HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS


Posted by Henry Bauer on 2008/04/29

Oh that one would hear me! … and that mine adversary had written a book
King James Bible, JOB 31:35

As a target of debunking, a review may serve as well as a book, especially when it happens to be a review of what’s [not!] known about HIV/AIDS: “The spread, treatment, and prevention of HIV-1: evolution of a global pandemic”, by Myron S. Cohen, Nick Hellmann, Jay A. Levy, Kevin DeCock, and Joep Lange, Journal of Clinical Investigation, 118 [2008] 1244-54; doi:10.1172/JCI34706. The authors are heavyweight white-coated HIV/AIDS gurus, at least two of whom (Levy, DeCock) have been in this business from the beginning. The review is a textbook case of cognitive dissonance or, using Thomas Kuhn’s term, incommensurability (1).

Cognitive dissonance is the inability to “see”, or to comprehend the implications of, evidence that—objectively speaking—disproves a belief. Popular parlance might describe it as a state of denial. In Festinger’s classic study (2), when the predicted end of the world did not come on the calculated date, the believers concluded only that they had gotten something in the calculations a bit wrong, and their basic belief hardened rather than weakened.

“Incommensurability” signifies that researchers get so vested in the prevailing paradigm (i.e., dogma) that they cannot understand—quite literally cannot understand—how data could be interpreted in any other fashion than the one dictated by their belief.

Imre Lakatos (3) identified a strategy researchers use quite routinely to preserve belief in the face of contradictory evidence: they invent ad hoc explanations for each new piece of data that their theory cannot accommodate. They do not modify at all the basic belief (the “core theory”); rather, they attach to it ad hoc extensions that are not genuine corollaries because they are not inherently demanded by the theory, and they are not necessarily consistent in any natural way with other such ad hoc extensions of the theory.

This aspect of science is not part of the conventional wisdom about “science”; the popular myth, oversimplified and reverential, holds science to be trustworthy under all circumstances (4, 5). But illustrations of the fallibility of science abound, and HIV/AIDS dogma offers some cogent examples of cognitive dissonance, for example:

— The prediction that the AIDS outbreaks in major American cities would be followed by a spread into the general population was almost immediately falsified; yet the belief that HIV is sexually transmitted hardened rather than weakened.

— The prediction that a vaccine would be available within a couple of years after 1984 has been falsified over and again, despite the deployment of every conceivable strategy for design of such a vaccine, not to speak of untold millions of dollars expended. These failures have brought only increasingly strident calls to continue the attempts.

— The finding that the observed apparent rate of sexual transmission is far too low to explain the observed distribution of “HIV-positive” people was met by the ad hoc postulate that there must be some higher rate of infectivity during short periods; and this unobservable and unobserved infectiousness is nowadays dogma without the benefit of proof.

The cited review by Cohen et al. of the state of the art of HIV/AIDS offers further illustrations of accepting as fact, and disseminating as fact, things that are plainly not true, or that are unproven or unprovable, or that border on the absurd. As well, interpretations are invoked or implied that in other contexts would be immediately recognized as unwarranted, and racist to boot.

Simply wrong:

“[M]ale circumcision provides substantial protection from sexually transmitted diseases, including HIV-1”
Four references are given, but left unmentioned is the study by the Centers for Disease Control and Prevention (6), which found no such effect.
Even were such an effect to be suggested by correlations (which are the only available evidence), one might question a causal interpretation for its extreme implausibility with respect to “HIV-1”: how could circumcision protect males from an agent whose apparent transmission from female to male is already significantly lower than the apparent transmission from male to female, which itself is only about 1 in 1000? And given those almost immeasurably small apparent rates of transmission, how massive a set of trials would be needed to gather potentially convincing evidence?
As to circumcision protecting against known STDs, there is controversy extending over centuries and still not resolved to the satisfaction of all researchers, see For example, Professor Andrew Grulich (National Centre in HIV Epidemiology and Clinical Research [Australia]) reported recently at the Australasian Sexual Health Conference (Gold Coast, 11 October 2007) that there was no association between infection and circumcision status for any disease apart from syphilis (Thaindian News, 14 November).

Hardened belief in face of contrary facts:

“28 years after AIDS was first recognized…, HIV-1 requires continued global focus and investment”
Required, presumably, only because researchers want the money; for in the very same paragraph, Cohen et al. acknowledge that “global HIV-1 prevalence seems to have been stable since around the turn of the 20th century; and HIV-1 incidence peaked worldwide in the late 1990s and has been declining ever since”.

“Perhaps one of the most surprising aspects of the HIV/AIDS pandemic is the unequal spread of HIV-1”
Exactly; “surprising” because no infectious agent behaves like that.
On the one hand, “HIV-1 does not respect social status or borders”—because no sexually transmitted agent does—yet on the other hand, “racial and ethnic minorities, especially African Americans and Hispanics, are disproportionately affected… in Europe … many infections today are found among immigrants from sub-Saharan Africa”. The obvious contradiction between “no borders” and “racially discriminatory” can only be resolved by recognizing that HIV is not sexually transmitted; but those hewing to the dogma are incapable of that recognition, as Festinger, Kuhn, and others have pointed out.

