think for yourself and not to rely on Duesberg as an authority. You had the arrogance to claim that you were going to demonstrate that HIV does not cause AIDS. The least you could do is respond to questions.

  215. #215 Chris Noble
    February 27, 2006

    It is worth reminding Hank Barnes that he has as yet neither attempted to defend his bold but stupid assertion that HIV is an endogenous retrovirus nor has he admitted he might have been in error

  216. #216 Richard
    February 27, 2006

    Did you have any comment on the age of Bialy’s cites, Stein? I didn’t spot anything amidst the insults. Do you think that, in 2006, something which hardly cites anything post-1990, let alone anything from the same decade, is a valuable contribution to scientific discourse?

  217. #217 Kristjan Wager
    February 27, 2006

    When one side of a debate cites references and links to statistics, and the other just insults and pimp their books, it would seem to me that the second group lacks any arguments to back up their stance.

    Like many others, I am reminded of the ID-crowd.

  218. #218 Dale
    February 27, 2006

    Does anyone know what post-modern immunology is supposed to be?

  219. #219 Orac
    February 27, 2006

    It is worth reminding Hank Barnes that he has as yet neither attempted to defend his bold but stupid assertion that HIV is an endogenous retrovirus nor has he admitted he might have been in error

    Nor will he do either, I predict.

  220. #220 Orac
    February 27, 2006

    Chris Noble to Dean Esmay:

    All I have ever asked you to do is to think for yourself and not to rely on Duesberg as an authority. You had the arrogance to claim that you were going to demonstrate that HIV does not cause AIDS. The least you could do is respond to questions.

    Cue Dean to accuse you of ad hominem attacks, repeat his assertions without answering your criticisms, and point out what great credentials Duesberg has.

  221. #221 Dave S.
    February 27, 2006

    Dale says:

    Does anyone know what post-modern immunology is supposed to be?

    Yes, it’s a branch of post-modern medicine. :)

  222. #222 Hank Barnes
    February 27, 2006

    Chris Noble,

    I do not think that Peter Duesberg has anything other than honourable intentions.

    Hey, that’s a good start!

    I do not think that he is homophobic.

    Ok.

    I think he truly believes what he claims.

    Ok.

    He has also made a far greater contribution to science than I have or probably ever will.

    Aw c’mon, Chris, don’t sell yourself short:)

    Just kidding. Good for you.

    He is quite possibly a nicer and better person than myself.

    You are draining all the bile out of this thread, with all this kindness. Maybe, we all should re-start the discussion, with civility, respect for each other’s views, without ad hominem, and then hammer out the issues.

    None of this means that he is right about AIDS.

    Totally true. The scientific evidence, not personalities, nor political agendas will determine whether or not HIV is the sole cause of T4-cell depletion.

    BTW, I’d be happy to argue the endogenous virus theory. But, it’s a 2-way street. You, Orac, and others have to answer this question:

    1. What evidence would falsify the contention that HIV causes AIDS?

    Tara sez: Find another “thing” causing it.

    Dale sez: Develop a vaccine that doesn’t work.

    So, let’s pick the forum, and get it on.

    Barnes

  223. #223 Pharma Bawd
    February 27, 2006

    Hank,

    A dozen volunteers from your side. A dozen needle sticks. A dozen years.

    No anti-virals, noillegal drugs, all the nutrition you want.

    Let’s see what happens.

  224. #224 Richard
    February 27, 2006

    Dale wrote:

    “Does anyone know what post-modern immunology is supposed to be?”

    No, but I quite like the idea of walking down a university corridor and seeing a sign that says: “Department of Post-Modern Immunology.” Anyway, it’s clear that even modern immunology has eluded the grasp of the denialists.

    Hank, apparently, is interested in what “will determine whether or not HIV is the sole cause of T4-cell depletion” despite his total igorance of what T4 cells (well, they tend to be called CD4 T cells these days Hank) actually do. The primacy of immune activation in disease pathogenesis would actually predict that during the asymptomatic phase of the infection, total body CD4 T cell counts might increase slightly despite their diminution in the blood. A German massacre of SIV-infected macaques, which sampled enough tissues to quantify ~50% of the CD4 T cell pool, reported exactly this finding.

  225. #225 David Lowenfels
    February 27, 2006

    Pardon me but are you guys and gals going to whine and argue all day about Duesburg and lame antibody tests or actually look into the pathophysiology and aetiology of this disease, which is oxidative stress!?

    Oxidation – the primary cause for AIDS and “HIV”
    21 January 2005

    Eleni Papadopulos-Eleopulos, Biophysicist

    http://www.rethinking.org/bmj/response_93597.html
    (reprinted from BMJ
    website, more info on the silencing of this debate at http://
    http://www.theperthgroup.com/bmjonline.html )

    Note that oxidative stress is needed in the cell cultures to elicit the “HIV particles”! Hellooo??

  226. #226 Richard
    February 27, 2006

    It’s always good to receive insights from a Biophysicist when you’re studying an immunological disease. Hellooo indeed.

  227. #227 Tara
    February 27, 2006

    homosexuals are exposed to relatively high levels of nitrites and anally deposited sperm,

    Not all of them, and heterosexuals can also be exposed to similar levels of “nitrites and anally deposited sperm.” I always find it amusing that these types of people assume only gay men have anal sex.

    David, can you please tell me where Papadopulos-Eleopulos published subsequent research backing up this hypothesis? Have reducing agents been administered (after all, this was presented 14 years ago!), and have they been successful?

  228. #228 Jean
    February 27, 2006

    Yes, Tara.
    For instance 3TC (epivir), FTC, efavirenz, lopinavir, nevirapine… are all reducing agents, contrary to AZT, wich is an oxidizing agent.
    How do I know that? Look at the metabolits ( http://www.rxlist.com) , and you will understand their properties :
    the only one which is reduced in vivo is AZT, giving aminothymidine or stavudine.
    For instance, 3TC gives S-oxy-3TC, nevirapine gives polyhydroxypyridine rings…
    You know well that the HAART has considerably reduced the full-blown aids and the death. The oxidative stress hypothesis allow also to explain it.

  229. #229 Richard
    February 27, 2006

    How would oxidative stress cause immune activation? The immune system gets activated by antigens. I think you’ll find oxidative stress is a consequence of immune activation due to the elevated number of cells that are committing suicide (activation-induced cell death/apoptosis); it is not the cause. Likewise, the decrease in immune activation which occurs on HAART is consistent with a reduction in antigen load and antigen presentation (you could also argue a direct reduction of T cell activation), but not a direct effect of HAART on oxidative stress.

  230. #230 Jean
    February 28, 2006

    For instance, this article :

    Platelet-Activating Factor and Oxidized LDL Induce Immune Activation by a Common Mechanism

    Johan Frostegard; Yi Hui Huang; Johan Rönnelid; ; Liselotte Schäfer-Elinder

    From the Department of Medicine, Division of Rheumatology, Karolinska Hospital (J.F., Y.H.H., J.R.), and the Department of Physiological Chemistry, Karolinska Institute (L.S.-E.), Stockholm, Sweden.

    (atvb.ahajournals.org/cgi/content/full/17/5/963)

    shows how oxidized LDL induces immune activation.
    I think that immune activation can also be the consequence of oxidative stress. The best word here is correlation between oxidation and immune activation, but not necessarily causation.
    Pr. Luc Montagnier said himself that the apoptosis of T-cells in AIDS is mediated by a strong oxidative stress (in french):

    “Enfin un des problèmes majeurs non totalement rĂ©solu de la pathogĂ©nèse du Sida, reste l’explication de la mort massive des lymphocytes T4. Contrairement ŕ Łe que l’on croyait il y a quelques annĂ©es, cette disparition, qui existe dès la pĂ©riode asymptomatique, n’est pas due Ă  l’infection directe des cellules par la souche virale, qui est alors peu cytopathogène, mais Ă  des mĂ©canismes indirects touchant les cellules CD4+ non infectĂ©es; celles-ci ont une propension Ă  mourir d’apoptose, comme d’ailleurs les cellules CD8+. En fait, toutes les sous-populations immunitaires sont touchĂ©es par ce phĂ©nomène, bien que ce soient les CD4+ qui disparaissent en nombre. Un des mĂ©diateurs de cette apoptose est l’existence d’un fort stress oxydant caractĂ©risĂ© par une prĂ©valence de molĂ©cules oxydantes (radicaux libres) sur les dĂ©fenses antioxydantes de l’organisme: ainsi le taux de glutathion oxydĂ© est-il très Ă©levĂ© de mĂŞme que celui des LDL (Low density lipoproteins) oxydĂ©es.”

    (www.robertogiraldo.com/brussels/montagnier.doc)

  231. #231 George
    February 28, 2006

    I think there is a definite case for the role of oxidative stresss in HIV disease pathogenesis.

    But as Richard adroitly points out, OS is not the CAUSE of AIDS. Immune activation leads to expression of inflammatory cytokines which can then lead to OS and apoptosis. Indeed, HIV invasion of the central nervous system is one where neuronal damage is not directly caused by infection but inflammatory responses arising from infected glial cells.

    The issue of massive depletion of bystander (uninfected) CD4+ lymphocytes I think is in part explainable by oxidative stress as one important mechanism (as it is in Hepatitis C disease).

    It IS something for which there are many intriguing therapeutic implications. Droge and his group have identified a MASSIVE loss of sulfur, primarily from loss of cysteine. That amino acid is the rate limiting step in the intracellular production of glutathione. Which is why I like whey proteins as an excellent and inexpensive (except for crap like Immunocal) intervention.

    Other interventions like N-acetylcysteine (NAC), acetylcarnitine, glutamine, alpha lipoic acid, omega-3 fatty acids and certain polyphenols all have important roles to play which are slowly being delineated in clinical trials.

    Indeed, the data show clearly that a mutlivitamin/mineral has significant effects on progression rates, morbidity and mortality.

    All that being said, it’s funny to see Eleni from Perth Group being raised. There’s one of the fascinating examples of cognitive dissonance in the Denialist community that somehow doesn’t bother them. She and her lot insist HIV doesn’t even exist. Yet Duesberg recognizes that it does. What to do?

    Vacilate between the camps depending on what idiotic denialist “argument” is being devastated by rational thought.

    But OS is an important issue and a manageable piece of HIV disease. Along with drug treatments as needed, such as antiretroviral therapy, and prophylaxis and treatment of opportunistic infections. NONE of that is yet the cure–but collectively, can help people stay alive and well. Possibly even to the point of anticipating a normal lifespan.

    Something denied to David Pasquarelli–something that denialism will result in the deaths of millions of South Africans who do not buy the denialist bullshit from people like Bialy, Duesberg, Eleni or Mbeki.

  232. #232 Tara
    February 28, 2006

    You know well that the HAART has considerably reduced the full-blown aids and the death. The oxidative stress hypothesis allow also to explain it.

    But no more so that the fact that the drugs are primarily antiretrovirals, and AZT works as well. What about reducing agents that *don’t* have antiretroviral properties?

  233. #233 Jean
    February 28, 2006

    For instance, you must look at this paper from Kalebic & al., from NIH, Bethesda :

    (www.pubmedcentral.nih.gov/picrender.fcgi?artid=50939&blobtype=pdf)

    This experiment can be easily reproduced.

  234. #234 Tara
    February 28, 2006

    But that’s still having the effect on HIV. You said that oxidative stress is the “primary cause” for AIDS. All that paper shows is that they have an antiviral effect, while I asked about agents that *don’t* have an antiviral effect. Whether the experiment “can” be reproduced with such agents isn’t the question–the claim put forth is that “Oxidation is the primary cause for AIDS and ‘HIV.’” I’m simply asking for evidence of that claim.

  235. #235 Jean
    February 28, 2006

    I give you this link, where Papadopoulos & al. question this more better as me :

    Reappraisal of AIDS–is the oxidation induced by the risk factors the primary cause?
    Papadopulos-Eleopulos E.
    Royal Perth Hospital, Medical Physics Dept., Western Australia.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3285143&query_hl=2&itool=pubmed_docsum

    you can find the whole paper here :

    http://www.theperthgroup.com/SCIPAPERS/reappraisalofaids.html

  236. #236 Tara
    February 28, 2006

    Jean,

    Medical hypotheses isn’t even a peer-reviewed journal. Still, even they note:

    The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific communication, which ideas must eventually enter if they are to be critiqued and tested against observations.

    That paper is 18 years old. Where are the experiments? That’s all I’m asking.

  237. #237 Jean
    February 28, 2006

    It is a review of experiments. Is it not scientific?

    Are these ideas been critiqued against observation? I don’t believe that.

    It should be interesting that you read this paper and scrutinize all the foot notes, to verify the reality of the described experiments, without any theoric prejudice.

  238. #238 Tara
    February 28, 2006

    It’s not a review of experiments–it’s a review of the epi with a focus on the “oxidation” hypothesis, published without peer review 18 years ago. Again, what I’m asking for are the experiments done since then to back up the hypothesis. There are all kinds of journals devoted to discussing hypothetical connections, causes, etc–but until the research is carried out to either support or falsify the hypothesis, that’s all they are: ideas.

  239. #239 George
    February 28, 2006

    Tara–there are data that show a role for oxidative stress in the context of HIV disease. NONE of them–even the one the nut job from Perth wrote about–are saying that OS is the CAUSE.

    Many diseases have oxidative stress as an important pathophysiologic component. Rheumatoid arthritis, Parkinson’s disease, HIV-associated dementia, hepatitis C disease, etc. Some references below.
    George M. Carter

    **
    Li W, Galey D, Mattson MP, Nath A. Molecular and cellular mechanisms of neuronal cell death in HIV dementia. Neurotox Res. 2005 Oct;8(1-2):119-34.

    RT Johnson Division of Neuroimmunology and Neurological Infection, Department of Neurology, Johns Hopkins University, Baltimore, MD 21287, USA.

    The deaths of neurons, astrocytes and endothelial cells have been described in patients with HIV (human immunodeficiency virus) dementia. HIV-1 does not infect neurons; instead, neurotoxic substances shed by infected glia and macrophages can induce a form of programmed cell death called apoptosis in neurons. These neurotoxins include the HIV-1 proteins Tat and gp120, as well as pro-inflammatory cytokines, chemokines, excitotoxins and proteases. In this article we review the evidence for apoptosis of various cell types within the brain of HIV-infected patients, and describe in vitro and in vivo experimental studies that have elucidated the mechanisms by which HIV causes apoptosis of brain cells.

    **
    Ozdener H. Molecular mechanisms of HIV-1 associated neurodegeneration. J Biosci. 2005 Jun;30(3):391-405.

    Monell Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104, USA. hozdener@yahoo.com

    Since identification of the human immunodeficiency virus-1 (HIV-1), numerous studies suggest a link between neurological impairments, in particular dementia, with acquired immunodeficiency syndrome (AIDS) with alarming occurrence worldwide. Approximately, 60% of HIV-infected people show some form of neurological impairment, and neuropathological changes are found in 90% of autopsied cases. Approximately 30% of untreated HIV-infected persons may develop dementia. The mechanisms behind these pathological changes are still not understood. Mounting data obtained by in vivo and in vitro experiments suggest that neuronal apoptosis is a major feature of HIV associated dementia (HAD), which can occur in the absence of direct infection of neurons. The major pathway of neuronal apoptosis occurs indirectly through release of neurotoxins by activated cells in the central nervous system (CNS) involving the induction of excitotoxicity and oxidative stress. In addition a direct mechanism induced by viral proteins in the pathogenesis of HAD may also play a role. This review focuses on the molecular mechanisms of HIV-associated dementia and possible therapeutic strategies.

    **
    Lanzillotti JS, Tang AM. Micronutrients and HIV disease: a review pre- and post-HAART. Nutr Clin Care. 2005 Jan-Mar;8(1):16-23.

    Nutrition/infection Unit, Department of Public Health and Family Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. jane.lanzillotti@tufts.edu

    Low serum micronutrient levels are common in HIV-positive individuals and have been associated with immune impairment, HIV disease progression, and increased mortality. Studies of micronutrient supplementation have yielded conflicting results, although several large trials suggest that multivitamin supplements, but not vitamin A, may decrease morbidity and mortality in some HIV-positive populations. Studies also suggest that antioxidant supplementation may decrease markers of oxidative stress in individuals with HIV, while selenium may enhance immune function by modulating cytokine production. Clearly, more research is needed, but current knowledge supports the use of a multivitamin supplement as a low-cost adjunct to antiretroviral treatment.

    …that’s just a start.

  240. #240 Tara
    February 28, 2006

    George–

    Sure, I don’t doubt there can be a role for OS in AIDS (or many other diseases). But Papadopulos-Eleopulos is pretty clear in that article:

    There is no compelling reason for preferring the viral hypothesis of AIDS to one based on the activity of oxidising agents. In fact, the latter is to be preferred, since unlike the viral hypothesis it leads to possible methods of prevention and treatment using currently available therapeutic substances.

    OS is *instead of* the “viral hypothesis of AIDS,” not in addition to it. I don’t know how tunes have changed since then, but that certainly seems to be David’s claim (stating that OS is the “aetiology” of the disease) and Jean hasn’t contradicted that either. Indeed, as you mention, what one group of “dissidents” may have long ago moved on from, others still hang onto and repeat.

  241. #241 Jean
    February 28, 2006

    I think that what you call hiv is called oxidative stress by these peoples.
    What puzzle me, is how you, biologists, know that the proteins detected below the cut’off are not “hiv antibodies”, while those detected above are actually hiv antibodies?
    If you don’t know it, but only assume it, thus aids is rather a metabolic disorder, better explained by oxidative stress than by hiv.