“Africa has witnessed the full devastation of the HIV/AIDS pandemic”
but the population there has continued to grow at an annual rate of a few percent!

Swallowing improbabilities:

“DNA sequences of viruses in distinct clades can differ by 15%-20%”
and yet all of them are supposed to do about the same thing, with only minor differences in efficiency of transmission and “pathogenic potential”.
But in other contexts we’re told that human and chimp genomes differ by less than 1%, which suffices to produce quite major differences in the products of those genes.

“In Eastern Europe … brisk and severe epidemics emerged among injecting drug users in the late 1990s”
Grant—for the moment—that HIV can be transmitted via infected needles: how to conceive “brisk and severe epidemics” from shared needles? Try to picture the orgies of needle-sharing that would be required, particularly when two decades of experience have revealed that catching “HIV-positive” from needle punctures is even less probable than the 1 in 1000 chance via unprotected intercourse.

How HIV is transmitted in different parts of the world:

Since this figure sports precise percentages, the casual observer might be tempted to regard this as scientifically established fact, instead of pausing to recognize how absurd it is on its face. Marital sex responsible for half of all infections in the most affected area, and for a quarter of them in Asia—but not at all in Eastern Europe? Casual sex more significant in Eastern Europe than transmission among men who have sex with men, who remain in the United States the group most regarded as at risk?! Mother-to-child transmission (MTCT) virtually unknown outside Africa, including in Asia where “marital sex” represents a quarter of all transmission?? Doesn’t marital sex in Asia ever lead to pregnancy?!? Medical injections, too, virtually unknown outside Africa; and in Africa allowed just a few percent, ignoring the numerous publications by Gisselquist, Potterat et al. that indict such injections as a more plausible source of the “pandemic” than sexual intercourse?!?! Sex workers a substantial risk in Asia and Latin America, but far less dangerous than marital sex in Africa, and no risk at all in Eastern Europe?!?!?
To believe all this, one would have to also believe that these various regions of the globe are characterized by cultures and lifestyles so different as to bespeak the presence of altogether different species of Homo.
The text of the review article notes that “the US epidemic remains a paradigm of HIV/AIDS in the developed world”, indicates that sex among males is the greatest source of infections there, and suggests something similar for Western Europe. Those are the regions for which the data are most copious and reliable; and moreover North America is the region where HIV/AIDS originated, the veritable “mother of all HIV/AIDS regions”; so why are Western Europe and North America absent from the figure, whose source is “Bringing HIV prevention to scale: an urgent global priority”?

Subterranean racism:

“even in settings of generalized epidemics [i.e., self-sustaining in the population], the risk of infection with HIV-1 is … increased in persons with higher rates of partner change or who acquire classical … STDs … [or] who experience other significant exposure(s) to HIV-1, such as injection drug use”
— those people who also happen to be endowed with black skin, in other words, because all our data has shown for a couple of decades that they, everywhere in the world, are the most likely to test “HIV-positive”: “In the US, racial and ethnic minorities, especially African Americans and Hispanics… in Europe … many infections today are found among immigrants from sub-Saharan Africa”.

Note how the term “minorities” is deployed as a euphemism in mainstream discourse about HIV/AIDS (and in many other contexts too). In the United States, Asians constitute a much smaller numerical minority, and Native Americans an even smaller minority again, than either blacks or Hispanics. But Asians are significantly less affected by “HIV” than are white Americans, and Native Americans are affected not much more than Caucasians and significantly less than Hispanics, let alone blacks. “Minorities” serves as a euphemism for both “liable to reprehensible behavior” and “black”.


This review article constitutes a goldmine of additional opportunities to debunk HIV/AIDS theory. It is replete with unproven assertions, for instance about “acute viral syndrome”, and contains the occasional nugget of acknowledgment that the most fundamental, central, matter of all remains as mysterious as when it was first declared that HIV destroys the immune system:

“To date, the destructive properties of HIV-1
have not been completely unraveled”

If one omits the misleading euphemistic weasel-word, “completely”, this statement is demonstrably true. None of the many suggested mechanisms have stood the test of reality. No plausible mechanism for the destruction of the immune system by HIV has been discovered in a quarter century, following more than $100 billion spent on research.