    Gallo and Zagury, in this paper :
    Long-term cultures of HTLV-III–infected T cells: a model of cytopathology of T-cell depletion in AIDS.
    Science, 1986,
    have shown that the decrease of T4-cells in 6 days culture was 26% in non activated (by phytohemagglutinin) hiv – culture, 70% in activated hiv – culture, and 91% in activated hiv + culture.
    thus, the “hiv” positivity acts in the same fashioning than phytohemagglutinin, which is an oxidative protein.

    This is backed by this paper :
    J Clin Invest. 1992 Nov;90(5):2123-9.
    Oxygen radical scavengers selectively inhibit interleukin 8 production in human whole blood.
    Deforge & al

    (www.pubmedcentral.gov/picrender.fcgi?artid=443281&blobtype=pdf)

    from which it is clear that phytohemagglutinin acts as an oxidant.

  242. #242 Richard
    February 28, 2006

    Jean, if the in vitro T cell activation in the study you cited had anything to do with the immune activation seen in HIV, it would not be inhibited by blocking MHC class II (a large part of the activation CD8 T cell activation). If CD8 T cells were getting activated by oxidized LDL, then the CD8 T cells that accumulated as a result would specific for oxidized LDL, not HIV (as they demonstrably are). Forget antibodies, people with HIV are have abundant HIV-specific CD4 and CD8 T cell responses.

  243. #243 George
    February 28, 2006

    Tara: I utterly agree. As I pointed out in my longer post, Eleni-whatsit is one of that whacko breed of denialists belonging to the so-called “Perth Group” who claim HIV does not exist at all.

    It’s part of what infuriates me about the fringe. OS then gets tarred with a broader brush because they mistakenly ascribe more to it than it warrants. Like Mathias Rath, that pig, telling people to drop ARV in favor of a multi. That’s criminal.

    Eleni-etc is wrong. Like Bialy and that lot of murderers who have swayed Mbeki to buy the BS and kill his own people in droves.

  244. #244 David Lowenfels
    February 28, 2006

    Tara wrote:

    >David, can you please tell me where Papadopulos-Eleopulos published subsequent research backing up this >hypothesis? Have reducing agents been administered (after all, this was presented 14 years ago!), and have they >been successful?

    BTW the Perth group are theorists, not clinical experimenters.

    NAC is a reducing agent which replenishes the sulfhydryl groups needed for maintaining the cell redox cycle (via glutathione)
    There is enormous clinical research evidence on the immune benefits of NAC administration in vivo. http://aliveandwellsf.org/library#sulfur

    With in vitro “HIV” research, strong reducing agents (antioxidants) prevent the expression of “HIV particles” because these cellular oxidation is what ultimately causes the polymerization of actin and subequent cellular breakdown. (not to mention mitochondrial dysfunction)

    Please have a look at the research of Hässig and Kremer for more background on the oxidative/hypercatabolic pathophysiology.

  245. #245 David Lowenfels
    February 28, 2006

    Richard wrote:

    It’s always good to receive insights from a Biophysicist when you’re studying an immunological disease. Hellooo indeed.

    Okay, while we’re playing Ad Hominem attacks…
    since when is it good to trust a lying self-aggrandizing man with a track record of shoddy lab techniques and trickery, who had financial interest in patenting his antibody test when he manufactured scientific consensus by press release? Duh, Bob Gallo circa 1984.

    Gallo used identical trickery with his HL23V which was later shown to be a laboratory artefact!

    Try these on for size:
    ( http://aliveandwellsf.org/library#isolation )

    Barbacid M, et al. Humans have antibodies capable of recognizing oncoviral glycoproteins: Demonstration that these antibodies are formed in response to cellular modification of glycoproteins rather than consequence of exposure to virus. Proc Natl Acad Sci USA. 77(3): 1617-1621, March 1980.

    Snyder HW Jr, Fleissner E. Specificity of human antibodies to oncovirus glycoproteins: Recognition of antigen by natural antibodies directed against carbohydrate structures. Proc Natl Acad Sci USA. 77(3): 1622-1626, March 1980.

    * Excerpt from abstract: “The results are consistent with the idea that the antibodies in question are elicited as a result of exposure to many natural substances possessing widely crossreacting antigens and are not a result of widespread infection of man with replication-competent oncoviruses.”

  246. #246 George
    February 28, 2006

    What Lowenfels posts re NAC is just the kind of distortion that drives me nuts. Hassig doesn’t know his ass from a hole in the ground. By contrast, the guys doing the real work on this issue are the Herzenbergs, Mario Roederer, the late Howard Greenspan and Wulf Droge.

    The REASON that there is a loss of sulfur in massive amounts is because people are infected with HIV, which in results in IMMUNE ACTIVATION that HIV likes since it results in activating cells and enhancing replication. And along with that comes the oxidative stress.

    This “vicious cycle” has been known for a long time. It’s just being better characterized. NAC thus is a therapeutic implication for HIV infection, in my view. And Hep C. I use it daily and have for years.

    Will it cure HIV or hep C? Unlikely. Might an agent like NAC help slow disease progression or offset mitochondrial toxicity resulting from some antiretroviral therapies? Evidence suggests it may. Whey proteins have a fair amount of cysteine and glutamine which is why I use them too. (Plus they showed some benefit in offsetting failure to thrive in kids with HIV….there’s another point. Kids with HIV don’t grow as fast as kids without HIV. Generally, I don’t think these kids are snorting poppers.)

    Otherwise, again, the denialists see a phenomonenon and have no clue what it means. People don’t just spontaneously lose a lot of sulfur. It happens for a reason. And no, Mary, not all gay men are drug users–and not all drug users develop AIDS. There’s a theory about as boneheaded and demonstrably wrong as Duesberg’s dithering about the expression of antibodies not ever being associated with clinical disease.

  247. #247 David Lowenfels
    February 28, 2006

    Richard wrote:
    “How would oxidative stress cause immune activation?”

    Jean had some good references for this.

    George wrote:
    “Immune activation leads to expression of inflammatory cytokines which can then lead to OS and apoptosis.”

    According to Kremer and others, the immune system is an effector of redox homeostasis. It is responsive to BOTH antigens AND oxidative toxins.

    Redox levels in the antigen-presenting cells modulate how the immune system is activated (Th1 cell-mediated response, or Th2 humoral antibodies)

    Peterson JD, Herzenberg LA, Vasquez K, Waltenbaugh C. Glutathione levels in antigen-presenting cells modulate Th1 versus Th2 response patterns. Proc Nat Acad Sci USA 1998; 95:3071-3076.
    ( http://aliveandwellsf.org/library#sulfur )

    Therefore any toxin that depletes the antioxidant thiol pool will lead to diminshment of cell-mediated immunity!

    The predictive outcome of thiol insufficency is a progressive Th1->Th2 shift: hypergammaglubulinemia leading to autoimmune inflammations via accumulation of circulating immune complexes, with concurrent inhibition of cell-mediated response due to downregulation of nitric oxide biosynthesis… Th2 activation and Th1 diminishment… sure sounds like AIDS to me.

  248. #248 Wheatdogg
    February 28, 2006

    A UC-San Diego team reports the HIV/AIDS rate in Tijuana is increasing alarmingly. The team, which worked with Mexican counterparts, blame needle-sharing by drug users and unprotected sex for the increase. The news release is at ucsdnews.ucsd.edu/newsrel/health/hiv_aids.asp.

    Do these findings support or refute the accepted transmission mechanism for HIV and AIDS? Any comments from anyone here?

    Wheatdogg the Curious

  249. #249 David Lowenfels
    February 28, 2006

    George wrote:

    “Hassig doesn’t know his ass from a hole in the ground.”
    Well he’s been dead for nearly 10 years, of course he is not up-to-date! :P
    Please read Kremer’s writings and then tell me why his head is up his ass.

    “The REASON that there is a loss of sulfur in massive amounts is because people are infected with HIV, which in results in IMMUNE ACTIVATION that HIV likes since it results in activating cells and enhancing replication. And along with that comes the oxidative stress.”

    WRONG. Continuous immune activation does not necessarily have to be caused by a pathogen.. especially if it is an AUTOIMMUNE disease.

    “(Plus they showed some benefit in offsetting failure to thrive in kids with HIV….there’s another point. Kids with HIV don’t grow as fast as kids without HIV. Generally, I don’t think these kids are snorting poppers.)”

    Kids with “HIV”/AIDS are basically malnourished and/or crack babies…

    “Otherwise, again, the denialists see a phenomonenon and have no clue what it means.”

    For the record I am not an AIDS denialist. But I am an “HIV” denialist. I believe that the postulation of a contagious retrovirus is not necessary to explain the course of the disease.

    “People don’t just spontaneously lose a lot of sulfur. It happens for a reason.”

    I agree. But there are more plausible reasons for amino acid dysregulation than viruses that cannot be found in real people except by nonspecific surrogate markers!
    I believe that the greatest block to finding the cure for AIDS is the fixation on HIV and sexual transmission.

    “And no, Mary, not all gay men are drug users–and not all drug users develop AIDS.”
    I never said that Duesberg or The Perth Group had all the answers.
    But they both deserve props for showing the gross holes in the HIV theory.

    Another factor which is often overlooked is antibiotic overuse in gay men. In the late 70′s and 80′s, Bactrim/Septra was handed out like candy for prophylactic use. And all the original AIDS patients were documented to abuse poppers. This poppers/antibiotic combo was the likely cause of the “first wave” of AIDS deaths.
    The second wave was linked to Bactrim/AZT poisoning, after faith was created in the bogus antibody test.

    These nitro/azido chemicals induce/metabolize into nitric oxide!
    Too much nitric oxide will cause an inhibitory counterregulation against cell damage (Th1->Th2 shift). No one knew about these things until the 90′s.

    Today people take 1/4 less AZT as before, of course they live longer!

    Now we have the bogus “viral load” test which can only show the biosynthesis of nonspecific RNA (which is used to repair DNA and damaged cells!)

    There is more trickery with T-cells and HAART:
    bone marrow toxicity leads to Th2 cells in the blood stream (Th2 cells don’t produce NO so are useless against OIs)

    Obviously the drugs have some short-term benefit. This may be due to their reducing ability, and also somehow they inhibit the inflammation/cellular activation. But in the longer term they damage the precious mitochondria, without which no one can live! (And for which there is no repair mechanism = PERMANENT GENETIC DAMAGE) It’s a double-edged sword and people taking these meds are absolute guinea pigs.

    I’m not saying AIDS is caused solely by drugs or sperm.
    I believe it is caused by biochemical (oxidative) stress, of a multitude of forms: nutritional, psychological, chemical, traumatic, infectious. The cumulation of these stress factors is not without consequence. However there are a multitude of NONTOXIC ways to manage and reverse these stress conditions, as you listed above (NAC, lipoic acid, whey protein, omega-3, phytonutrients, etc)

    On this level we probably agree more on this topic than disagree.

  250. #250 George
    February 28, 2006

    Lowenfels wrote: “Therefore any toxin that depletes the antioxidant thiol pool will lead to diminshment of cell-mediated immunity!”

    Feh. What a load of crap. No toxins cause a persistent and chronic decline in CD4+ T lymphocytes numbers, skew their function, upset subsets, increase CD8+ mediated cell activation–and otherwise screw with the immune system as Richard has so eloquently summarized above.

    OS is a CONSEQUENCE of HIV disease. And thus a target for therapeutic intervention that may at least help attenuate the effect of OS.

    The study you cite does NOT dispute that notion. The Herzenbergs realize that HIV exists and causes AIDS. The glutathione pool is diminished as a CONSEQUENCE of that.

    What other theory works as well to describe AIDS? Go on. And provide some data.

    Toxins. What a crock.

  251. #251 Tara
    February 28, 2006

    David,

    Kids with “HIV”/AIDS are basically malnourished and/or crack babies…

    Including Christine Maggiore’s?

    But they both deserve props for showing the gross holes in the HIV theory.

    I noted this earlier and in the previous thread and don’t know if you saw it amid the mess, but those types of “gross holes”, as you assert, exist in *every* infectious agent/disease relationship. Are they all caused by “toxins” instead of microbes?

  252. #252 David Lowenfels
    February 28, 2006

    Another reference for intracellular redox balance controlling immune activation:

    Murata, Y et al. The polarization of Th1/Th2 balance is dependent on the intracellular thiol redox status of macrophages due to the distinctive cytokine production. International Immunology 2002, 14(2): 201-212.

    George wrote:

    “No toxins cause a persistent and chronic decline in CD4+ T lymphocytes numbers, skew their function, upset subsets, increase CD8+ mediated cell activation–and otherwise screw with the immune system as Richard has so eloquently summarized above.”

    WRONG. For instance Mercury can do these things, via the Type-II shift.

    Look deeper… the apparent decline in CD4s (those which circulate in the blood stream are Th1 CD4s) can be explained by the Th2 shift. Th2 cells live in the lymph system, and will not be found in blood counts unless there is bone marrow toxicity occurring.. but common CD4 counts do not differentiate between Th1/Th2 function.

    More food for thought: ( http://aliveandwellsf.org/library#tcells )

    Roederer, M. Getting to the HAART of T cell dynamics. Nature Medicine 4: 145-146. 1998

    * Synopsis: From a Stanford press release:

    “Mario Roederer of Stanford University describes the [1998] papers as the final nails in the coffin for the proliferation model of T cell dynamics. Roederer concludes that only by understanding how T cell numbers are regulated will we find the mechanism by which HIV destroys the immune system.”

    * From the article itself:

    “First and foremost, we must always remember that the blood is an imperfect reflection of the immune system. It is not representative of the [entire body]…

    The facts (1) that HIV uses CD4 as its primary receptor, and (2) that CD4+ T cell numbers decline during AIDS, are only an unfortunate coincidence that have led us astray from understanding the immunopathogenesis of this disease. HIV leads to the progressive destruction of all T cell subsets, irrespective of CD4 expression. Ultimately, AIDS is a disease of perturbed homeostasis. Only when we understand how the body regulates T cell numbers will we be able to find the mechanism(s) by which HIV destroys the immune system.”

    Again, I invoke “Post Hoc Ergo Proper Hoc”
    Is “HIV” the chicken or the egg? Cause or symptom?
    Oxidation is always part of the picture, even with in vitro cell expression.

    Tara wrote:
    “What about reducing agents that *don’t* have antiretroviral properties?”
    Conversely one could argue according to the evidence, that ALL strongly-reducing agents are antiretroviral.

  253. #253 George
    February 28, 2006

    Lowenfels mentions mercury. Show me the data.

    Then you quote Roederer, who makes some cogent and interesting remarks (upon which “postmodern” immunology has more to say) and underscores the role of HIV in the disruption of CD4 dynamics.

    So just how does this support the notion that either HIV doesn’t exist or doesn’t cause AIDS? Answer: it doesn’t.

    Try again.

  254. #254 David Lowenfels
    February 28, 2006

    sorry for the messy quoting, not sure how to do it fancier..

    Tara wrote:

    “David wrote: Kids with “HIV”/AIDS are basically malnourished and/or crack babies…
    Including Christine Maggiore’s?”

    If you scratch the surface, there was NO PROOF that Eliza Jane had HIV antibodies.. they only found some abnormal brain cells long after her death. There was no experimental control.

    “David wrote: But they both deserve props for showing the gross holes in the HIV theory.

    I noted this earlier and in the previous thread and don’t know if you saw it amid the mess, but those types of “gross holes”, as you assert, exist in *every* infectious agent/disease relationship. Are they all caused by “toxins” instead of microbes? ”

    The sheer quantity of these posts make the thread hard to follow…
    Let me rephrase it as a question:
    Does *every* infectious agent/disease relationship have such faulty nonspecific evidence for “isolation” and no gold standard?
    Does *every* such relationship have political and economic interests motivating the science? (Gallo’s greed for fame and patent money, greedy pharmaco’s in africa, etc.)

    I think not.

    I won’t defend Duesburg, I think his ideas are now passe, but I admire him for sticking his neck out for what he believed in. I think the real crux of all this comes down to “Is Gallo/Montagnier’s published evidence for ‘HIV’ sufficient prove the existence contagious/exogenous retrovirus?”
    I believe the answer is NO. HIV only exists in the test tube.

    Have you read the HIVgate.pdf article yet? Please do, I’d like to hear your response.

    Also, could you respond to Jeane’s question:
    “What puzzle me, is how you, biologists, know that the proteins detected below the cutoff are not “hiv antibodies”, while those detected above are actually hiv antibodies?”
    ( referring to Giraldo’s paper http://www.robertogiraldo.com/eng/papers/EveryoneTestsPositive.html )
    ( see also Kremer’s “Did Gallo manipulate the ‘AIDS test’ to order?” http://www.virusmyth.net/aids/data/hkgallo.htm )

    How is it that a small number of autoantibodies is “HIV negative” and a large number of autoantibodies is “HIV positive”. Where is the specificity?? And where does this arbitrary threshold come from??

  255. #255 Chris Noble
    February 28, 2006

    Tara wrote:

    Are they all caused by “toxins” instead of microbes?

    Yes. Everything is caused by oxidative stress.

    This paper proves that oxidative stress causes influenza.


    Protective effect of n-acetylcysteine in a model of influenza infection in mice.

    Influenza virus has never been isolated. You can’t show me a single electron micrograph of isolated influenza virus.