(1) Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press (1970, 2nd ed., enlarged; 1st ed. 1962)
(2) Leon Festinger, Henry Riecken, & Stanley Schachter, When Prophecy Fails: A Social and Psychological Study of A Modern Group that Predicted the Destruction of the World, University of Minnesota Press (1956)
(3) Imre Lakatos, “History of science and its rational reconstruction”, pp. 1-40 in Method and Appraisal in the Physical Sciences, ed. Colin Howson, Cambridge University Press (1976)
(4) Henry H. Bauer, Fatal Attractions: The Troubles with Science, Paraview Press (2001)
(5) Henry H. Bauer, Scientific Literacy and the Myth of the Scientific Method, University of Illinois Press (1992)
(6) Millett GA et al., “Circumcision status and HIV infection among Black and Latino men who have sex with men in 3 US cities”, JAIDS 46 (2007) 643-50


  1. Martin said

    Excellent post. I have one comment, your statement: “but those hewing to the dogma are incapable of that recognition, as Festinger, Kuhn, and others have pointed out”, would make more sense if the word “incapable” would be replaced with unwilling. Many times (especially psychiatrists) do not distinguish between unable and unwilling. That’s a crucial distinction. I sincerely believe that those HIV/AIDS researchers are very capable (in fact have enhanced capability) to recognize error in scientific procedures. There are very existential reasons why they are unwilling (not unable) as you know — money (livelihood) and professional status/power. Saying they are incapable gives them an excuse. Helen Keller was incapable of sight and deaf — she became a very learned person in spite of her disabilities. The HIV/AIDS researchers have no such disabilities.

  2. hhbauer said


    These waters may be too deep for me, “unable” or “unwilling”. I tend to think that career, etc., interests can produce blind spots via subconscious emotional-psychological mechanisms; so that people may be potentially “capable” of seeing that they are wrong but in practice unable to see it. I speculate that if the training of scientists included learning about the REAL history of science they might be more aware of their own fallibility.

    Of course I don’t want to allow Gallo, for instance, room for excuse; but he has committed plenty of scientific sins that are inexcusable because much more blatant than not being able to comprehend the significance of certain data.

  3. Chris Noble said

    DNA sequences of viruses in distinct clades can differ by 15%-20%”
    and yet all of them are supposed to do about the same thing, with only minor differences in efficiency of transmission and “pathogenic potential”.
    But in other contexts we’re told that human and chimp genomes differ by less than 1%, which suffices to produce quite major differences in the products of those genes.

    Ever thought to check how much different strains of poliovirus differ from each other?

    Sabin 1,2 and 3 isolates have all been sequenced.

    [ ad hominem deleted]
    [relevance of] … Kuhn, Lakatos, Popper and Feyerabend [to knowledge about] … HIV and RNA viruses in general

  4. Martin said

    Psychiatrists lock people up for not wanting to talk to them. They diagnose them claiming they are unable to talk as opposed to unwilling. I call that punishment not treatment.
    Gallo (and Fauci, Altman, Maddox etc.) are much more cabable than most to understand what they have wrought. They are equivalent to the so-called corporate CEO “psychopath” — you know, the ones who have no compunction about shifting their companies to foreign soil to increase profit, killing entire towns and cities economically in the process.

  5. hhbauer said

    Chris Noble:

    Thanks for the substantive parts of your comment. You may have neglected to read my “Re Comments” page about avoiding ad hominem remarks, they distract from the issues.

    Thanks for reminding us that the Sabin attenuated vaccines against 3 polio virus clades involved only a few substitutions, quite a contrast to the proliferation of HIV clades and CRFs that all supposedly remain pathogenic.

    Science studies is relevant to science policy because it is able to take an unbiased view of what makes for scientific progress and what doesn’t. I do think that Kuhn and Lakatos contributed important insights. Popper was wrong about “falsifiability” as a criterion of what’s scientific, but his more basic point was well worth making, that theories can be disproved but not proved (though this is really a re-statement of the underdetermination insight). Feyerabend’s contribution was more as provocateur, and I haven’t had occasion to cite him, you may have overlooked that it was Darin Brown who quoted from him.

    So Kuhn et al. are relevant to knowledge about HIV, etc., insofar as they remind us to be wary of mainstream consensus that ignores anomalies (Kuhn) or fails to stimulate progress (Lakatos). That we still don’t know how HIV kills immune-system cells raises a Lakatosian doubt about the validity of the consensual theory. So does the fact that two decades of working toward a vaccine have been totally unsuccessful even though the HIV genome is comparable in size to the polio genome.

  6. Chris Noble said


    you seem to be confusing direct language with ad hominem.

    Your comparison of variability of the HIV genome with the difference between the human and chimp genomes is absurd. (I trust I am allowed to use the word “absurd” as it seems to be one of your favourites)

    The Sabin poliovirus strains all differ from each other by 20% and yet they are all pathogenic.

    The alleged “anomaly” that you highlight is not an anomaly at all.

  7. MacDonald said

    Dr. Noble,

    Welcome aboard. It’s good to have you with us. I hope you don’t mind a couple of questions.

    (1) In your response to Prof. Bauer’s Post, you seem to accept the cited 15-20% divergence in DNA sequences between different clades of HIV. This number seems to be quite arbitrary. Mark Wainberg, for example, has,

    “HIV-1 clades are phylogenetically classified on the basis of the 20–50% differences in envelope (env) nucleotide sequences. The Env proteins of groups M and O may differ by as much as 30–50%. The N subtype, in turn, appears to be phylogenetically equidistant from M and O. Within M subgroups, inter-clade env variations differ by 20–30% whereas intra-clade variation of 10–15% is observed.”

    Why do you think it’s so difficult for HIV scientists to agree on the exact extent of the genetic variability of the HIV genome?