  256. #256 David Lowenfels
    February 28, 2006

    George wrote:
    “Lowenfels mentions mercury. Show me the data.”
    The immunotoxic properties of mercury are well known…
    You can look it up yourself. Google, google scholar and medline.
    “mercury Th2″ “mercury CD4″ etc
    Here’s a start: http://www.cqs.com/immune.htm

    Mercury is an oxidative toxin, not an antigen.
    I’m not saying it causes AIDS, just that you are incorrect that immune activation is caused solely by antigens.

    “Then you quote Roederer, who makes some cogent and interesting remarks (upon which “postmodern” immunology has more to say) and underscores the role of HIV in the disruption of CD4 dynamics.”

    In the very same issue of Nature Medicine, there is an article about how HAART causes *redistribution* of T-cells from lymphoid organs, but not de-novo Th1 formation. Can’t recall the title, but it’s linked to Roederer’s editorial.

    “So just how does this support the notion that either HIV doesn’t exist or doesn’t cause AIDS? Answer: it doesn’t. Try again.”

    I’m not going to waste my time… obviously you are not going to be convinced no matter what I say.

    Besides, there is no “100% conclusive” evidence either way, otherwise we would not still be debating this 20 years later. You believe in the “chicken”, I believe in the “egg”.

    However I do think you would do well to look deeper into Gallo’s fraud… what this whole house of cards is based on.
    He lied about a lot more than just stealing from the French…
    http://www.sparks-of-light.org/HIVGATE%20-%20review%20copy.pdf

    Personally I believe there is sufficent evidence for reasonable doubt of the entire “HIV”/AIDS theory. For me, that’s enough.

  257. #257 George
    February 28, 2006

    Oh, Chris!

    My hero!

    It’s true. In fact, ALL infectious disease and cancer are just made up by Industry and Government.

    Just eat well, lots and laugh and everything will be ever so peachy! Mmmmm….peaches.
    Homersexual

  258. #258 David Lowenfels
    February 28, 2006

    Chris Noble rwote:
    “Influenza virus has never been isolated. You can’t show me a single electron micrograph of isolated influenza virus.”

    Oh, come on. Nice try but that’s a red herring. There IS a standard of procedure for isolating a RETROvirus, of which influenza is NOT in the same category.

    To see the EM pictures of the junk proteins that were called “purified HIV isolate” for over 10 years, have a look at these papers: ( http://aliveandwellsf.org/library#microvesicle )

    Bess et al, Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virology. 1997 Mar 31;230(1):134-44.

    Gluschankof P, Gelderblom HR, et al. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virol. 1997;230:125-133.

    Gallo couldn’t even get an EM photo himself (see definitive documentation in HIVgate.pdf), so he stole the one that Montagnier had already published! Pretty ballsy…

    And according to a Djamel Tahi’s interview with Montagnier himself, they could not find “HIV particles” in the “isolate” either (after a “Roman effort”), so they found a “virus-[like] particle” from human fetal cord blood (known for ubiquitous virus-like particles and even “HIV antibodies” [Faulk WP, Labarrere CA. HIV proteins in normal human placentae. Am J Reprod Immunol. 1991 Apr;25(3):99-104.])

    Repeat after me class… NON-SPECIFIC

    Please read what EM retrovirology expert Etienne de Harven has to say about it: “Problems with isolating HIV”
    http://aliveandwellsf.org/articles/isolation/deHarven_ProblemsWithIsolatingHIV_2003.pdf
    He is an expert in the field of EMs and retroviruses.. not a “nutjob” Australian “biophysicist”

  259. #259 Chris Noble
    February 28, 2006

    George writes:

    It’s true. In fact, ALL infectious disease and cancer are just made up by Industry and Government.

    Now you are trying to make me look like some sort of conspiracy theorist!

    You don’t need to resort to these cheap tactics when it is obvious that most of the scientists working in these fields are just stupid sheep who blindly believe the orthodox pap that they are spoon fed in University. The few who should know better are too busy driving around in their shiny new cars that they just bought from the profits from their new “vaccines”. No, you don’t need conspiracy theories when stupidity and greed explain everything.

    Besides, the Perth Group conclusively proved that oxidative stress causes cancer in this seminal paper.

    A Mitotic Theory

    In 25 years nobody, not one person, has managed to refute the contents of this paper.

    Not a single refutation in 25 years. What is the orthodoxy afraid of?

  260. #260 Karen Lynne Lambert
    March 1, 2006

    HIVists are:

    1) CFS denialists
    2) HHV6 denialists

    HIVists use the racist and homophobic HIV/AIDS
    paradigm to hide the white heterosexual CFS/AIDS
    epidemic. They’re CFS/AIDS denialists.

    In the name of protecting heterosexuals from the
    HIV/AIDS stigma, they condemn their fellow
    heterosexuals to the very real life-altering problems
    of having CFS/AIDS.

    Because of HIVism, the virus associated with CFS/AIDS
    is not being screened from the blood supply.
    Unacknowledged CFS/AIDS continues to spread throughout
    the population, unleashed.

    Because of HIVism, white heterosexuals are not being
    advised that there is a much, MUCH bigger epidemic of
    CFS/AIDS out there that they can contract
    sexually–but not only sexually. HIV testing will not
    save anyone from CFS/AIDS.

    Because of HIVism, the medical establishment does not
    recognize that many children have CFS/AIDS. Sometimes
    these children are taken away from their parents
    because the state does not recognize CFS/AIDS as real
    disease and accuses the parents of “Munchausen by
    Proxy.” (A Boston woman recently had to pay $25,000 in
    court costs to keep the state from taking her two
    children who are afflicted with CFS.)

    The real debate should not be whether heterosexuals
    can get HIV/AIDS. The debate should be about whether
    heterosexuals can get CFS/AIDS. Because of the medical
    establishment’s CFS denialism, we don’t have hard
    numbers on CFS in this country. But some educated
    estimates are in the millions. Also, healthcare workers are
    especially vulnerable to CFS and may even be spreading
    CFS in hospital settings. Why isn’t CFS a reportable illness?

    And of course, one of the most entertaining questions
    is, given the massive problem of HIV/AIDS in the gay
    community, where is the massive CFS/AIDS epidemic in
    the gay community and how do you tell CFS/AIDS and
    HIV/AIDS apart? Can a gay man have both CFS/AIDS and
    HIV/AIDS? Does this show the absurdity of the
    bifurcation of what is probably one epidemic with one
    cause?

    And where is the massive CFS/AIDS epidemic in the
    African-American community? And in Africa? We’re told
    that African-Americans are more at risk for HIV/AIDS.
    How many African-Americans have HIV/AIDS and CFS/AIDS?
    Are African-Americans with CFS/AIDS being stigmatized
    with the label of HIV/AIDS? Maybe it’s time for civil
    rights leaders to ask whether the political wall
    between CFS/AIDS and HIV/AIDS is stigmatizing their
    community, and leaving them vulnerable to being used
    as medical guinea pigs for bogus HIV/AIDS experiments.

    ramblings….on a rare night that I just can’t get any restful sleep…..I swear this idiopathic illness is going to get the best of me, but at the very least, I am going down fighting…

  261. #261 Kristjan Wager
    March 1, 2006

    WTF? So the people dealing with realities in their attempt to find a cure for this dreadful ailment base it on a racist and homophobic view? Trying to cure someone is racist? Or homophobic?

    The people who says AIDS is God’s punishment on gays are the homophobic ones – none of the people here have said that, no matter which side they are on.

  262. #262 David Lowenfels
    March 1, 2006

    My posts didn’t come through for about 5 hours, so I’m posting them again all in one go. Sorry if they become duplicated.

    George wrote:
    “Lowenfels mentions mercury. Show me the data.”
    The immunotoxic properties of mercury are well known…
    You can look it up yourself. Google, google scholar and medline.
    “mercury Th2″ “mercury CD4″ etc
    Here’s a start: http://www.cqs.com/immune.htm

    Mercury is an oxidative toxin, not an antigen.
    I’m not saying it causes AIDS, just that you are incorrect that immune activation is caused solely by antigens.

    “Then you quote Roederer, who makes some cogent and interesting remarks (upon which “postmodern” immunology has more to say) and underscores the role of HIV in the disruption of CD4 dynamics.”

    Actually, he underscores that the direct role of HIV is UNKNOWN because the normal homeostasis of CD4 cells was not well understood.

    In the very same issue of Nature Medicine, there is an article about how HAART causes *redistribution* of T-cells from lymphoid organs, but not de-novo Th1 formation. Can’t recall the title, but it’s linked to Roederer’s editorial.

    “So just how does this support the notion that either HIV doesn’t exist or doesn’t cause AIDS? Answer: it doesn’t. Try again.”

    I’m not going to waste my time… obviously you are not going to be convinced no matter what I say.

    Besides, there is no “100% conclusive” evidence either way, otherwise we would not still be debating this 20 years later. You believe in the “chicken”, I believe in the “egg”.

    However I do think you would do well to look deeper into Gallo’s fraud… what this whole house of cards is based on.
    He lied about a lot more than just stealing from the French…
    http://www.sparks-of-light.org/HIVGATE%20-%20review%20copy.pdf

    Personally I believe there is sufficent evidence for reasonable doubt of the entire “HIV”/AIDS theory. For me, that’s enough.

    sorry for the messy quoting, not sure how to do it fancier..

    Tara wrote:

    “David wrote: Kids with “HIV”/AIDS are basically malnourished and/or crack babies…
    Including Christine Maggiore’s?”

    If you scratch the surface, there was NO PROOF that Eliza Jane had HIV antibodies… they only found some abnormal brain cells long after her death. There was no control comparison. There is also no proof that she died from PCP, on the contrary there is evidence that she died from an allergic reaction to amoxicillin!

    “David wrote: But they both deserve props for showing the gross holes in the HIV theory.
    Tara wrote:
    I noted this earlier and in the previous thread and don’t know if you saw it amid the mess, but those types of “gross holes”, as you assert, exist in *every* infectious agent/disease relationship. Are they all caused by “toxins” instead of microbes? ”

    The sheer quantity of these posts make the thread hard to follow…
    Let me rephrase it as a question:
    Does *every* infectious agent/disease relationship have such faulty nonspecific evidence for “isolation” and no gold standard?
    Does *every* such relationship have political and economic interests motivating the science? (Gallo’s thirst for fame and patent money, greedy pharmaco’s in Africa, etc.)

    I think not.

    I won’t defend Duesburg, I think his ideas are now passe, but I admire him for sticking his neck out for what he believed in. I think the real crux of all this comes down to “Is Gallo/Montagnier’s published evidence for ‘HIV’ sufficient prove the existence contagious/exogenous retrovirus?”
    I believe the answer is NO. HIV only exists in the test tube.

    Have you read the HIVgate.pdf article yet? Please do, I’d like to hear your response.

    Tara, could you respond to Jeane’s question:
    “What puzzle me, is how you, biologists, know that the proteins detected below the cutoff are not “hiv antibodies”, while those detected above are actually hiv antibodies?”
    ( referring to Giraldo’s paper http://www.robertogiraldo.com/eng/papers/EveryoneTestsPositive.html )
    ( see also Kremer’s “Did Gallo manipulate the ‘AIDS test’ to order?” http://www.virusmyth.net/aids/data/hkgallo.htm )

    How is it that a small number of autoantibodies is “HIV negative” and a large number of autoantibodies is “HIV positive”. Where is the specificity?? And where does this arbitrary threshold come from??

    Chris Noble rwote:
    “Influenza virus has never been isolated. You can’t show me a single electron micrograph of isolated influenza virus.”

    Oh, come on. Nice try but that’s a red herring. There IS a standard of procedure for isolating a RETROvirus, of which influenza is NOT in the same category.

    To see the EM pictures of the junk proteins that were called “purified HIV isolate” for over 10 years, have a look at these papers: ( http://aliveandwellsf.org/library#microvesicle )

    Bess et al, Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virology. 1997 Mar 31;230(1):134-44.

    Gluschankof P, Gelderblom HR, et al. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virol. 1997;230:125-133.

    Gallo couldn’t even get an EM photo himself (see definitive documentation in HIVgate.pdf), so he stole the one that Montagnier had already published! Pretty ballsy…

    And according to a Djamel Tahi’s interview with Montagnier himself, they could not find “HIV particles” in the “isolate” either (after a “Roman effort”), so they found a “virus-[like] particle” from human fetal cord blood (known for ubiquitous virus-like particles and even “HIV antibodies” [Faulk WP, Labarrere CA. HIV proteins in normal human placentae. Am J Reprod Immunol. 1991 Apr;25(3):99-104.])

    Repeat after me class… NON-SPECIFIC!!
    (How can HIV antibodies be nonspecific and yet still show infection with a retrovirus? Answer: they cannot.)

    Please read what EM retrovirology expert Etienne de Harven has to say about Gallo’s experiments: “Problems with isolating HIV”
    http://aliveandwellsf.org/articles/isolation/deHarven_ProblemsWithIsolatingHIV_2003.pdf
    He is an expert in the field of EMs and retroviruses.. not a “nutjob” Australian “biophysicist”

  263. #263 Karen Lynne Lambert
    March 1, 2006

    HIV+ individuals, the majority of whom are already part of socially-repressed classes (African Americans, homosexuals, the impoverish), are being falsely stigmatized/demoralized and in some cases criminalized, and possibly, and quite literally, drugged to death by an orthodoxy that is questionably inaccurate.

    Racist? homophobic? Sounds like both to me.

    I don’t even see agreement on a cause, and you believe someone is working on a cure? Please enlighten me.

    I anxiously await the point in the discussion where we get to the millions of neglected CFS/AIDS patients, who are chronically suffering, destined to be ailing HIV-NEGATIVE AIDS (idiopathic CD4 lymphocytopenia) patients. HIVists use the racist and homophobic HIV/AIDS paradigm to hide the white heterosexual CFS/AIDS epidemic (E.g. my case)). They’re CFS/AIDS denialists.

    This is a 3 dimensional debate, and you people have been missing the 3rd prong for over two decades. WAKE UP!!! Your ideologies are stale and innocent people are needlessly dying.

  264. #264 Chris Noble
    March 1, 2006

    Well, we seem to have drifted a long way from the famous Padian study which according to Harvey Bialy “demonstrated so well that sexually transmitted HIV was a figment”.

    I note that Bialy never once made a comment that was relevant to the study.

    These are the people that claim that HIV cannot possibly cause AIDS. You ask them for justification and they give you the “Padian study”.

    You demonstrate that this study cannot be used to conclude that HIV is not sexually transmitted and they go all silent, bring up other studies or in Bialy’s case proceed to insult everyone that doesn’t worship Peter Duesberg.

    I predict that in the future the exact same people will again cite the “Padian study” as proof that HIV is not sexually transmitted.

  265. #265 Kristjan Wager
    March 1, 2006

    HIV+ individuals, the majority of whom are already part of socially-repressed classes (African Americans, homosexuals, the impoverish), are being falsely stigmatized/demoralized and in some cases criminalized, and possibly, and quite literally, drugged to death by an orthodoxy that is questionably inaccurate.

    You have an extremely US-centric view. The majority of HIV+ individuals are Africans of all types.

  266. #266 Kristjan Wager
    March 1, 2006

    I don’t even see agreement on a cause, and you believe someone is working on a cure? Please enlighten me.

    It might surprise you, but there is actually a worldwide work going on. You might not agree with their premise, but to say it doesn’t exist is mind-numbing ignorant.

  267. #267 George
    March 1, 2006

    Chronic fatigue syndrome exists. HHV-6 exists. Syphilis exists. As do schistosomiasis, leishmaniasis, dengue fever, filiarisis, yellow fever, malaria, tuberculosis, mycoplasmas, HHV-8 and a range of other diseases and disorders.

    None of that means HIV does not exist or does not cause AIDS.

    None of them, I don’t believe, are necessary for HIV to cause AIDS (the “co-factor” theory).

    ALL of them deserve more PUBLIC funding in basic science research and development of new drugs and diagnostic techniques.

    The PRIVATE model of discovery has deteriorated into a massive marketing campaing that has long since lost sight of the patients it was meant to serve–and now merely serves it’s stockholders. This has also turned intellectual property into a mockery of itself, where those stockholders rape—er—reap the benefit of the original individual or team’s discovery.

    Then they price gouge us to death. And ignore the vast majority of diseases noted above because they won’t generate enough profits to sate the voracious maw of the Ferengi-like stockholders.

    Who, happily, will suffer and die one day. My only consolation at this point for all the blood they have spilled, especially in collusion with those murdering, low-life thugs, George W. Bush, Dick Cheney, Donald Rumsfeld, Condoleeza Rice, Bill Frist (MD-mad dog) and other and various scum that have destroyed the United States perhaps permanently.

  268. #268 Richard
    March 1, 2006

    George wrote:

    “Then you quote Roederer, who makes some cogent and interesting remarks (upon which “postmodern” immunology has more to say) and underscores the role of HIV in the disruption of CD4 dynamics.”

    David wrote:

    Actually, he underscores that the direct role of HIV is UNKNOWN because the normal homeostasis of CD4 cells was not well understood.

    In the very same issue of Nature Medicine, there is an article about how HAART causes *redistribution* of T-cells from lymphoid organs, but not de-novo Th1 formation. Can’t recall the title, but it’s linked to Roederer’s editorial.

    George wrote:

    “So just how does this support the notion that either HIV doesn’t exist or doesn’t cause AIDS? Answer: it doesn’t. Try again.”

    David wrote:

    I’m not going to waste my time… obviously you are not going to be convinced no matter what I say.

    - This is a great exchange, which inevitably ends with David waving the white flag. You’re completely right David that Roederer “underscores that the direct role of HIV is UNKNOWN because the normal homeostasis of CD4 cells was not well understood.” It is is still not fully understood. But Roederer works on, among other things, analyzing HIV-specific T cell responses and developing HIV vaccines at the NIH’s Vaccine Research Center. The idea that there’s some kind of homogenous “AIDS establishment” consensus that cytopathicity is key to AIDS and that to call this into question undermines the causative role of HIV is a completely artificial construct made up by the denialists. Roederer is in no way calling into question the fact that HIV causes AIDS. Even though it’s eight years old, his commentary is a nice summary of the understanding of HIV’s effects on the immune system and the fact that the paper is posted on the Alive & Well website and is being cited by you in the service of your erroneous point of view is a testament to the sheer bizarreness of this debate.

  269. #269 Karen Lynne Lambert
    March 1, 2006

    In 3rd world countries, where HIV diagnostic tests do not exist CFS patients are labeled AIDS patients by sheer symptomatology alone. Since when did Africans have the money to purchase HIV diagnostic tests? AIDS and CFS are the same epidemic because viral/bacterial diagnostic tests do not exist. It is just nature running its natural course.

    Back to my question, how many African-Americans have HIV/AIDS vs. CFS/AIDS?

    My case currently sits at the apex of three disparate paradigms: Chronic Fatigue Syndrome (clinical diagnosis: “CFS”), HIV/AIDS (clinical diagnosis: “viral syndrome of unknown etiology”), and AIDS Myth (clinical diagnosis: “idiopathic CD8 lymphocytopenia” – a.k.a. HIV-NEGATIVE AIDS) –> potentially representing over a billion ailing patients worldwide.

    Your belief that my views are “US-centric” and “mind-numbing ignorant” are quite disturbing to me. Perhaps, one day, when the United Nations gets involved in your healthcare you’ll truly appreciate human welfare.

  270. #270 Hank Barnes
    March 1, 2006

    George,

    Much of what you write is true (notwithstanding the melodrama)

    The PRIVATE model of discovery has deteriorated into a massive marketing campaing that has long since lost sight of the patients it was meant to serve–and now merely serves it’s stockholders. This has also turned intellectual property into a mockery of itself, where those stockholders rape—er—reap the benefit of the original individual or team’s discovery.

    That’s mostly right. But the primary benefactors of the HIV=>AIDS paradigm are the pharmaceutical companies who see AIDS victims as potential customers, not patients. To them, Africa is a big ‘ole marketplace to sell more drugs!

    And, they really don’t care if you bad-mouth them, as long as you support and defend the existing paradigm, and, more importantly, buy a lotta AZT, Crixivan, Epivir, Nevirapine, etc, etc.

    Who, happily, will suffer and die one day. My only consolation at this point for all the blood they have spilled, especially in collusion with those murdering, low-life thugs, George W. Bush, Dick Cheney, Donald Rumsfeld, Condoleeza Rice, Bill Frist (MD-mad dog) and other and various scum that have destroyed the United States perhaps permanently.

    A little over the top, but I grant you literary license:) What you fail to recognize is that the folks you named are all big supporters/benefactors of Big Pharma (particularly surgeon Frist). Derivatively, they all support the HIV=>AIDS paradigm, which, ironically, you support.

    So, in essence and in great irony, you’re doing the bidding for those whom you despise. It’s like the liberal activist, who blasts oil companies, yet drives a large SUV.

    Barnes, Hank

  271. #271 George
    March 1, 2006

    Hank, that’s what makes you such a fucking idiot.

    Of course, Bush/Cheney/Frist et al. support big business and esp. Big Pharma. What you and Lynne fail to realize is so much it is almost breathtaking that you even have the audacity to scribble your nonsense.

    1) Africans have a range of incomes. HIV tests are not that costly. Some places even provide free testing.

    2) HIV medications are largely NOT available, tho this is changing due to the arrival of generics.

    3) Big Pharma doesn’t give a rat’s ass about Africa or other developing nations as they seem them as

    a) not an important market (knowing people can’t afford the prices they regularly screw Americans, Europeans, etc., tho the latter have price controls);

    b) a threat if generics come out of Africa and are purchased in developing nations (not that this has ever happened tho sometimes I think it should).

    So I don’t “fail to recognize” what the scum in Washington DC are doing. I see it quite clearly.

    And 3 million men, women and children died of AIDS, many in Africa, because Bush worked his ass off and continued the lobbyist dream legacy of blocking or vastly limiting access to generics. Hell, they even got the FDA to be the arbiter of the world’s access to such medications. Not to mention despicable unilateral trade deals, etc.

    The only ones that don’t get it are you and your denialist buddies–who by the way convinced that neo-liberal jackass, Thabo Mbeki, to buy your bullshit, adding to the suffering and death in South Africa.

    So. Economic genocide it is.

    Nothing that I have said supports your braindead notion that HIV either does not exist or does not cause AIDS.

  272. #272 Hank Barnes
    March 1, 2006

    George,

    Whenever you prattle on about HIV causing AIDS, Big Pharma smiles. Well done!

    Fondly,

    Hank

  273. #273 Tara
    March 1, 2006

    Whenever you prattle on about HIV causing AIDS, Big Pharma smiles. Well done!

    “Big Pharma” also make vaccines and antibiotics. Again, Hank, what you limit to HIV applies to the entire spectrum of infectious disease.

  274. #274 Kristjan Wager
    March 1, 2006

    Your belief that my views are “US-centric” and “mind-numbing ignorant” are quite disturbing to me. Perhaps, one day, when the United Nations gets involved in your healthcare you’ll truly appreciate human welfare.

    When you describe AIDS-victims in terms that only makes sense when you focus on the US, it’s US-centric. When you think that no one is working on a cure, it’s ignorant, even mind-numbing so.

    And I didn’t get your point about the UN getting involved in my health care – that’s hardly likely, as it’s a political body. Maybe you are refering to the expert panels that the UN regularly holds? Or maybe UNICEF, WHO or one of the other globale organizations, some of which are connected to the UN?

  275. #275 Kristjan Wager
    March 1, 2006

    What Tara is too polite to point out, is that HIV/AIDS medicine isn’t a field that big pharma earns much money from. That’s anti-depresants and similar stuff. Many ‘big pharma’ companies even have a non-profit policy in regard to HIV/AIDS medicine (to some degree becuase of political pressure).

  276. #276 Hank Barnes
    March 1, 2006

    Tara,

    That’s true — Big Pharma does some good, which is why I tried (gently) to distance myself from George’s hysteria. But, they have gone real bad with HIV/AIDS.

    Barnes

  277. #277 George
    March 1, 2006

    Big Pharma hasn’t gone “real bad” with HIV/AIDS. They’ve been bad and getting worse.

    They focus only on profitable diseases. Cancer, heart disease, etc. A new monoclonal antibody to treat lung cancer is being introduced at the stellar price of $100,000 per year.

    They make a HUGE amount from overpriced–and overprescribed–statins. The biggest selling drug is atorvastatin.

    The industry has invaded many hospital and university settings, resulting in distortions and spinning of data of clinical trials. They paint the rosiest pictures to make money, period.

    That is not good science. That is not good medicine.

    That’s not to say everyone in pharma is evil. Mostly, the ones I admire and get along with the best are the bench scientists who are actually trying to do the work and make the discoveries.

    Political pressure indeed has forced them to make some changes–but many more changes need to be made. AIDS, as it has done with so much, has merely shown the stark spotlight of reality upon the many deficiencies of our society.

  278. #278 Hank Barnes
    March 1, 2006

    Big Pharma hasn’t gone “real bad” with HIV/AIDS.

    Well, they sold a lot of AZT, which is highly toxic cancer chemotherapy, to a lotta people, probably killing them.

    What Tara is too polite to point out, is that HIV/AIDS medicine isn’t a field that big pharma earns much money from.

    Heh! Riiiiight. Burroughs Welcome=>Glaxo Wellcome => GlaxoSmithKline — all those lucrative mergers since 1987, and nothing to do with AIDS drugs:)

    Hank

  279. #279 David Lowenfels
    March 1, 2006

    Goddamit. Someone please explain to me how NONSPECIFIC PROTEINS can used as specific proof of infection??!!

    Faulk WP, Labarrere CA. HIV proteins in normal human placentae. Am J Reprod Immunol. 1991 Apr;25(3):99-104.

    ShivRaj L, et al. Antibodies to HIV-1 in sera from patients with mycobacterial infections. J Lepr Other Mycobact Dis. 1988 Dec;56(4):546-51.

    Papadopulos-Eleopulos E et al [The Perth Group] HIV Antibodies: further questions and a plea for clarification, Curr Med Res and Opinion 1997; Vol. 13: 627-634

    Tomiyama T, Lake D, Masuho Y, Hersh EM. Recognition of human immunodeficiency virus glycoproteins by natural anti-carbohydrate antibodies in human serum. Biochem. Biophys. Res. Commun. 1991; 177:279-285.

    Kashala O, et al. Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among and antibodies to lipoarabinomannan. J. Infect. Dis. 169:296-304, 1994.

    Barbacid M, et al. Humans have antibodies capable of recognizing oncoviral glycoproteins: Demonstration that these antibodies are formed in response to cellular modification of glycoproteins rather than consequence of exposure to virus. Proc Natl Acad Sci USA. 77(3): 1617-1621, March 1980.

    Snyder HW Jr, Fleissner E. Specificity of human antibodies to oncovirus glycoproteins: Recognition of antigen by natural antibodies directed against carbohydrate structures. Proc Natl Acad Sci USA. 77(3): 1622-1626, March 1980.

    Did anyone read any of the papers I cited other than that Roederer review? HIVgate.pdf? Kremer’s writings? Someone explain to me why Gallo is not a liar and a thief, and why his 1985 papers still have any scientific validity.

    PS I quoted Roederer not to “prove HIV doesn’t cause AIDS” but to show that the CD4 thing is more complex than virus cytopathicity, and to support that Th1 CD4 counts are not raised by killing virus by HAART, but that it is bone marrow toxicity that increases CMI-useless Th2 cells… juicing them from the wrong place back into the bloodstream.
    A persistently low CD4 count in the bloodstream implies that there is a high Th2 CD4 count in the lymph, and that there is chronic hypercortisolism. See the Fauci’s doctoral research in the 70′s…

    The effect of in vivo hydrocortisone on sub-populations of human lymphocytes.
    Fauci A.S. & Dale D.C.
    J. Clin. Invest., 53:240-246 (1974). 1974

    The effect of hydrocortisone on the kinetics of normal human lymphocytes.
    Fauci A.S. & Dale D.C.
    Blood, 46:235 (1975).

    In the mid-’70s Fauci and his working group showed that after the administration of cortisol (a hormone produced by the adrenal glands in response to stress) the body appeared to respond with a selective reduction in the number of CD4-cells. This was found to be because most of this sub-group of white blood cells migrated from the blood circulating in the blood vessels into other areas of the body outside the vascular system. After the withdrawal of cortisol, the CD4-cells return to the circulating blood and CD4/CD8 ratio returns to normal.

  280. #280 Richard
    March 1, 2006

    HIV encodes multiple proteins, and you can reproducibly find T cell responses directed against most or all of them in HIV-infected people. Gag tends to be most recognized, followed by Pol and Nef. Ask Mario Roederer.

  281. #281 Hank Barnes
    March 1, 2006

    Richard,

    Why not simply culture HIV from an AIDS patient? Surely, if CD4 cells are dying, high titers of HIV are present, no?

    Barnes

  282. #282 McKiernan
    March 1, 2006

    Barnes,

    Give it up,already. Neither Bialy, nor Duesberg nor yourself can falsify the HIV/AIDS hypothesis. All you do is ask another question. PHD’s and academics need to be held to a higher standard that simply deconstruction and cleverness.

    If you could it falsify it, it wouldn’t be taking 30 years of moanings.

    You guys cannot even address the totally bogus, contrived,
    reconstituted autopsy reconstruction of LA coroner’s Office report by Dr.Mohammed Ali Al-BAyati, PHD.

    If your standard is no higher than ask another question, why should anyone respect you ?

  283. #283 Hank Barnes
    March 1, 2006

    Mckiernan,

    Lemme explain:

    HIV has 9000 nucleotides, which makes it a genetic “simpleton.” (Human cells have 3 billion nucleotides). So, the only way for this genetic simpleton to destroy mighty, powerful T4-cells, would be in large numbers, ie, high titers.

    If high titers of said genetic simpleton are present — which purportedly account for the destruction of said T4-cells — one would expect to be able to extract said viruses from AIDS patient, and culture them. You would then isolate these viruses, purify them, and photograph them with an electronmicroscope at 1.16 grams/mil, density gradient.

    One would not need various indirect methods such as the presence of various proteins, which may or may not be unique to HIV, nor the presence of anti-bodies, which may or may not respond uniquely to HIV, nor fragmented DNA sequences, which may or may not be unique to HIV.

    You culture HIV from AIDS patients, you’re half-way to refuting Duesberg. Neither Gallo, nor Motagnier were able to do this.

    Gluschankof first tried to do it in 1997, but found tons of contamination.

    Has it been done? If not, Why not?

    Barnes

    p.s. BTW, no need to follow me around, particularly when you have nothing to add.

  284. #284 Dale
    March 1, 2006

    Hank writes: HIV has 9000 nucleotides, which makes it a genetic “simpleton.” (Human cells have 3 billion nucleotides). So, the only way for this genetic simpleton to destroy mighty, powerful T4-cells, would be in large numbers, ie, high titers.

    Fallacious argument Hank. Introduction of a single gene, if it’s the right gene, can destroy a cell. Besides, as has been pointed out to you numerous times, the current thinking is that T cells don’t have to be infected with HIV to be destroyed.

  285. #285 Richard
    March 1, 2006

    “Why not simply culture HIV from an AIDS patient? Surely, if CD4 cells are dying, high titers of HIV are present, no?”

    This is a perfect example of the denialist approach. Ask a question (“Why not simply culture HIV from an AIDS patient”) which you believe to be important because of your own specious predictions (“Surely, if CD4 cells are dying, high titers of HIV are present, no”). Duesberg’s “17 predictions” paper does exactly the same thing. CD4 (and CD8) naive T cells are depleted slowly over time in association with persistent immune activation, while increasing numbers of memory CD4 and CD8 T cells become dysfunctional (including losing proliferative capacity) and the numbers of functional memory CD4 and CD8 T cells specific for opportunistic pathogens declines. Even if we did not know this, your statement “Surely, if CD4 cells are dying, high titers of HIV are present, no?” would simply be your assumption, not anyone elses.

    The reason AIDS is the end stage of the disease is that, by that point, immune activation has greatly depleted the pools of T cells capable of proliferating (which you can measure using something like CD3 stimulation, which will stimulate all T cells capable of proliferating to proliferate). And given HIV replicates far better in proliferating T cells, it is not surprising that amount of virus typically declines. There are still plenty of viral antigens around to continue driving immume activation, however. If you want to culture HIV, you’d be better of doing it in primary infection when the number of proliferating T cells is highest.

  286. #286 Hank Barnes
    March 1, 2006

    Besides, as has been pointed out to you numerous times, the current thinking is that T cells don’t have to be infected with HIV to be destroyed.

    The current thinking is based on voodoo, witch-craft, and superstition then:)

    Hank

  287. #287 Dale
    March 1, 2006

    Hank writes: The current thinking is based on voodoo, witch-craft, and superstition then:)

    And data, Hank. Don’t forget the data!

  288. #288 Richard
    March 1, 2006

    “So, the only way for this genetic simpleton to destroy mighty, powerful T4-cells, would be in large numbers, ie, high titers.”

    Same again. This is your (and Duesberg’s) assumption, it sure ain’t the assumption of any scientists I’ve come across. The genetic complexity is irrelevant. The virus encodes nine proteins – Env, Gag, Pol, Nef, Tat, Rev, Vpr, Vpu, Vif – all of which are antigenic i.e. the immune system treats them as foreign and epitopes within all of them are typically targeted by the T cell (and, for that matter, B cell) response. Plus the sloppy nature of the RNA genome also means that variant epitopes get generated which then also become targets.

    It’s a bit ironic that you – like most other denialists – are simply busily dismantling your own deeply flawed predictions and assumptions. Well done there! I don’t really see why you feel the need to try and get other people involved, you could do this on your own at home. Maybe I’ll have a go: the only way cancer could start is if Raquel Welch crashed into a healthy cell in a miniaturized submarine! But wait, there aren’t any miniaturized submarines! Cancer doesn’t exist!

  289. #289 Richard
    March 1, 2006

    Hank wrote:

    “The current thinking is based on voodoo, witch-craft, and superstition then:)”

    It’s called immunology, actually Hank. This is what I have (perhaps, I’ll concede, with a surfeit of pomposity) been trying to point out. When you activate a T cell it will typically divide ~15-18 times (as for how many new T cells one T cell can thereby generate, you do the math). Most of these newly generated cells will die in 1-2 days. You have a burst of activation and cell division like this when you get the flu. You’ll lose some naive T cells, too, because those that are specific for the flu will go through this activation process and the few that don’t undergo activation-induced cell death will be recruited into the memory T cell pool. Kind of like graduating from being a rookie (naive) to becoming an expert (memory). Vaccines work by getting T cells and B cells to do just this. But with the flu, this is a very time-limited phenomena, it’s over in a week or less. New naive T cells being produced by the thymus will rapidly “top up” the naive T cell pool back to normal levels. With HIV, the initial wave of activation occurs in similar fashion to flu, but it does not full resolve. There is a continuous, demonstrable low level of immune activation that persists, along with a persistent activation of naive T cells that – just slightly – outpaces the replenishment capacity of the thymus. It is a small effect, which is why it typically takes quite a while before there are any noticeable consequences. This is a unique effect of HIV infection, I might add, with the exception of HIV-2 where the situtation is similar but the persistent activation is at a lower level.