    (2) Dr. Noble, you have previously stated that, “two subtypes of hemagglutinin from influenza A, isolated from humans at approximately the same time, differ from each other by 81% at the amino acid level”, and yet retain identical biological (pathogenic) functions. Is this still your
    opinion? If so, could you provide a reference explaining this?

    (3) You state above that, “Sabin 1,2 and 3 [Polio virus] isolates have all been sequenced”, as if this were an argument in itself. Could you please refer me to the scientific precedent for accepting the existence and biological properties of one member of a class of beings by referring to other members within the same class? Or put differently, would you accept the argument that all variants of Bigfoot allegedly observed in North America have identical biological properties because three different strands of Yeti hair from the Himalayas have been sequenced?

  8. hhbauer said


    “Ad hominem” doesn’t mean “direct”, it means “addressed at a person”, and stands in contrast to “ad rem”, addressing the substantive issue. I deleted comments you made about me instead of about statement(s) I had made.

    There’s more than one good reason for avoiding ad hominem comments (apart from the obvious one of courtesy or good manners). The proper purpose of discussing matters of science, medicine, public policy, and so on, is to advance understanding, for oneself as well as for others. Most people find it easier to recognize their errors if they are pointed out in a non-aggressive manner, and so ad hominem commentary is not only rude but also counterproductive. My aim with this blog is to build on the insights I gained when looking at the epidemiology of “HIV”, and you will have noticed, I hope, that it has concentrated on adducing and critiquing evidence. (Incidentally, I hesitated for quite a long time before starting the blog, because so much blogging is little more than venting emotions, and I didn’t want to waste time trying to moderate that sort of stuff.)

    I should have either not made the comparison you criticize or done so at greater length. Here’s the greater length. When, many years ago, I first came across the comparison of chimp and human genomes, coupled with expressions of amazement that so small a difference in “genes” could produce such different results, I thought that the expressed amazement totally missed the point, which was that the “one gene, one protein” view was obviously wrong. Ever since, I’ve just taken for granted that “percentage differences” between genomes provide no useful information. So the statement by Cohen et al. fits into my general critique of their review as illustrating how little is actually understood about “HIV”—not least, of course, how it’s supposed to arrange for the immune system to be destroyed. But I realize that I was far from making my meaning clear. You are surely not the only reader led astray by my ineptness here, and I appreciate the chance to rectify that.

    My remark about the Sabin clades of polio was also too abbreviated, apparently. The clades are all pathogenic, yes, but the attenuated versions of each one, developed for the Sabin vaccine, in each instance involves only a small number of substitutions in the genome. Once again, there is no correlation between the “percentage” composition of a genome and its biological activity.

    Thanks for the opportunity to clarify this small point. I’m also gratified that, apparently, you found nothing else to take exception to in my critique of the current state of (lack of) knowledge about HIV/AIDS as expounded by Cohen et al.

  9. hhbauer said


    Re variability of the HIV genome, my favorite quote has been

    “no two virus isolates are identical…. Within a single … host, HIV-1 population represents a complex mixture, or swarm, of mutant virus variants … [whose] prevalence … is changing … on almost a daily basis (intrahost evolution). Moreover, infected individuals within a human population harbor distinct viruses (interhost or populationwide heterogeneity). Finally, the global HIV-1 pandemic is composed of many local epidemics, which generally differ in … virus genotypes in circulation (global variation) [Lukashov, Goudsmit, and Paxton 2002]” cited at p. 168 in my book.

  10. Steve said

    So I’m kind of curious about how researchers such as Lukashov (yes, I’m too lazy to find the actual article, or even to buy your book, Henry 🙂 manage to determine that no two virus isolates are identical. My limited understanding of DNA sequencing, a process which seems to be a prerequisite for a statement like that one, is that you can only do it if you start with billions of *identical* copies of the DNA in question, along with a template primer. (How many copies you need to start with depends on how long the target DNA is, and there are limits to how long it can be for the sequencing operation to work…) So how do HIV researchers get billions of identical copies of one particular HIV instance out of a human host? I thought that the step of getting just one HIV particle intact out of a human host, which itself seems to be a prerequisite for making billions of identical copies, had never been done.

    And then to determine that each individual HIV particle in a given human host is different, you need to isolate not just one of them, but *every* one of them, or at least some large fraction. I have never heard of a technique that is capable of doing this, even for viruses that can be successfully isolated using standard techniques such as sucrose gradients and centrifugation, of which HIV is not one. I would envision someone with an electron microscope and a nanopipette picking HIV particles off the microscope plate one by one, and putting them in separate jars… how else would one accomplish such a thing?

    I get the feeling that someone is making something up here. The pieces don’t seem to add up.

    My suspicion is that what is happening is that the sequencing data that researchers are getting are not consistent with the view that a large population of identical virus copies is present, as one would expect in traditional virology, and so they are forced to come up with another hypothesis, in this case that there is nevertheless a large population of viruses, but they are all different. This would contrast with the view that what is being sequenced is not viral fragments at all, but cellular debris, endogenous DNA expressed under conditions of varying stress, etc.