  290. #291 Richard
    March 1, 2006

    Oh please Hank, is this what you do when the facts elude you? For your information I do not work for, or have anything to do with, The Body. I work at a non-profit community-based organization called Treatment Action Group (TAG). Sometime before I started, there was an agreement whereby The Body (which is indeed for-profit) puts up TAG materials on their community site, they do not give TAG any money for this. TAG does – gasp – receive some funding from drug companies (the financials are all on the website if you feel like you’ve reached a point where you need to try and use them in your arguments) but my project (and salary) is funded with a grant from the Michael J. Palm Foundation. Anything more substantive to say?

  291. #292 Richard
    March 1, 2006

    Perhaps you might also wish to know that I have, on occasion, done freelance writing. Here, for example, is an article I wrote several years ago for another non-profit group, the Community Research Initiative on AIDS (who also appear to allow The Body to reprint their materials).

    http://www.thebody.com/cria/summer01/road.html

    The work I do now is about pathogenesis, immunology, basic science, vaccines and other prevention technologies.

  292. #293 David Lowenfels
    March 1, 2006

    Richard wrote:

    “HIV encodes multiple proteins, and you can reproducibly find T cell responses directed against most or all of them in HIV-infected people. Gag tends to be most recognized, followed by Pol and Nef.”

    No shit “HIV-infected” people have weird proteins I agree. But this is still circular logic to call them “HIV proteins”. Lots of weird things happen to cells when they are subjected to oxidative stress.
    It is a well known fact that the pH and redox status of a cell can radically change the expression of genes and proteins, even activating weird archaically preserved ones that we don’t normally see.

    Where is the proof that these “HIV proteins” are endogenously acquired? Where are the control studies subjecting uninfected cells to the same oxidative mechanisms of “HIV cultures”?

    How do we know that these proteins are not encoded somewhere in the 3 billion nucleotides of the human genome, much of which is endogenous retroviral DNA?

  293. #294 Richard
    March 2, 2006

    Because the human genome has been sequenced, I think. And because they are encoded by the HIV genome (which you seem to be suggesting does not exist). And because there are so many similarities with the proteins encoded by other similar viral genomes: HIV-2, SIVsm, SIVagm, SIVcpz, SIVmnd, SIVrcm, FIV , EIAV.

  294. #295 David Lowenfels
    March 2, 2006

    Richard wrote:
    “Because the human genome has been sequenced, I think. And because they are encoded by the HIV genome (which you seem to be suggesting does not exist). And because there are so many similarities with the proteins encoded by other similar viral genomes: HIV-2, SIVsm, SIVagm, SIVcpz, SIVmnd, SIVrcm, FIV , EIAV.”

    Similarity to other retroviral genomes doesn’t mean squat in showing exogenicity. The human genome consists of at least 1% retroviral sequences (do the math, that’s 30 million endogenous nucleotides to “HIV”‘s 9000)

    Obviously there is genetic material associated with “HIV particles”, I just haven’t seen evidence that shows that these originally came from OUTSIDE the cell.

    Again, you all seem to be ignoring my most pertinent questions and going for the weakest link in the chain. WHERE ARE THE PROPER EXPERIMENTAL CONTROLS FOR STRESSING UNINFECTED CELLS? And most importantly: HOW CAN PROTEINS BE BOTH PROVEN-NONSPECIFIC AND YET STILL CLAIMED SPECIFIC??

    Here is a pertinent reference, showing that cancer cells (which Gallo used in his cultures) can make microvesicles that cause T-cell death No need for an exogenous virus to explain it. Immunology in 1984 was in the stone age, now it’s just coming into the bronze age.

    Huber V, et al. Human colorectal cancer cells induce T-cell death through release of proapoptotic microvesicles: role in immune escape. Gastroenterology. 2005 Jun;128(7):1796-804.

    http://aliveandwellsf.org/articles/huber_microvesicle_Tcell_death_2005.pdf

  295. #296 David Lowenfels
    March 2, 2006

    Richard wrote:

    “HIV encodes multiple proteins, and you can reproducibly find T cell responses directed against most or all of them in HIV-infected people. Gag tends to be most recognized, followed by Pol and Nef.”

    T-cell responses to these proteins are not proof of exogenicity.
    I am not arguing that there are no pathogenic cellular modifications in AIDS, just that they are not necessarily exogenously acquired. They could very well be due to modification of cellular processes under abnormal cell stress conditions.

    For a thorough treatment of the endogenicity of these proteins, and their connections with polymerized actin and myosin, Class II histocompatability DR proteins, etc.
    refer to Section 5 of
    “THE ISOLATION OF HIV — HAS IT REALLY BEEN ACHIEVED?
    THE CASE AGAINST”
    http://www.virusmyth.net/aids/data/epreplypd.htm
    Continuum Vol.4 No.3 Sept./Oct. 1996

    and also the PNAS 1980 Barbacid and Synder papers that I referenced earlier, regarding glycoproteins

    As a tangential note, no one has mentioned the previously believed “scientific” notions of the contagiousness of scurvy, pellagra, and
    *especially* a decade of Japanese SMON which even had an “isolated virus” before they realized it was caused by pharmaceutical poisoning.
    http://www.virusmyth.net/aids/data/besmon.htm

  296. #297 Richard
    March 2, 2006

    Sigh. I try and focus on questions that seem to make some kind of sense to me. What has T cell death in Gallo’s culture got to do with anything? Why are you concerned with “stressing uninfected cells.”? Because it might make them die? I thought we’d already covered the irrelevance of cytopathicity. I think there are online databases where you can scan the human genome for sequences encoding the HIV proteins I mentioned above, let us know if you find anything. I guess, trying perhaps foolishly and pointlessly to be thorough, that leaves “HOW CAN PROTEINS BE BOTH PROVEN-NONSPECIFIC AND YET STILL CLAIMED SPECIFIC??”

    Is there a particular HIV protein you’re talking about here that you think is “proven non-specific”? Which one? Or perhaps I am just not understanding what you mean.

  297. #298 David Lowenfels
    March 2, 2006

    Richard:
    My points is that stressing uninfected cells might elict abnormal proteins and apoptotic microvesicles.. I am guessing there may be an overlap. There are no control studies that I know of, that submit uninfected cells and “infected” [overstressed/cancerous] cells to the same mitogenic and oxidative stress [hydrocortisone, etc] and then look for identical proteins/particles in both sets of cultures.

    “Is there a particular HIV protein you’re talking about here that you think is “proven non-specific”? ”
    How about p24? Gallo’s putatively “most specific” HIV protein?
    And the similarities between gp40 and cellular actin (gp60 and gp120 also as oligomers of actin)

    Refer to the Perth Group paper that I just referenced, section 5.

    These proteins are found in normal ["uninfected"] human placenta where there is admittedly no HIV. How can they then be called “HIV-specific” proteins??

  298. #299 Richard
    March 2, 2006

    David wrote:

    “How about p24? Gallo’s putatively “most specific” HIV protein?
    And the similarities between gp40 and cellular actin (gp60 and gp120 also as oligomers of actin)

    Refer to the Perth Group paper that I just referenced, section 5.

    These proteins are found in normal ["uninfected"] human placenta where there is admittedly no HIV. How can they then be called “HIV-specific” proteins??”

    And we have to assume that similar “similarities” exist throughout all nine proteins, including at the CD4 and CD8 T cell epitope level (~9-20 mers). And T cell responses are being generated against actin-that-looks-like-gp120-because…why? What’s making it immunogenic? Is this connected to the idea of retroviral genes in the human genome, or is it something different?

  299. #300 David Lowenfels
    March 2, 2006

    Richard wrote:

    “And we have to assume that similar “similarities” exist throughout all nine proteins, including at the CD4 and CD8 T cell epitope level (~9-20 mers).”
    I’m not following you here… why do you say this?

    “And T cell responses are being generated against actin-that-looks-like-gp120-because…why? What’s making it immunogenic? Is this connected to the idea of retroviral genes in the human genome, or is it something different?”

    My guess is that altered cell-structural proteins are immunogenic, because they signify some kind of defect. The CMI doesn’t just kill infected cells, but also scavenges defective ones. The task is essentially one and the same.

    Though you quoted it, you have not addressed my point about so-called “HIV” proteins found in normal human placenta: p17, p24, gp120
    While we’re at it, antibody cross-reactivity with intracellular agents such as TB and mycobacteria. Not to mention pregnancy and malaria.

    Given this evidence of nonspecificity, how can anyone claim that so-called “HIV-antibodies” are specific for anything other than modified cell-structural proteins?

  300. #301 David Lowenfels
    March 2, 2006

    Richard wrote:

    “And we have to assume that similar “similarities” exist throughout all nine proteins, including at the CD4 and CD8 T cell epitope level (~9-20 mers).”
    I’m not following you here… why do you say this?

    “And T cell responses are being generated against actin-that-looks-like-gp120-because…why? What’s making it immunogenic? Is this connected to the idea of retroviral genes in the human genome, or is it something different?”

    My guess is that altered cell-structural proteins are immunogenic, because they signify some kind of defect. The CMI doesn’t just kill infected cells, but also scavenges defective ones. The task is essentially one and the same.

    Though you quoted it, you have not addressed my point about so-called “HIV” proteins found in normal human placenta: p17, p24, gp120
    While we’re at it, antibody cross-reactivity with intracellular agents such as TB and mycobacteria. Not to mention pregnancy and malaria.

    Given this evidence of nonspecificity, how can anyone claim that so-called “HIV-antibodies” are specific for anything other than modified cell-structural proteins?

  301. #302 George
    March 2, 2006

    David Lowenfels raises some points that can easily be resolved by a BLAST search of the relevant proteins primary structure. And indeed, when such has been suggested, there is NOTHING in the human genome that looks like HIV proteins, nor even anything with a significant degree of sequence homology.

    Again, OS is PART of the problem in AIDS with direct therapeutic implications. But HIV proteins are the CAUSE of that disruption–and to a certain degree, antiretroviral therapy (despite the unsupported claims that some ARV act as antioxidants; may be modestly true but I doubt it).

  302. #303 jean
    March 2, 2006

    “despite the unsupported claims that some ARV act as antioxidants; may be modestly true but I doubt it”

    learn chemistry, George, and it becomes you obvious

  303. #304 George
    March 2, 2006

    Re the list of citations that attempt to show something that supports Denialist Cant….I have only reviewed the abstracts so far. But from what I see, they don’t support denialist rhetoric.

    The first only shows that some proteins of similar weight to some HIV proteins may be found in the human placenta. This appears to be the ONLY paper that discusses HIV proteins and responses. I’d like to review the full paper. The rest of the sites are below and a couple are available for free online. Not ONE of them supports the theory that HIV proteins are found endogenously in humans. And I rather doubt the Faulk paper does either.

    Faulk WP, Labarrere CA. HIV proteins in normal human placentae. Am J Reprod Immunol. 1991 Apr;25(3):99-104.
    Cryostat sections of human normal term placentae were studied for evidence of immunopathology by using antibodies to lymphocytes, macrophages, platelets, and coagulation factors. Areas of so-called chronic villitis of unestablished etiology were identified in all placentae. The same tissues were examined for HIV protein antigens gp120, p17, p24, and gp41. No evidence for gp41 was found. Antigens gp120 and p17 were identified in normal chorionic villi in vimentin-positive fibroblast-like cells and in endothelium, respectively. Antigen p24 was localized to HLA-DR positive cells that morphologically resembled macrophages in areas of villitis. The distribution of gp120 and p17 was similar to that observed for tissue factor. These findings prompted speculation that retroviral proto-oncogenes that are known to encode for certain placental receptors could be involved in the presentation of tissue factor, and that gp120 may be a hitherto unrecognized immunobiological mechanism for the blockade of CD4 on maternal lymphocytes if and when such cells gain entrance to chorionic villi.
    ***

    The next paper’s abstract below talks about ANTIBODY responses. No one argues that diagnostic tests can have limitations; there is some evidence for cross-reactivity. But this one basically shows the FIRST test, ELISA, were all negative. Western blot wouldn’t be done normally at that point.

    ShivRaj L, et al. Antibodies to HIV-1 in sera from patients with mycobacterial infections. J Lepr Other Mycobact Dis. 1988 Dec;56(4):546-51.
    Sera from 478 persons (348 leprosy patients, 33 tuberculosis patients, 29 healthy contacts of leprosy patients, 38 normal healthy Indians, and 30 normal healthy Europeans) were screened for anti-HIV-1 IgG antibodies by ELISA. None was positive. In addition, 132 samples (from 43 leprosy patients, 21 tuberculosis patients, 5 healthy contacts of leprosy patients, 33 normal healthy Indians, and 30 normal healthy Europeans) were also tested by Western blot assay for anti-HIV-1 IgG antibodies. Only 1 of the 63 healthy subjects expressed a prominent p17 band. One or more bands were found in 44 (leprosy patients 33/43, tuberculosis patients 7/21, and leprosy contacts 4/5) of the remaining 69 sera. Antibody to the HIV-1-specific antigen p24 was expressed by 17 of these subjects (14/43 leprosy patients, 1/21 tuberculosis patients, and 2/5 leprosy contacts), either as a single band or in combination with other bands. This raises the possibility of a common antigenic pattern between HIV-1 and mycobacteria, especially Mycobacterium leprae.

    **
    Papadopulos-Eleopulos E et al – not a credible site or worth reviewing in my view. I’ve read her crap before and have been completely unimpressed.

    **
    The following talks again about ANTIBODIES, not HIV proteins–and here, to the “sugars” that coat the gp120, not even those directed against the protein itself. So irrelevant to any “case” against HIV.

    Tomiyama T, Lake D, Masuho Y, Hersh EM. Recognition of human immunodeficiency virus glycoproteins by natural anti-carbohydrate antibodies in human serum. Biochem. Biophys. Res. Commun. 1991; 177:279-285.
    Anti-carbohydrate antibodies were isolated from Human immunodeficiency virus (HIV) negative human serum by affinity chromatography using yeast mannan followed by protein A. The purified mannan-binding IgG (MBIgG) bound to HIV glycoproteins gp 160, gp 120 and gp 41 in Western blot. Immunofluorescence revealed that MBIgG bound to HIV/IIIB-infected H9 cells but not to uninfected H9 cells, suggesting that carbohydrate structures recognized by MBIgG are specifically expressed on HIV-infected cells. MBIgG did not neutralize infectivity of HIV. These results show that normal human serum contains natural antibodies reactive to carbohydrate structures of HIV glycoproteins propagated in human cells.

    **
    Again, a study looking at the reliability of HIV testing (from 1994) among patients with leprosy. And indeed: “Sera from leprosy patients and leprosy contacts were often false-positive for HIV-1 by ELISA and were indeterminate by Western blot.”

    Kashala O, et al. Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among and antibodies to lipoarabinomannan. J. Infect. Dis. 169:296-304, 1994.
    To determine the association between leprosy and human retroviral infections, 57 leprosy patients, 39 leprosy contacts, and 500 pregnant women were investigated serologically for antibodies to human immunodeficiency virus type 1 (HIV) and human T cell lymphotropic virus (HTLV) types I and II. Antibodies to Mycobacterium leprae phenolic glycolipid I (PGL-I), and lipoarabinomannan (LAM) were also analyzed. A low prevalence of HIV-1 infection was observed among leprosy patients (3.5%), leprosy contacts (0), and pregnant women (3.6%). Antibodies to HTLV-I but not -II were found more often in leprosy patients (8.7%) and contacts (12.8%) than in pregnant women (0). Sera from leprosy patients and leprosy contacts were often false-positive for HIV-1 by ELISA and were indeterminate by Western blot. LAM IgM and PGL-I IgM antibodies in sera from leprosy patients yielded significant cross-reactivities with HIV-1 pol and gag proteins. These data suggest that mycobacterial cell wall antigens may share common epitopes with HIV. Caution should be exercised when interpreting HIV-1 ELISA and Western blot data from regions where leprosy or other mycobacterial diseases are endemic.

    **
    This talks about growing viruses in various cell types. Interesting paper! Irrelevant to supporting denialist bollocks.

    Barbacid M, et al. Humans have antibodies capable of recognizing oncoviral glycoproteins: Demonstration that these antibodies are formed in response to cellular modification of glycoproteins rather than consequence of exposure to virus. Proc Natl Acad Sci USA. 77(3): 1617-1621, March 1980.
    There is controversy in the literature concerning the presence in humans of antibodies directed against the envelope glycoproteins of known oncoviruses. In the present report, we show that antibodies capable of precipitating a wide variety of oncoviral glycoproteins can be demonstrated under certain assay conditions. Substances as diverse as normal components of serum, extracts of bacteria, and even nonprotein molecules such as glycogen also shared the oncoviral glycoprotein determinants recognized by normal human sera. It was found that immunoprecipitation of a given viral glycoprotein by human sera was entirely dependent upon the cell in which the virus was grown. Human sera specifically did not recognize glycoproteins purified from oncoviruses grown in human or higher primate cells. These findings not only demonstrate that the antibodies were directed against cellular rather than the virus-coded antigenic determinants but also exclude the possibility that this immune response was elicited as a consequence of oncovirus exposure.

    **
    Again, this does not support the case in any meaningful way. It talks about ANTIBODY responses to SUGARS, not proteins. Try again.

    Snyder HW Jr, Fleissner E. Specificity of human antibodies to oncovirus glycoproteins: Recognition of antigen by natural antibodies directed against carbohydrate structures. Proc Natl Acad Sci USA. 77(3): 1622-1626, March 1980.
    Antibodies in human sera from healthy individuals were shown to be reactive with highly purified 70,000-dalton envelope glycoprotein (gp70) of the simian sarcoma virus-simian sarcoma-associated virus (SSV-SSAV) complex in radioimmunoprecipitation assays under certain conditions. The specificity of the reaction was analyzed in absorption tests with normal human serum proteins, assays of viral gp70 antigenicity after exposure to exo- and endoglycosidases or trypsin, and carbohydrate hapten inhibition studies. On the basis of the results obtained in these experiments we have concluded that immune recognition of SSV-SSAV gp70 can be mediated by naturally occurring heterophil antibodies in human sera that are reactive by virtue of binding to the carbohydrate moiety of the viral gp70 molecules. The results are consistent with the idea that the antibodies in question are elicited as a result of exposure to many natural substances possessing widely crossreacting antigens and are not a result of widespread infection of man with replication-competent oncoviruses.

  304. #305 George
    March 2, 2006

    Post a convincing cite, Jean, and I’ll be happy to look at it. The only one that seems to exert some modest activity is lamivudine. But these are not antioxidants in the same was as glutathione, catalase or superoxide dismutase.

    God. What a crock. You couldn’t get away with saying AIDS was caused by AZT when people started taking handsfull of drugs that were supposedly causing AIDS, so now you have to resort to fantasizing that ARV cocktails are somehow antioxidant therapy?

  305. #306 jean
    March 2, 2006

    “The only one that seems to exert some modest activity is lamivudine. But these are not antioxidants in the same was as glutathione, catalase or superoxide dismutase.”

    What you miss, George, is the fact that epivir (3TC), emtriva (FTC), dOTC and dXG, all five studied by Dr. Mark Wainberg, are acetals which are hydrolyzed at pH=1 (stomach). dXG is quickly hydrolyzed at this pH, and, strangely, is more efficient vs VL than dOTC and 3TC.

    The hydrolysis rate evolve in the same fashioning.

    What are they giving in this hydrolysis : first glycolic aldehyde. The electrode potential of the couple carboxylic acid/aldehyde is about 0 V at pH = 0, while the one of GSSG/GSH is 0,3 V at the same pH. Aldehyde is a stronger educing agent than glutathion. At pH = 7, the respective electrode potential are 0,63 V and 0, 72 V (because the carboxylic acid is ionized). But aldehyde remain a stronger oxidant.

    secondly, the oxathiolane rings (3TC, FTC and dOTC) release mercaptoethanols, which are thiols, like glutathion.

    We can also study the other ARV, lopinavir for instance.

    You can learn in RXLIST (http://www.rxlist.com/cgi/generic4/kaletratabs_cp.htm)
    that kaletra undergoes oxidative metabolism. Why?

    If you look at the chemical structure (http://www.rxlist.com/cgi/generic4/kaletratabs.htm)
    you can see a very nucleophilic aromatic ring (right)(o,o-dimethylalkoxybenzene), which is very quickly nitrated by peroxynitrite for instance.

    How you it know, peroxynitrite is the first accountable for apoptosis.

  306. #307 jean
    March 2, 2006

    Sorry, some errors in my precedent post :

    “The only one that seems to exert some modest activity is lamivudine. But these are not antioxidants in the same was as glutathione, catalase or superoxide dismutase.”

    What you miss, George, is the fact that epivir (3TC), emtriva (FTC), dOTC and dXG, all four studied by Dr. Mark Wainberg, are acetals which are hydrolyzed at pH=1 (stomach). dXG is quickly hydrolyzed at this pH, and, strangely, is more efficient vs VL than dOTC and 3TC.

    The hydrolysis rate evolve in the same fashioning.

    What are they giving in this hydrolysis : first glycolic aldehyde. The electrode potential of the couple carboxylic acid/aldehyde is about 0 V at pH = 0, while the one of GSSG/GSH is 0,3 V at the same pH. Aldehyde is a stronger reducing agent than glutathion. At pH = 7, the respective electrode potential are 0,63 V and 0, 72 V (because the carboxylic acid is ionized). But aldehyde remain a stronger reducing agent.

    secondly, the oxathiolane rings (3TC, FTC and dOTC) release mercaptoethanols, which are thiols, like glutathion.

    We can also study the other ARV, lopinavir for instance.

    You can learn in RXLIST (http://www.rxlist.com/cgi/generic4/kaletratabs_cp.htm)
    that kaletra undergoes oxidative metabolism. Why?

    If you look at the chemical structure (http://www.rxlist.com/cgi/generic4/kaletratabs.htm)
    you can see a very nucleophilic aromatic ring (right)(o,o-dimethylalkoxybenzene), which is very quickly nitrated by peroxynitrite for instance.

    How you it know, peroxynitrite is the first accountable for apoptosis.

  307. #308 jean
    March 2, 2006

    “God. What a crock. You couldn’t get away with saying AIDS was caused by AZT when people started taking handsfull of drugs that were supposedly causing AIDS, so now you have to resort to fantasizing that ARV cocktails are somehow antioxidant therapy?”

    I have never believed that ARV cocktails were causing Aids, and it is obvious that the aids deaths decline from the introduction of HAART. But AZT is for me very poisonous, like all drugs which contain a bonding between nitrogen and an atom with an electronegativity higher than the one of carbon. For instance N-N, N=N (AZT), N-Cl (chloramines), N-O, N=O (nitroimidazoles, nitrofuranes,…)

    The human redox metabolism (immune system) handle very well the oxygenated radicals (with SOD, catalase, GPx), but I doubt that it is able to handle correctly those new structures, which don’t exist in such amounts 50 years before.

  308. #309 jean
    March 2, 2006

    I want to add that, yes, AZT, like other oxidants, (N-oxyde from tertiary amines – cocaďne – , hydroxylamines frome secondary amines – crystal meth – , isoxazoles compounds – sulphamethoxazole – , oximes or oxime ethers – cefixime – , nitrites – poppers – ) is a good candidate for the first cause of Aids.

  309. #310 George
    March 2, 2006

    Jean–First, I am delighted to hear you have not bought the idiotic idea that ARV cause AIDS. Though with your last comment, you seem to being veering toward the discredited and ridiculous “drugs cause AIDS” theory put forward by Duesberg.

    Second, the notion that ARV may exert some modest antioxidant activity is intriguing but not demonstrated biochemically. Though the chemistry suggests that they may act as reducing agents, aldehydes, for example, are, I believe, more involved with reducing H2O2 and certain metals–but it has to be free.

    It may be that there is some small degree of antioxidant activity as a secondary effect of some antiretroviral drugs. That doesn’t make them “antioxidants” per se. Though it is a fascinating topic and I shall look into it more closely.

    Third, no question, AZT is toxic. It has an azide group (N=N=N) that basically abrogates the newly forming DNA. It thus can have adverse effects on mitochondrial DNA but doesn’t appear to have such on nuclear DNA. By contrast, the same problems arise with stavudine, same exact structure except no azide group, just the hydroxyl snipped off. And it is seriously toxic.

    In fact, ALL the ARV demonstrate toxicities. That does not mean that they are not effective. AIDS death rates have declined because their primary effect is inhibiting the replication of HIV. This in turn has demonstrable effects on the intracellular redox status as the viral load declines, at least in the peripheral blood. (Other sanctuary sites like the central nervous system have other problems).

    However, the nucleoside analogs and probably other drug classes used against HIV also exert a certain PRO-OXIDANT activity through their disruption of the mitochondria.

    So to suggest (maybe you are, maybe you aren’t) that the reason ARV are successful in reducing AIDS deaths is because they are antioxidants is just ridiculous. They are successful–and that success is limited by side effects and resistance–MOSTLY because they reduce HIV load.

  310. #311 jean
    March 2, 2006

    A beautiful study from feb 2006 :

    Unsafe Sexual Behavior and Correlates of Risk in a Probability Sample of Men Who Have Sex With Men in the Era of Highly Active Antiretroviral Therapy.

    Brewer DD, Golden MR, Handsfield HH.
    From the Department of Medicine and the Center for AIDS and STD, University of Washington, and Public Health-Seattle & King County, Seattle, Washington.
    Sex Transm Dis. 2006 Feb 7;Publish Ahead of Print

    (look at pubmed)

    Among HIV-negative men, the strongest bivariate correlates of potential exposure to HIV were recent bacterial sexually transmitted disease (odds ratio [OR], 5.8, number of recent male sexual partners (OR, 1.01 per partner), recent sex at a bathhouse (OR, 9.1), and recent use of sildenafil (OR, 4.4), amyl nitrite (OR, 6.2), and methamphetamine (OR, 8.0). Among HIV-infected men, the strongest correlates of potential HIV transmission were recent use of amyl nitrite (OR, 3.1), number of recent male sex partners (OR, 1.07 per partner), and having a male spouse or domestic partner (OR, 0.3).

    The strongest correlations are with chemical stuffs which increase the intracellular amount of nitric oxide : nitric oxide gives peroxynitrite with the dioxygen anion…
    You must note that the Dr. Heinrich Kremer in 2000 had forecasted that sildenafil would increase the risk of “transmission”, thanks to his oxidative stress hypothesis.

  311. #312 jean
    March 2, 2006

    aldehyde oxidase exists, allowing the reduction of nitrocompounds and the oxidation of aldehydes… I would like to say “allow the reduction of nitrocompounds by aldehydes”

  312. #313 Richard
    March 2, 2006

    David wrote:

    “And we have to assume that similar “similarities” exist throughout all nine proteins, including at the CD4 and CD8 T cell epitope level (~9-20 mers).”
    I’m not following you here… why do you say this?

    Epitopes are small slices of protein recognized by the T cell receptor, typically around nine amino acids in length for the class I MHC receptor on CD8 T cells and ~12-20 for the class II MHC receptor present on CD4 T cells. The point being, you can identify recognition of epitopes throughout the nine HIV proteins. These T cell responses are present in people identified as HIV infected using the tests that you and others believe are so meaningless, and they are absent in people that are uninfected (with occasional exceptions at the single epitope level and in some highly exposed seronegative individuals).

    David wrote:

    “My guess is that altered cell-structural proteins are immunogenic, because they signify some kind of defect. The CMI doesn’t just kill infected cells, but also scavenges defective ones. The task is essentially one and the same.”

    I’m so glad you have a guess to reassure us with. The CMI response to things like cancerous cells and the antiviral CMI response are not “essentially one and the same.” Your theory now David is positing that all these altered cell structural proteins (mysteriously resembling the nine HIV proteins) all suddenly appear simultaneously at the time of acute HIV infection and become so immunogenic that dendritic cells are ferrying them off to the lymp nodes causing a massive wave of T cell activation (the specifity of which is easily demonstrable and perhaps might be something you want to think about instead of antibody responses, which you seem to want to insist on believing are always cross reactions with something else).

    “Though you quoted it, you have not addressed my point about so-called “HIV” proteins found in normal human placenta: p17, p24, gp120
    While we’re at it, antibody cross-reactivity with intracellular agents such as TB and mycobacteria. Not to mention pregnancy and malaria.

    Given this evidence of nonspecificity, how can anyone claim that so-called “HIV-antibodies” are specific for anything other than modified cell-structural proteins?”

    See above.

  313. #314 David Lowenfels
    March 2, 2006

    George wrote:
    “In fact, ALL the ARV demonstrate toxicities. That does not mean that they are not effective. AIDS death rates have declined because their primary effect is inhibiting the replication of HIV. This in turn has demonstrable effects on the intracellular redox status as the viral load declines, at least in the peripheral blood.”

    Can you point me to the data for these demonstrable intracellular redox effects? My understanding is that the Herzenbergs showed that GSH redox status was worse in HAART medicated individuals.

    To Jean: please shoot me an email, it would nice to correspond with you further. dfl AT.. aliveandwellsf dot org

  314. #315 jean
    March 2, 2006

    David, your mail adress don’t work.
    j.umber@ac-nancy-metz.fr

  315. #316 George
    March 2, 2006

    Here’s one study below in answer to the query about ARV effects on improving antioxidant status. Another study by Tang et al. I believe show similar effects among intravenous drug users. However, I should point to the second abstract which suggests a therapeutic approach to offset the damage to mitochondria induced by some antiretroviral drugs.

    **
    de Martino M, Chiarelli F, Moriondo M, Torello M, Azzari C, Galli L. Restored antioxidant capacity parallels the immunologic and virologic improvement in children with perinatal human immunodeficiency virus infection receiving highly active antiretroviral therapy. Clin Immunol. 2001 Jul;100(1):82-6.

    Department of Pediatrics, University of Florence, Florence, Italy. maurizio.demartino@unifi.it

    CD3+CD4+ T-lymphocyte numbers, viral load, and serum antioxidant capacity were evaluated in 20 children with perinatal human immunodeficiency virus (HIV) infection one month (T = -1) and one day (T = 0) before and one month (T = 1) and two months (T = 2) after a treatment switch to highly active antiretroviral therapy (HAART). Antioxidant capacity micromol/L) was evaluated by measuring the cuprous ion deriving from a known amount of cupric ion. Compared to control values (998 +/- 113 micromol/L), values in HIV-infected children were lower before HAART (T = -1, 848 +/- 211 micromol/L, P = 0.008; T = 0, 732 +/- 131 micromol/L, P < 0.0001), but similar during HAART (T = 1, 914 +/- 121 micromol/L, P = 0.089; T = 2; 957 +/- 155 micromol/L, P = 0.528; T = 1 and T = 2 vs T = 0, P < 0.0001). Immunologic and virologic improvement paralleled the restored antioxidant capacity. HAART may restore antioxidant capacity suppressing HIV, which inhibits antioxidant capacity. A positive feedback may be triggered since restored antioxidant capacity counterbalances the oxidative stress, which enhances lymphocyte apoptosis and HIV replication. Copyright 2001 Academic Press.

    **
    Lopez O, Bonnefont-Rousselot D, Edeas M, Emerit J, Bricaire F. Could antioxidant supplementation reduce antiretroviral therapy-induced chronic stable hyperlactatemia? Biomed Pharmacother. 2003 May-Jun;57(3-4):113-116.

    Service des Maladies Infectieuses et Tropicales, Groupe Hospitalier Pitie-Salpetriere (AP-HP), 47 boulevard de l’Hopital, 75651 cedex 13, Paris, France.

    OBJECTIVE: To determine if asymptomatic stable chronic hyperlactatemia in human immunodeficiency virus (HIV)-infected patients under highly active antiretroviral therapy (HAART, including nucleoside analog reverse transcriptase inhibitors (NRTI)) could be improved by antioxidant supplementation. DESIGN: To match two groups of patients taking NRTI for at least 24 months: 15 without and 15 with antioxidant supplementation (vitamin E, beta-carotene, N-acetylcysteine, selenium, Gingko biloba extracts and nutritional supplements). For both the groups, the supplementation by antioxidants or its lack was carefully assessed. Venous lactatemia, blood oxidative stress markers (plasma lipid peroxidation, enzymatic and non-enzymatic antioxidants), CDC revisited classification, CD4 count and viral load, NRTI (with or without stavudine) and other antiretroviral drugs used, lipoatrophy, central fat accumulation were assessed. RESULTS: Patients were not statistically different with respect to the CDC classification, CD4 count, viral load and characteristics of antiretroviral therapy. Blood oxidative stress markers, i.e. vitamin E, vitamin A and beta-carotene tended to be higher in the supplemented group. The difference observed in venous lactate concentration between the two groups was significant (1.37 +/- 0.10 vs. 1.82 +/- 0.19 mmol/l in the supplemented and non-supplemented groups, respectively P = 0.04). CONCLUSION: Antioxidant supplementation improves the asymptomatic stable chronic hyperlactatemia observed in HIV-infected patients taking HAART including NRTI for a long time. Controlled studies are needed to demonstrate the efficacy of this supplementation on mitochondrial toxicity observed during HAART and the possible usefulness of its combination with mitochondrial cofactors like carnitine, riboflavine, coenzyme Q, alpha-lipoic acid.

  316. #317 jean
    March 3, 2006

    George,

    The study on oxidative or antioxidative effects of HAART are very contradictory. But I mean that one should look at the composition of each regimen : do it contains AZT or not? I think that is the nail in the coffin.

  317. #318 George
    March 3, 2006

    jean: je crois que non.

    AZT has toxicities–but so do all the rest of the AIDS medications. All of them….like most medications. Still, it is pretty clear that ARV is a much better bet than dying of AIDS. And those toxicities can be attenuated, I believe. Indeed, data show that a) glutamine and/or calcium can offset protease inhibitor related diarrhea, and b) acetylcarnitine at 3000 mg/day can offset nuke-related neuropathy.

    Of course, the REASON that people don’t die of AIDS when taking ARV is because it is affecting the replication of this thing–you may have heard of it–called Human Immunodeficiency Virus? It’s an infection that’s been killing a lot of people lately.

    Focusing on AZT is a mistake. Although I think one could argue that a 300 mg/day dose (total) works as well as 600 mg and could further reduce toxicities while not sacrificing efficacy.