    (Naturally I could be mixing up DNA and RNA here, which may affect the validity of assumptions about sequencing processes and prerequisites.)

  11. hhbauer said


    I have the same questions as you, and know less about PCR than you do. I would have ventured the same guess, that whatever they do to identify the strain of HIV produces a mix of products that are then interpreted as coming from different strains. But, sorry, I can’t help.

  12. Dave said

    Hi Henry,

    Stupendous blog, and stupendous book you have written. You have done a brilliant job of analyzing the HIV testing from the macro perspective and how it is completely screwy. They are certainly testing for *something”, but it remains unclear what they are testing for.

    As for the occasional critic who shows the courage to appear on this august blog, they should first answer the following 2 questions:

    1. If there was sufficient evidence undermining the claim that AIDS was caused solely by a retrovirus, would you change your mind?

    2. What evidence, in your view, would tend to falsify the claim that AIDS was solely caused by a retrovirus?

    The reason these 2 preliminary questions are necessary is because the phrase “HIV causes AIDS” has permeated the collective psyche of millions of people. They uncritically accept this idea, although, in general, they have no idea why they believe this, nor have read any critiques of the claim (nor want to). They mostly think AIDS is a “bad thing” involving sex and disease, and are glad they don’t have it.

    Again, you are a scholar and a gentleman, Henry.

  13. hhbauer said


    Thank you! What can I do except blush? Since this is a moderated blog, I pretended to be a politician and said to myself, “Well, I do approve this message” 🙂

  14. Dave said


    No more flattery of your great blog:) Back to work!

    Chris Noble,

    The only reasonable, civilized scientific debate that I’ve seen on this topic was published in the esteemed journal, Science about 20 years ago. There, Drs. Blattner, Gallo and Temin squared off against Dr. Duesberg.

    During the debate, the proponents of the conventional theory admitted the following:

    “It is true that HIV does not cause AIDS in chimpanzees” (Science, 241:518 (1988).)

    Curiously, they cite no reference for this statement. I assume AIDS reseachers infected chimps with copious amounts of HIV, based on the a priori hypothesis, that the virus, if pathogenic in humans, would no doubt be pathogenic in their closest primate relatives. Do you know where these (negative) results are published? I haven’t been able to find them.

    On the substance, though, it seems to me there are 1 or 3 options:

    1. The HIV did not infect T4 cells of the Chimpanzees

    2. The HIV did infect the T4 cells of the Chimpanzees, but did not kill these cells.

    3. The HIV did infect the T4 cells of the Chimpanzees, did kill these cells (either directly or indirectly), but did not lead to any opportunistic infections.

    Which of the 3 options do you think it was, and why?

    I think this is an important question. It would seem paradoxical that a conventional retrovirus could kill 40 million humans, but not one chimpanzee.

    Also, I’m not interested in SIV or other viruses that allegedly don’t cause disease in chimps. Focus solely on HIV, please.

  15. Frank said


    There was another reasonably civilized debate, hosted by the British Medical Journal between 2003 and 2005. Chris Noble was a frequent participant. An archive of the debate can be found at:

  16. Dave said

    Hi Frank,

    Thanks for the wonderful suggestion. Your first link worked fine and greatly piqued my interest, but I couldn’t get the subseqent links to open up. Let me know if they work for you.

  17. Martin said

    Dave, There is a fourth option: The chimps were not infected with HIV because there wasn’t any HIV in the serum used to infect the chimps. If HIV has never been isolated, how did the researchers know if there was really HIV in the serum used to infect the chimps? It’s all hypothesis, nothing more.

  18. Frank said


    The links have all been in place and working for years now. Not sure what trouble you’re having but they should all work. Here’s the first one, by Dave Rasnick:

    Here’s one of the sorted lists:

  19. Dave said

    Yes, I changed computers and it worked beautifully. What a wonderful robust debate in the BMJ! I wish there had been a moderator to probe a bit and perhaps reign it in some. A lot of entrenched views.


    Excellent observation. Perhaps, the chimpanzee researchers simply injected the blood of AIDS patients into the chimps, but there was no detectible HIV in it.

  20. Alain1 said

    The problem is how those researchers are selected. The problem is that they are precisely selected often because they have a great will power (you need it to succeed in those hard studies). They are kind of bulldozers. Qualities that don’t make very much those people to be able to change of idea very often. In the research field, we need artists, not draft horses.

    If you asked these people what they would do when facing a problem, they would often say that they would focus on it intensively for weeks, or even months (depending of the problem of course) until the problem would be resolved. But, to the contrary, we need people who are able to give up. Of course coming back after some times to the problem, but people able to give up. Not over focusing bulldozers. Those kind of people are good engineers or technicians, but very bad researchers.

  21. Martin said

    Hi Alain1:
    Those “researchers” (if you want to call them that) are nothing but acolytes with scientific degrees. If they dared suggest, say, that the serum used to infect the chimps had no HIV in it, or to actually verify that the serum had HIV through the classical methods — not the invalid methods — Ah! another problem — to suggest the tests themselves don’t work either., then they would be looking for work in another field because they, like Duesberg and Rasnick, would be black-balled.