  318. #319 Dave S.
    March 3, 2006

    I was reading the paper this morning and came acrossed the following story:

    NEW WESTMINSTER, B.C. (CP) An HIV-positive man who had unprotected sex with seven women has been sentenced to 15 years in prison.

    But the sentence for Adrien Nduwayo was not imposed until after he delivered a long tirade in B.C. Supreme Court in New Westminster.

    He stared at several of his accusers during his address, reducing the women to tears as he declared he would never hurt them and criticized police and doctors.

    Justice John Truscott sentenced Nduwayo to 15 years after deducting two years already served.

    Nduwayo was convicted in December of five counts of aggravated sexual assault, one of attempted aggravated sexual assault and one of sexual assault.

    He was accused of deceiving sexual partners about his HIV status and deliberately engaging in unprotected sex.

    Now my question is this. Given that HIV does not cause AIDS, given that it’s a harmless passenger virus, and given that even then it can’t be transmitted by heterosexual contact (or so our HIV/AIDS “skeptic” friends keep telling us), what are they doing to ensure these obvious travesties of justice do not occur? What actions are they taking to see to the release of Mr. Nduwayo and others in his situation?

  319. #320 George
    March 3, 2006

    To: letters@harpers.org
    Subject: Farber article

    To whom it concerns,

    I was shocked and disgusted to see the huge spread and waste of print space you provided to this crank writer who promotes the despicable notion that HIV somehow doesn’t cause AIDS.

    You completely abrogate your responsibility to people struggling with this disease worldwide while rendering your magazine non-credible. An otherwise important article on impeaching Bush can now be dismissed, tarred by the broad brush of coddling a long-discredited conspiracy theory that ignores the genuine and horrific issues faced by people living with HIV/AIDS worldwide.

    I presume that your magazine has no fact checkers. That can be the only explanation for providing such an incredible amount of space to these dangerous and unsupportable ditherings.

    If you like, you can see how quickly the denialist garbage is demolished. Aside from a set of arguments in the British Medical Journal forum, please review
    http://scienceblogs.com/aetiology/2006/02/discussion_of_the_padian_paper.php

    I hope you will print as lengthy an article underscoring the genuine issues, political, social and moral, faced by people living with HIV/AIDS.
    Yours sincerely,

    George M. Carter
    Director, FIAR

  320. #321 Hank Barnes
    March 3, 2006

    George Carter,

    Hmm. I thought you wrote that FIAR was closing as of June 2005,?

    Hank Barnes

  321. #322 George
    March 3, 2006

    FIAR almost closed but we’re still operating.

    If for no other reason than to annoy you, dear.

  322. #323 Hank Barnes
    March 3, 2006

    Annoy me? Not in the least. I have no beef with non-profits tryin’ to make a few bucks off this AIDS boondogle:)

    But, don’t take the AZT, my friend

    Hank

  323. #324 George
    March 3, 2006

    LOL…FIAR does not pay me.

    You really always have to resort to that when you run out of arguments, don’t you?

  324. #325 Hank Barnes
    March 3, 2006

    Hello!?!?

    I said “non-profits” makin’ a buck; I didn’t say you , now did I?

    You really always have to resort to that when you run out of arguments, don’t you?

    No, I have a whole lotta arguments left:) But, don’t you think we’ve exhausted this thread? Mebbe, later on we can talk about all the AZT that was overprescribed between the years (1987-1996), that probably killed a lot of folks — despite Duesberg’s warning — but that might upset some of your pharmaceutical buddies (or is it enemies, I forget which?:)

    Also, perhaps you can cut and paste from your ANGRY letter and send it in response to this fine piece, by Dr. Rebecca Culshaw.

    That’d be a hoot!

    Your humble friend,

    Hank

  325. #326 George
    March 3, 2006

    LOL…bullshit. Use of high dose (1200 mg) AZT didn’t last that long and CERTAINLY does not account for the AIDS deaths during that period.

    Dr. Culshaw is an idiot and sounds like she has been one for at least 10 years. She’s good at regurgitating the same pap that has been refuted and discredited while adding nothing new from her purported specialty that I can see.

    So she joins the tiny legion of cranks! Good for her. Bad if she becomes infected or her foolishness encourages others to unsafe sex or horrible public policies that kill people, as in denying folks proper treatment.

  326. #327 George
    March 3, 2006

    Oh and she babbles: ” It was around this time, too, that I became increasingly perplexed by the stories I heard about long-term survivors. From my admittedly inexpert viewpoint, the major thing they all had in common – other than HIV – was that they lived extremely healthy lifestyles. Part of me was becoming suspicious that being HIV-positive didn’t necessarily mean you would ever get AIDS.”

    AIDS victims are all druggies and live those HOMO lifestyles? That old tired bullshit?

    If that were true, there’d be a lot more of my friends alive who had HIV and were pretty modest if not abstemious with regards to sex and/or drugs–and a lot more folks I know would be dead. This is just brain dead stupid.

    Sigh. Does she also need a proctologist to find her head?

  327. #328 George
    March 3, 2006

    But wait!! You should really tell one of the Big Kahunas in the world of Denialists!

    David Pasquarelli will simply SWOON when he sees her marvy smart letter full of glib commentary!!

    Go on tell him!

    Oh–oops. Sorry. I forgot.

    He died of AIDS believing your crap.

  328. #329 Richard
    March 3, 2006

    Hank wrote:

    “No, I have a whole lotta arguments left:) But, don’t you think we’ve exhausted this thread?”

    You haven’t responded substantively to the points that have been raised to rebut your arguments, because you’re incapable of doing so. Is that the same as exhausting the thread?

  329. #330 Hank Barnes
    March 3, 2006

    Richard,

    Check the title of the thread:”Discussion of the Padian paper.”

    Have we not discussed the Padian Paper?

    You haven’t responded substantively to the points that have been raised to rebut your arguments, because you’re incapable of doing so..

    Sigh. My capabilities aren’t at issue. The evidence supporting or refuting this worthless, er, consensus, HIV paradigm, is the issue.

    Of course, if one makes his financial living by propping up the paradigm, well, I would not expect said person to honestly examine the evidence.

    I doth quote the great Upton Sinclair:

    It is difficult to get a man to understand something when his job depends on not understanding it.

    Now, Richard, if you want to discuss this, without all your biases and blinders, great.

    Let’s start with the basics:

    1. What peer-reviewed paper first determined that HIV causes AIDS?

    2. If you contend that HIV causes AIDS, what evidence would falsify this causal connection?

    Those 2 are the starting blocks of a fruitful discussion.

    Fondly,

    Hank

    p.s. George, dumping on DP is pretty crummy. It shows that you are an immature man, without much honor.

  330. #331 Francis
    March 3, 2006

    hank: what relevance is the first determination that HIV causes AIDS?

    If HIV does, in fact, cause AIDS (in the manner that Tara and others have described), what difference does it make whether the first peer reviewed paper came out yesterday?

    Isn’t it the case that what matters more than a “first” publication are the multiple threads of evidence, as cited by NIH?

    I look forward to your response.

  331. #332 George
    March 3, 2006

    LOL. Hank, you’re so full a shit ya need a QTip just to get a start on it.

    I’m not dumping on David P. Hardly. Can’t say I loved the guy but I certainly didn’t want to see him die. Frankly, I don’t think you did either, at least I should hope not.

    But here you go again, asking stupid fucking questions about THE paper. Show me THE paper that shows influenza virus causes flu.

    You should answer your second question yourself.

    And indeed–the thread started with the Padian paper. The silly and inane arguments brought forth by you, Bialy etc. underscore too horrifically the dreadful weaknesses of the denialist position.

    But you cling steadfast as I knew well you would. As will Bialy. The consequences for people that buy this line of nonsense can be fatal. And for David, he met that fate that awaits us all. If there is something after this life, then maybe we’ll get a chance to meet and share each other’s joy and pain.

    And I shall bear the responsibility for any pain or suffering I have caused, intentionally or inadvertently. Unless it’s just oblivion in which case it matters not a whit. (Tho I keep praying that certain pharma execs, Rumsfeld-Cheney-Bush and other shits will get to experience the suffering of all those they have murdered with their hubris and greed.)

    But in this life–you need to do MUCH better than you have to show why any of these other hypotheses that explain why young people’s immune systems crash and otherwise rare opportunistic infections arise. Recreational drugs? Nonsense. Just doesn’t fly.

    Nor does it explain the very distinct and strong correlation between HIV and AIDS among children, men, women, the elderly, people with hemophilia, people with a drug use history, people without a drug use history, gay men who have lots of sex, those that don’t, etc.

    Happily, at least, I don’t see any denialists here trying to claim it is ARV causing AIDS.

  332. #333 George
    March 3, 2006

    A quite thorough disquisition and dissection of Farber’s misleading, inaccurate and delirious Harper’s article has just been published by quite an esteemed group. Richard–is there a URL where people can go to review it?

  333. #334 Hank Barnes
    March 3, 2006

    Francis,

    hank: what relevance is the first determination that HIV causes AIDS?

    You’re a lawyer, right?

    It’s called citing the source. Can you imagine a future Supreme Court case over abortion in 2008, that somehow conveniently forgets to cite Roe v. Wade from 1973?

    Same principle with science. There should be a paper or group of papers, that says, essentially, we hypothesized that this 9Kilobase virus wrecks the immune system, we tested this hypothesis, doing X,Y,Z, to ensure we were not dealing with a harmless passenger virus, we conclude A,B,C.

    For example, if I’m writing a paper on the structure of DNA, I would probably cite, Watson & Crick’s seminal paper in Nature in 1953.

    This should be very easy to understand.

    So from the top:

    1. In 1979, there was no AIDS, nor HIV.

    2. By 1981, there was AIDS, but the cause was unknown.

    3. In 1984, there was AIDS, and the cause was said to be HIV.

    What was the peer-reviewed paper in 1984 that served as the scientific foundation of that statement?

    Aren’t you interested in reading about the rigorous scientific tests undertaken in said paper, by the men/women who undoubedtly won the Nobel Prize for such a brilliant discovery?

    Hank

  334. #335 George
    March 3, 2006

    And so we come full circle in the Denialist Merry-Go-Round.

    Hanklet, my dear little bubble of gas, are you unable to review the papers on the isolation of LAV? Do you want the papers by Francoise Barre-Sinoussi, the discoverer of what later became known as HIV? Or Jay Levy’s seminal work (pardon the pun)?

    Or are you going to trot off to the Perthies to claim HIV doesn’t exist? And then off to Duesberglet for a course of “it does but it’s them drugs causin’ AIDS”?

    And then the circle goes on….the data are presented. You trot off to the next bullshit claim, utterly ignoring all the evidence presented, raising more spurious, foolish questions and bubbling off to another whiskey bar for yet another round….in the modern parlance of the net, Hanklet my dear, you are a troll.

  335. #336 Hank Barnes
    March 3, 2006

    George,

    Francis wrote:

    I look forward to your response

    So, I responded to him, not you.

    George writes: ….the data are presented

    By you? Where?:)

    Hank

    p.s.

    George writes above:

    (Tho I keep praying that certain pharma execs, Rumsfeld-Cheney-Bush and other shits will get to experience the suffering of all those they have murdered with their hubris and greed.)

    You’re a unwitting tool of those certain pharma execs and Rumsfeld et al. Your’re just too stupid to understand it.

  336. #337 George
    March 3, 2006

    You didn’t reply…you just waved your hands and squealed, letting out a stream of nothing. No evidence. No data. Nothing but the same old gas….

    …and au contraire. I propose ideas that pharma does not like and that will eventually come to pass.
    1) Single payer healthcare;
    2) Price controls;
    3) Patent law reform to reward discoverers, not stockholders;
    4) Increased public funding for drug discovery from the lab to phase IV;
    5) Access to generics;
    6) Greater regulation and oversight of industry products.

    That’s what I want my tax dollars for. Not wars based on lies that are then horribly botched by a jackanape with an IQ possibly lower than yours.

  337. #338 Francis
    March 3, 2006

    Hank:

    two problems with your comment. first, science is more evidentiary, law more philosophical. why do people believe the world is 4.5 billion yrs old? for most people, it’s because they’re told. for those who have a deep understanding of the issue, it’s because multiple lines of evidence all support that conclusion and there is no strong evidence that the conclusion is erroneous (or so i’m told). there is no one arbiter of truth. by contrast, the US Sup Ct. is, by definition, the ultimate arbiter of what the law is.

    second, in most cases where the application of legal principles is hotly disputed (as compared to cases where the facts are disputed), there is no one authoritative case. (if there were, then there’d be no case.) lawyers weave arguments together out of multiple threads, including analogous precedent, legislative intent, common sense, efficiency and whatever else is applicable.

    put simply, most of the time in a lawyer’s life there is no one Roe v. Wade to cite. but the absence of the one seminal case does not mean that the law is then unclear. (hmm, don’t want to end on a double negative.) Even when there is no one seminal case on a particular legal doctrine, there is often no dispute as to what the doctrine is, because instead of one case there are hundreds of cases which collectively establish the doctrine at issue.

    you pose an interesting question in the context of the history of science. but i think you ask too much of both scientists and lawyers to be able to point to single sources as proof of answers to complex problems.

  338. #339 Richard
    March 3, 2006

    Now, Hank, if you want to discuss this, without all your biases and blinders, great.

    Let’s start with the basics:

    1. What peer-reviewed paper first determined that herpes zoster causes chickenpox and shingles?

    2. If you contend that herpes zoster causes chickenpox and shingles, what evidence would falsify this causal connection?
    -

    I think that document will go up soon on the TAC website George, but I don’t have a link yet. It’ll probably just be another instant Durban Declaration for the denialists, they love that document because it made them feel like they were having an impact. They came up with a fresh bunch of sophistry in response. Duesberg’s response to the seven bullets of the Durban Declaration was to invent 17 specious “interpretations” of his own with a few quotes laced in, then, of course, he was able to question his own specious predictions and show that they didn’t match reality. This, we are supposed to believe, represents a serious challenge to the scientific consensus (one that is being stifled!). The other amazing thing about Duesberg’s “predictions” is that they’re so rooted in his own arrogant certainty that he knows everything that is possible (and that might ever be possible) in the virological universe. An example:

    Duesbergian prediction

    All viruses are most pathogenic prior to anti-viral immunity. Therefore, preemptive immunization with Jennerian vaccines is used to protect against all viral diseases since 1798.

    Fact (his word)

    But, AIDS is observed “by definition” only after anti-
    HIV immunity is established, a positive HIV/AIDS test. Thus HIV cannot cause AIDS by “the same criteria” as conventional viruses.

    - It’s the words “by definition” and “the same criteria” that are quoted from the Durban Declaration.

    As for the remaining words, which are all contributed by Duesberg, what does the prediction mean really? “All viruses”? In perpituity? Jennerian vaccination should work because it’s worked for a couple hundred years? And for the “fact” part, the Durban Declaration nor anyone else is saying that the virus causes disease the same way as other viruses; they’re saying that it has met the same criteria to be identified as the causative agent of the disease. That last sentence doesn’t even mean anything – what does it mean to cause disease by the same criteria? Since he was making up the prediction, you’d think he’d have been able to come up with a better rebuttal really.

    I suspect the response to the Farber article will produce something similar, but then it’s not the denialists that are the intended audience. More like Harper’s fact checkers, for starters.

  339. #340 Reggie
    March 3, 2006

    ** claims to have ICL and in the link below states she has PML for quite some time, aside from various other devastating illnesses.

    http://www.reason.com/hitandrun/2005/10/does_a_mothers.shtml

    I imagine her immune system is shattered to develop PML and it’s quite a miracle that she’s able to write so extensively across the web and on her blog. She describes her bout with ICL by an infectious agent after a sexual encounter.

    ** what are your CD4/CD8 numbers and percentages? Wondering how you are managing so lucidly with PML for so long. Many others on the web wonder too.

  340. #341 George
    March 4, 2006

    Thanks, Richard. I hear TAC may have it up on their website soon–I hope so!

    And you’re undoubtedly correct…the denialists will vomit up a reply undoubtedly. But this is not about them. There have been only a couple of denialists I’ve known who changed their mind. James Scutero was one–he looked at the science and realized it was HIV causing his CD4 count to erode away. Sadly, he committed suicide a few years later due to other demons. Casper Schmidt I think was open to the idea that HIV caused AIDS–it killed him in the end. I think even Pasquarelli got it at the end–a bit too late. Root-Bernstein seems to almost have gotten although he still thinks there is a role for a co-factor.

    (Indeed, one of the revolting things is that list of so-called scientists who “question” HIV–an ancient list, cobbled together with misleading questions; one idiot denialist has a website with a photo of Joe Sonnabend and a caption saying it’s Casper…and Joe, of course, is not a denialist.)

    No, I’m not in this fight to convince them. I know they won’t be. I remember when Duesberg called me after the Berlin conference based on a white paper I’d written and he misinterpreted as representing incipient denialism. I still am astonished that this guy can persistently burble that presence of antibodies indicates the disease has been overcome. What a rigid, fascistic mind! Such boneheaded persistence in embracing a demonstrable falsehood! (He gives Bush/Rumsfeld/Cheney et al. a run for the stolen money.)

    The real audience is the people who are at equipoise. Who may be swayed by what appear to be cogent arguments from the denialists but upon closer scrutiny turn out to be weak, hollow, misleading or false.

    Hanklet represents the fundamental approach too: bring up a “question!” which appears to be devastating and turns out to be nothing. Responded to, he flits off to the next conspiratorial Big Wink.