  22. Lucas said

    I had been trying to read the Book of Job, and was shown a friendly banner, “Share the gift of life with a mother in Africa, $25 saves an African baby from being born with HIV”, clicking which brings one to Gospel Communications, the producer of the movie “The Gift” and further their “communique”: “if only pregnant women received were [sic] educated about the behavioral and medical options available to them.”

    Cognitive dissonance might be distinct from the incommensurability, like “I can’t see” is distinct from “my eyes ache”.

  23. Cee said

    How are the antibody and/or the PCR tests supposed to work if the virus is constantly changing potentially producing billions a day of DNA/RNA?

    Do the PCR tests assume there is a sequence that never changes?

    For antibodies, if there is that much change in the virus that frequently, wouldn’t the antibodies produced be unique and therefore not be comparable to any standardized test?

  24. hhbauer said


    I’d love to see a mainstream response to your excellent questions

  25. hhbauer said

    From MacDonald, via e-mail:

    To illustrate Cee’s point a little more vividly, let’s begin with the words of an expert on viruses and their genomes, Dr. Brian Foley Of Los Alamos Gene Bank:

    “The HIV-1 M group of viruses and the HIV-1 O group of viruses are not ‘one and the same thing’. Calling them ‘one and the same thing’ just because they have been named ‘HIV-1’ and because they infect CD4+ T-cells of primates and cause AIDS in humans, is analogous to calling mice, elephants and cats ‘one and the same thing’ because they have been named ‘mammals’ and because they produce live young , feed them milk and breathe air.” [End excerpt]

    The answer to the question of how the antibody test can pick up on all HIV infections is that the antigens used have been modified and updated to detect all subtypes of HIV. Or as Dr. Foley would have put it, nowadays they don’t merely test for elephants, they also test for mice. The controvery is summed up nicely in the BMJ exchange between the Perth Grop and the illustrious Dr. Noble:

    [Perth Group writes:] “Christopher Noble wrote: ‘You have previously asked me a question “how it is possible with such variability to have proteins which have the same function, to induce the same antibodies which can be detected with a single antibody test, and to define ‘HIV’ infection in molecular terms?” Contrary to your assertion I have answered this question. There is not a single antibody test but a multitude of them. The initial antibody tests were based on viral lysates isolated from a small number of AIDS patients. Since then antibody tests have incorporated recombinant proteins, synthetic peptides or a combination of the three. Originally the antibody tests that are approved by the FDA were based only on HIV-1 group M. Since then antigens specific to HIV-2, HIV-1 group O and other non group M virus types have been added precisely because these tests were failing to detect non HIV-1 group M viruses(6)”

    [Perth Group answer:] Christopher Noble has never answered our questions regarding protein functions and the identification of “HIV” infection in molecular terms or design of vaccines. His reference 6 is the web address for these rapid responses but there Christopher Noble did not give any references apart from a reference to the Vironostika test kit. The Vironostika test is an ELISA test which is considered to be not sufficient to prove “HIV” infection in developed countries.

    Christopher Noble wrote: “The Vironostika HIV Uni-Form II is one of the antibody tests that includes HIV-1 group O specific antigens.(7) It is not an exception as you claim it is one of many tests that incorporate HIV-1 group O specific antigens.”

    [Perth Group answer:] Where are the other tests? As far as Vironostika is concerned, here is the answer to our questions from Biomerieux: “The Vironostika HIV-1 assay reacts well with subtypes A-J of Group M strain. Also the assay can detect some of Group O strain. As for the MN or N strain, we do not have any information on this strain and we have no documentation that this assay can detect the N strain…The answer to your question regarding whether the antigens used in the Vironostika HIV-1 and Oral Fluid Vironostika assays are viral lysates or recombinant is that both assays contain antigens that are viral lysates.”

    [Perth Group cont.:] Note that: (i) the Vironostika “includes HIV-1 group O specific antigens” yet cannot detect even all the “Group O” “HIV-1” strains; (ii) since the antigens are “viral lysates” and since “HIV” has never been purified, the antigens could have originated from anywhere.” [End excerpt]

    Dr. Noble’s reply to the Perth Group: “Regarding the antibody tests that include HIV-1 group O specific antigens Eleni Papadopulos-Eleopulos asks: “Where are the other tests?” Enzygnost® HIV Integral: recombinant proteins (HIV-1 gp41, HIV-2 gp36, HIV-1 group O gp41) and synthetic peptides (HIV-1 gp41). (1) AxSYM HIV Ag-Ab assay: recombinant antigens (HIV-1 group M gp41, HIV-1 group O gp41, and HIV-2 gp36) (2) Murex antigen/antibody assay: recombinant antigens and peptides from HIV-1 group M gp41 and polymerase (pol), HIV-1 group O gp41, and HIV-2 gp36 (2) Genscreen HIV Plus assay: HIV-1 and HIV-2 antigens (recombinant gp160, artificial functional consensus group O gp41 polypeptide, and synthetic gp36 polypeptide) (2) VIDAS HIV Duo Ultra assay: antigens (gp160 of HIV-1, immunodominant region peptides of HIV-2 and HIV-1 group O) (2) BioRad HIV-1/HIV-2 PLUS O EIA: synthetic polypeptide mimicking an artificial HIV-1 Group O-specific epitope (3) I repeat. The Vironostika HIV Uni-Form II is not an exception as you claim. It is one of many tests that incorporate HIV-1 group O specific antigens. Why did you claim it was an exception when you have obviously not researched this area? Your previous question “how it is possible with such variability to have proteins which have the same function, to induce the same antibodies which can be detected with a single antibody test, …?” is based on a set of false premises. The divergent strains of HIV, such as HIV-1 group O that you have specifically referred to, do NOT induce the SAME antibodies, they CANNOT be detected reliably with antibody tests based on group M strains. The antibody tests that I have listed above now include HIV-1 group O specific antigens precisely because the previous tests lacked sensitivity for these strains.”[End excerpt]

    There is of course much more, but I think this is a fine introduction which shows that HIV researchers are aware and agree with rethinkers that there is a problem, although they tend to trivialize it. The PCR test is even more problematic. First a clear admission that NO HIV GOLD STANDARD EXISTS:

    “Considerable controversy remains about the diagnostic accuracy of PCR. Some studies report that the test has perfect sensitivity and specificity, but others report high false-positive and false-negative rates. An understanding of the diagnostic performance of PCR for HIV infection is essential in determining the appropriate role of PCR in the clinical diagnosis of such infection. However, evaluation of the performance of PCR poses difficult methodologic challenges. To evaluate the sensitivity and specificity of PCR, investigators must ascertain whether study participants are infected with HIV. Typically, a new test is compared with a superior reference (or gold standard) test, but PCR is an example of a class of diagnostic technologies (including, for example, genetic screening tests) that have the potential to outperform and displace existing tests. At least in certain clinical circumstances, PCR may be more sensitive or more specific than the current reference tests (enzyme immunoassay followed by confirmatory Western blot analysis). The lack of an appropriate reference test substantially complicates evaluation.” reference

    The PCR answer to the genomic variability of HIV seems to be to increase the number of primers. This approach was illustrated by a study by Damond et al. brought up in another BMJ exchange between Dr. Noble and the Perth Group:
    “[Damond et al] evaluated a new human immunodeficiency virus type 2 (HIV-2) DNA amplification strategy based on peripheral blood mononuclear cell long PCR (XL PCR) followed by nested PCR amplification. The primers used were located in the highly conserved long terminal repeat in the pol regions of the genome. Five primer pairs corresponding to different regions of the HIV-2 env gene were used in the nested step”. Samples from 42 HIV-2 positive patients were tested and amplification with one primer was considered a positive PCR.” [End excerpt]

    However, even though 5 primer pairs from “highly conserved regions” were used as part of a “strategy to bypass HIV-2 genetic diversity”, 2 out of the 42 samples were still not amplified (detected) at all! The results were as follows:

    “Two samples were not amplified by any of the five primer pairs. Two samples were amplified by only two primer pairs; Four samples were positive with three primer pairs; five samples were positive with four primer pairs and twenty nine with five primer pairs.”

    The Perth Group concludes: “In particular we have claimed that, given the genetic diversity of “HIV-1”, it would not be possible to define “HIV” infection in molecular terms, that is by hybridisation and PCR. The Damond et al findings support our claim. Although they used a small number of patients (42) and 5 primers they could not detect the “HIV-2” env gene in all the 42 “HIV-2” positive individuals. To detect the env gene in all “HIV-2” positive individuals many more primers would be necessary. If similar numbers of primers are necessary for the detection of all the other genes the detection of the whole “HIV-2” genome would require the use of a very large number of primers. Given that the “HIV-1” genome is more diverse than that of “HIV-2” and that many more people are infected with “HIV-1” the number of primers needed to detect the whole “HIV-1” genome in all “infected” individuals, that is, to define “HIV-1″ infection in molecular terms in these individuals, would be prohibitory.” [End excerpt]

    As far as I know, neither Dr. Noble nor Dr. Foley has explained how five primer pairs located in highly conserved regions were not able to detect HIV in 42 out of the millions of supposedly HIV-infected people worldwide; or how this problem can be overcome.

  26. MacDonald said

    Dear friends,

    The question we need to ask of Dr. Noble and HIV scientists is not whether HIV infects the CD4 cells of chimps (it does by all the markers of retrovirology), or why it is not pathogenic in them, since retroviruses are not obliged to behave consistently in this way – especially considering that retroviruses similar to HIV (SIV) are supposed to have infected and co-evolved with chimps long before they did humans.

    What we need to ask in the year 2008 is, why is there no functioning animal model of HIV infection and AIDS at all?