    The consequences of this dancing with denialism are of course horrifically clear. Needless suffering and death.

    And a deflection from the more important issue of HOW HIV causes AIDS–and what the therapeutic implications are.

  341. #342 Karen Lynne Lambert
    March 4, 2006

    Hi Reggie, Thank you for your care and concern. My NeuroAIDS physician, at the world’s finest hospital in downtown Boston, enrolled me in his PML research studies, so yes it was accurate statement when I made it and — amongst numerous other AIDS-like opportunistic infections –it remains an accurate statement today.

    As you will note, Tara chose to initiate a discussion about my case (http://scienceblogs.com/aetiology/2006/02/post_3.php), not vice versa. While I have my guesses, I have no idea how she even came to know about me. Subsequently, she and I have had several communications, and I have no reason to believe that she would compromise her integrity and reputation for sake of mine…I have given her no reason to question otherwise. Much to many people’s dismay, every word I speak is the truth (so, doubt it if you wish, because it all still horrifies me too, but it will all still be true).

    Not really sure what you perceive people who are chronically ill, with impaired immune systems do with their free time (Hillenbrand became a best seller while bedridden with severe CFS–link to the story on my blog), since my very active, triathons days are long since over. With toothpicks holding my eyes open most days, rather than watching drivvle on tv, I usually chose to spend time continuing to research undiagnosed acquired idiopathic immune disorders, work with scientists and Rx companies all over the world, try to continue to understand where my case sits in the HIV/AIDS, CFS, AIDS Myth debate, and educate others about my plight. I am a humanitarian.

    Also, you also faslely assume that I am a team of one. Very, VERY far from the truth…

    ICL cases are a really big deal, so I hope everyone will get over their skeptism. My bloodwork will be provided, if protected by HIPAA.

    My goal has been unwavering since Day1: systemic diagnosis. I promised it then, and I promise it now…I am going down fighting.

  342. #343 George
    March 4, 2006

    KL: I don’t think anyone disputes the reality or existence of ICL. It appears to be a genuine condition of unknown etiology–and a very rare one.

    But the existence of ICL does not mean HIV does not exist or does not cause AIDS!

  343. #344 Reggie
    March 5, 2006

    Yes George, that is one of my issues with K’s claims that are blindly insistent with ICL (which, by definition, is not understood) being infectious. Laura Hillenbrand has never claimed she is infectious and my understanding is that she’s had a long term partner who PRE-DATES her CFS, yet he is perfectly healthy. Please don’t use her as an ally in your claims of having an infectious disease. I simply don’t know why you insist on having an infectious disease when there is no evidence that you do, not in the eyes of science and medicine anyway.

    I do admit being very suspicious of your claims however. I was on a couple of boards where people brought up flagrant inconsistencies with your claims and some had even done what they called “homework” and found holes. You have even been banned on AIDS Myth Exposed, a radical board of conspiracy theorists of the highest order (one would think they’d embrace you with open arms). One claim that posters have often raised is that you claim to have PML for a couple of years now (on the link I provided). That is a rare and severe opportunistic infection that would cause one to scratch their heads to understand how you can write, discuss, debate and argue so passionately and articulately. It remains a mystery.

  344. #345 Reggie
    March 5, 2006

    Oh K, your CD4/CD8 numbers/percentages? Care to share? Would be very helpful to understanding how you have had PML for so long yet have managed to survive it and be doing so well cognitively.

    What was your number when diagnosed? And now? Was there some kind of treatment in the interim? How do the many prominent researchers you work with explain your current condition?

  345. #346 George
    March 5, 2006

    Reggie, whether Lynn actually has ICL is not the point. I commented on the condition existing–which I think it does.

    I too find it difficult to believe she has had PML. Some few people have indeed survived it–but it is damned rare. One of my dearest friends in the world died of PML. She had had HIV and developed AIDS and was a long time survivor, a fierce and incredible activist and did so much for women’s rights. I miss her and think of her often.

    It is not impossible that she had a milder form and if she has some idiopathic condition which causes CD4 declines that are episodic, she may have had a bout of a flare up of the JC Virus that subsided during a remitting portion of her disease? It’s not impossible. But I am not here to determine the veracity of her claims. That’s up to her!

    And I’d be curious to learn more of her history as well.

  346. #347 Reggie
    March 5, 2006

    Sorry George, I probably misread your comment. Khas made a great many claims across the web that change and contradict one another frequently, which is why she has been banned from websites and her very claims challenged. Even Christine Maggiore, whose beliefs are outrageous, is perceived as being genuine (Gulp! I can’t believe I just said something positive about Maggiore).

    ICL DOES exist, there is no question (and it’s said to be rare). She may or may not suffer from ICL. That is not my issue.

    PML (among other fantastic claims of illness) is my point of contention. Per the NIH, PML is fatal (http://www.ninds.nih.gov/disorders/pml/pml.htm) and at the very least, does impair mental and physical functions. I don’t know how often you have come across her posts but they are extensive on the blogosphere. They range from complete allegiance to the HIV does not equal AIDS delusion to government conspiracies of ICL to CFS is AIDS to ICL is induced by a strain of HIV not yet discovered. She has posted various times to the pros at thebody.com and some of their responses are frustrated.

    When the conspiracy theorists at “AIDS Myth Exposed” have asked members not to respond to her, it says something. These are the folks who give wide latitude in credibility to Kary Mullis’ alien encounters.

    I don’t know if she has ICL, she may. But to have the list of ongoing fatal infections she has claimed is implausible at best and to try to insist ICL is infectious is inconsistent with current medical literature.

  347. #348 Tara
    March 5, 2006

    To go back to Hank’s point for a moment–

    For example, if I’m writing a paper on the structure of DNA, I would probably cite, Watson & Crick’s seminal paper in Nature in 1953.

    But, y’see, Hank, that paper still built on years of work on DNA. Where would Watson and Crick’s work be without the context of Griffith’s work showing transformation in pneumococcus, or Avery’s work identifying DNA as the material that provided the genetic material? Science doesn’t work in isolation–it builds upon the previous literature, and therefore even your Watson and Crick paper doesn’t do it alone. Heck, even they admit that the previous X-ray data isn’t enough to “prove” their findings, and that more research needs to be done. What if you saw this kind of sentence in a paper discussing HIV causation of AIDS, Hank? My guess: you’d hone in on that point and dismiss the paper.

  348. #349 Karen Lynne Lambert
    March 5, 2006

    Reggie, There remain no “holes”, inconsistencies, contradictions, or changes to my story now (or ever). If acclaimed critics have done their homework they would know that my story is flawless, so I really do not know what you are referencing.

    Using AIDS Myth Exposed in an argument is actually laughable to me.

    My bloodwork will be provided, if protected by HIPAA.

    Extended response is on my blog.

  349. #350 Reggie
    March 5, 2006

    K, the inconsistencies are endless and detailing them all is tiresome. I’ll reference some but you’re on your own after that.

    May I ask why you have, twice, referenced HIPAA privacy issues regarding your bloodwork. If ** is your real name and you have ICL (and the dozen other fatal OI’s you’ve claimed to suffer from) then you’ve already broken HIPAA while discussing your “condition.” Hell, you’ve disclosed having PML. What uglier, more fatal and terrifying revelation could your medical records produce, Ebola?

    And if that is not your name, I don’t know why it matters if you do provide CD4/CD8 numbers/percentages, course of illness, treatment plans, stage of PML — no one would know who you were anyway. You have been asked for the numbers many many times, not documentation. My theory is that detailing fictitious figures and treatment plans that would have to correspond with fictitious OI’s around bona fide scientists, who would easily smell a rat, would quickly prove disastrous for your stories.

    Once the scientists and physicians start asking direct questions, you become evasive and fly away.

    Most troublesome of all is that your favorite tangent has nothing to do with illness and everything to do with labeling. The basis of your fury is that you are not called an AIDS patient. Your myelin is eroding (so doubtful, truly), your future is short and bleak and you’re pissed off that scientists use the term AIDS only to describe HIV+ patients?

    AIDS Myth Exposed is laughable, correct. And that’s why their banishing you for outrageous claims makes you even more incredible.

    The L claims change radically given the predominant view on the blog. If it’s an “orthodox” blog, HIV is accepted. If it’s a denial/conspiracy blog, ** works with whatever culprit they identify. But the underlying thread is always the same: Why why why do I have ICL? Why don’t I have AIDS? No matter how many times scientists explain idiopathic to **, she doesn’t get it. No matter how many times scientists tell K that AIDS is used to describe HIV+ individuals and that their immunosuppression is not idiopathic, she persists as if her question was not answered.

    Endless claims of close association with the nation’s foremost scientific and medical authorities in epidemiology abound (ICL isn’t that fascinating; you should have picked another disease). Now “crash and bleed out” from the Mayinga strain of Ebola Zaire in downtown Los Angeles and you’ll garner so much attention from USAMRIID and the CDC, you’ll wonder if they all abandoned the east coast.

    -claims of having and being studied for PML, claims that HHV6 is the cause of AIDS, CFS, ME, Fibromylgia, MS, and autism.
    http://www.reason.com/hitandrun/2005/10/does_a_mothers.shtml

    -claims of having and being studied for PML
    http://thetyee.ca/News/2006/02/01/AIDSTrialsRisky/

    http://www.windsofchange.net/archives/008106.php

    http://www.thebody.com/Forums/AIDS/SideEffects/Archive/Testing/Q160149.html

    http://www.nypress.com/18/2/mail/themail.cfm (even Celia Farber is perplexed over ** insistence that her immunodeficiency is infectious)

    Yes, this is the last post on L. I just thought some of you should know you’re wasting your time.

  350. #351 Hank Barnes
    March 6, 2006

    Tara,

    What if you saw this kind of sentence in a paper discussing HIV causation of AIDS, Hank? My guess: you’d hone in on that point and dismiss the paper.

    Well, why not show me the paper?

    Barnes

  351. #352 Chris Noble
    March 6, 2006

    Hank, you still haven’t attempted to support your claim that HIV is an endogenous virus.

  352. #353 George
    March 6, 2006

    “Show me the paper” he says.

    Hanklet, does this mean that you are completely ignorant of the literature you’ve been holding forth on with such bombast and pomp?

    My heavens. That you don’t know the various papers means that you, my little bubblet of gas, have been merely speaking in tongues of flatulence, exuding your ersatz knowledge from the lips of your ass….

  353. #354 George
    March 6, 2006

    To: letters@harpers.org
    Subject: Further to Farber

    To whom it concerns,

    I am sure by now you have seen the extensive dissection of Farber’s article–but another aspect concerns me.

    By embracing denialist cant, aside from discrediting other articles and raising suspicions about your editorial quality, I think the biggest loss is that the story of all the MANY horrendous ways the AIDS pandemic has been addressed are swept aside. An opportunity is lost then to understand the ways in which:

    1) Yes, clinical trials in developing nations suffer from sometimes serious ethical lapses. Recent evidence of a hep E vaccine’s mismanagement in Nepal by Glaxo SmithKline, for example. The “pre-exposure prophylaxis” studies in various countries of the drug, tenofovir, represent another set of ethical issues (not the least of which is that data subsequent to the studies development in a macaque model showed that the drug failed to prevent infections).

    2) The pernicious influence of the pharmaceutical industry and the aggressive and vicious stance of the United States government through horrific unilateral trade deals and a psychotic office of the US Trade Representative which have done their level best to deny access to antiretrovirial therapy, positing that intellectual property rights (read: “Profit”) trump human life.

    3) The Bush administration’s Gag Rule on family planning while ramming “abstinence only” policies down the throats of non-governmental organizations and governments, facilitating the spread of HIV. Makes “intelligent design” nonsense look mild by comparison.

    4) The invidious and despicable activities of Matthias Rath in telling people to stop taking ARV and rely on a multivitamin. This sets up a false and evil polemic that it is one or the other. Nothing could be further from the truth. A simple and inexpensive multivitamin has been shown to dramatically slow progression and can help reduce morbidity and mortality. This information comes from well-controlled and conducted studies. But it’s not a cure and unfortunately won’t obviate the need for ARV therapy.

    5) The failure to address many “orphan diseases” such as parasitic infections (schistosomiasis, leishamaniasis, etc.) which dramatically increase progression rates and are easily treated.

    6) The distortion of intellectual property rights, further to point 2, that instead of rewarding discoverers now reward stockholders. The profit motive has further narrowed drug-discovery pipelines for many infectious diseases, deemed unprofitable by a voracious industry that has abjectly lost sight of its putative beneficiaries, i.e., patients, in favor of ever-increasing profits. This has had horrific implications for drug discovery.

    7) The suffeirng and plight of children, often living with HIV, from Russia to Rwanda. (Oh, right, those kids are all out doing poppers, I forgot. That’s what causes AIDS, right? Feh.)

    8) The stigma and discrimination faced by same gender loving individuals, recreational drug users, sex workers, women, ethnic minorities from the south Bronx to Bangkok….

    There are SO many stories you COULD have told that are well documented. Yet, instead, you chose a crank like Celia Farber to write an incredible piece of trash.

    Again, I point you to
    http://scienceblogs.com/aetiology/2006/02/discussion_of_the_padian_paper.php

    That and the work of Nathan Geffen et al. should show how deeply embarrassed and ashamed you should be for having published that crap. I hope you will retract the article and give equal time and space to GENUINE issues in the war against AIDS, a pandemic that has indeed shown a bright and horrific light on our public policy failures from local to global levels.

    George M. Carter
    Director, FIAR
    http://www.fiar.us

  354. #355 Karen Lynne Lambert
    March 6, 2006

    Reggie, Thank you for continuing to bring more attention to my case, to HIV-Negative AIDS, and to my undiagnosed infectious and communicable disease. I take your word, that your last post, was truly your “last post” on the “Lambert case”, as I am too tired to deal with your nonsense any longer. Since you clearly made no initiative to read my response to you, let me cut a blurb from my blog:

    If acclaimed critics have “done their homework” as you suggest, they would know that my non-risk group body has been saying the same unwavering, progressively-worsening, story for the last 1,000+ — rather enduring — days.

    I do not know how to resolve critics’ skepticism about my case and ensure your comfort with the facts that I have presented (without compromising my privacy), other than to say that my request for an investigation — and my selfless activism for the betterment of mankind — was initiated from The White House (on March 23, 2004) and was transferred to The Commissioner at the Massachusetts State Health Department on May 12, 2004, http://lemonfoundation.blogspot.com/2005/07/few-highlights-of-my-plight_12.html. If you have concerns about who I am, of my creditability, or of my research affiliations, please feel free to write them: http://www.mass.gov/dph/about/feedback/feedback_health.htm, since investigations have already been opened (on my own merits and accord). Ask them to confirm that I am who I say I am. Ask them to confirm their investigation of me. Ask them to confirm the contents of my medical file. Ask them to systemically diagnosis me. Demand them to conduct a Reappraisal of AIDS. You clearly are an imaginative bunch, making up all sorts of fabricated things about me, so I am sure you’ll come up with something grandious to say.

  355. #356 Hank Barnes
    March 6, 2006

    Chris,

    Hank, you still haven’t attempted to support your claim that HIV is an endogenous virus.

    I offered above to do that on a separate thread. Tell me when and where?

    There are a lotta distractions on this thread from folks who believe in stuff without evidence found in the literature.

    Hank

  356. #357 George
    March 6, 2006

    Talking to yourself again, Hank?

  357. #358 George
    March 7, 2006

    The extensive rebuttal to the incompetent and inaccurate Farber article in Harper’s is available here:
    http://www.tac.org.za/

  358. #359 Chris Noble
    March 7, 2006

    Hank you have diverted the thread numerous times. You quickly gave up trying to defend your characterisation of the Padian paper when people demonstrated you were making stuff up.

    What you have not done is provide evidence for the claims that you make.

    You are again trying to avoid the inconvenience of actually finding evidence to support your claim that HIV is an endogenous virus.

    Remember? You claimed that the Padian study provided evidence that HIV was an endogenous virus.

    You are a troll.

  359. #360 George
    March 10, 2006

    End of thread…denialists rush of to spew the same dismal, refuted crap on the Nation website or some such!

  360. #361 Jörg Hartmann
    March 22, 2006

    Every 1000th sexual intercourse transmits “*”? (Put there “HIV” or “sexually transmitted herpes simplex 2″ or whatever you like.)

    How do you know? Is sexual intercourse the only thing those couples did in these periods of time? Or are these things transmitted by eating donuts, too, because there’s a correllation between eaten donuts and “transmissions” (the second person getting a positive test) in a ratio of –say– 1/500 (assuming that people eat 2times more donuts than they have sex)?

    Not a single one of these expensive “studies” has really studied anything like a causal connection, just correllations. 1/1000 ratios. How insanely stupid …

  361. #362 Dale
    March 22, 2006

    Evidence that it’s sex, among other things? People who share lifestyles or even households but don’t have sex with, get blood transfusions from or be born to HIV positive individuals don’t become HIV positive themselves.

  362. #363 windy
    March 22, 2006

    (assuming that people eat 2times more donuts than they have sex)

    Dude, that doesn’t sound healthy.

    (Assuming an active sex life and that the people aren’t cops or working in a donut shop)

  363. #364 Rob
    March 26, 2006

    The final version of the Harper’s rebuttal is available at AidsTruth.org. The site also features some of the letters sent to the magazine in response to the article, and links to more resources.

  364. #365 Rob
    March 27, 2006

    I think this thread is dead. However if anyone is still interested in evidence of sexual transmission of HIV then they should check the many references in this fact sheet.

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