    HIV scientists will tell us that there are indeed animal models for infection with HIV (SIV, SHIV). However, not only is HIV not pathogenic in chimpanzees, SIV, in spite of its name, is not pathogenic in any of its host species, Pan Troglodytes, African Green Monkeys and Sooty Mangabeys. Researchers have therefore been forced to rely on artificially infected macaques as their animal model of HIV infection and AIDS. Countless papers describing successful cross-species infection of macaques with SIV and SHIV, and resulting ‘AIDS-like’ diseases, have been published to date. Let’s leave aside the ‘AIDS-like’ diseases and focus on the practicalities of ‘HIV’ infection.

    The scientists who have successfully managed to infect macaques with SIV have, to my knowledge, never published a study showing an artificially infected macaque in turn infecting and causing AIDS in another macaque the ‘natural way’, by sexual intercourse. An example of what the scientists call a ‘model of sexual transmission in Rhesus Macaques’ can be found here:

    “One ml of contraceptive foam (12.5% N-9 [v]]/v]) was placed into the vaginal vault of six female rhesus macaques prior to the intravaginal infusion of one ml of cell-free SIVmac (10(4) intravenous animal infectious doses [IVAID]). This procedure was repeated twice a week for 2 weeks. (We have previously shown that this stock and dose of SIV produces infection in 100% [6/6] of females inoculated.). We found that the infusion of the contraceptive foam prevented the genital transmission of the virus in 3 of the 6 animals. In a second experiment, one ml of contraceptive gel (4% N-9 by weight) was placed in the vaginal vault of six additional female rhesus macaques prior to the intravaginal infusion of 1 ml of cell-free SIVmac (10(4) IVAID). This procedure was repeated twice a week for 2 weeks.”

    To date, the results of human trials with microbicides have ranged from disastrous to ‘seemingly harmless’; statistically speaking not a single HIV-infection has been prevented.

    But it was also in experiments of this kind that Merck’s researchers successfully vaccinated macaques. The indications of these animal studies were so encouraging that they proceeded to human trials (Phambili, STEP) with the greatest optimism. The result was once again a complete disaster; the vaccine seemed to heighten the risk of HIV-infection rather than lowering it. Thus, successful prevention of infection in animal models of HIV infection and AIDS has yet to translate into success in a single human trial. These failures have now resulted in calls for more human experimentation in recognition of the fact that the animal models are useless. Richard Jefferys and Treatment Action Group (TAG) put it this way in their commentary:

    “One of the implications of Merck’s results is that vaccine challenge studies conducted in macaques are not predictive of what happens in people, making the information from vaccine and other prevention studies even more important to the future research effort.”

    Another way of putting it is that, after 25 years of hype, there is still no useful animal model of HIV infection and AIDS, and that HIV scientist are despairing of ever finding one

  27. Nick Naylor said

    Chris Noble shows up and makes his standard point re poliovirus and then leaves us breathlessly hanging.

    Can you tell us anything about the non-synomous to synomous codon substitution ratio in RNA picorna-viruses? Does this number (low) tell us anything about “negative selection” of viral “master sequences” or “quasispecies” by cell-cultures?

    There’s no need to belabor the Perth Group’s response to good old one-note Chris. But how typically does his substantive point leave the area of constructive as he attacks those who refuse to give acceptance to any of the endless fascinating “ad hoc extensions” of the HIV hypothesis. Another question ol’ buddy, how many “HIV proteins – purified” do we have now and how do they stack up with the genes that have been associated with the processing of cellular reverse transcriptases? Is this too much of Leibniz (parsimony) for you taste?

    If three “clades” of poliovirus are successful in culture, what does this tell us about Eigen’g quasispecies PLUS hypercycle model IN VIVO? And what can this tell us about retroviruses endogenous or exogenous, constrained as they are by the cell’s proviral stage and exosome to budding pathway? Can “viral load” possibly be real evidence for a putative hypercycle phase (replicase feedback to new template processing) in vivo?

  28. hhbauer said

    Nick Naylor:

    Thanks for the substantive comment. However, I’ve just refused to accept another comment from Noble that contains nothing new but does contain more ad hominem remarks despite my private e-mail to him reminding him to avoid it. So, after this one, I will also not post further responses to his comment.

  29. Interesting paper that MacD references there. I went and looked at it.

    “Polymerase Chain Reaction for the Diagnosis of HIV Infection in Adults: A Meta-Analysis with Recommendations for Clinical Practice and Study Design”, Owens DK et al., Annals of Internal Medicine, 1 May 1996

    The authors are hopelessly confused, as are most medical professionals, about the meaning of the term “gold standard”, “sensitivity”, and “specificity”.

    It is true as MacD states, they admit there is no GS for HIV infection. However, the problem is considerably worse than this. They fail to realize that without a GS, it is impossible to determine “sensitivity” or “specificity” of anything, and that a GS is a matter of definition, and cannot be determined by empirical findings. A GS is not “the best available diagnostic tool [for the condition]”, it is defined to indicate the condition.

    A number of contradictory statements appear:

    “We accepted positive results on conventional antibody tests (if they included a confirmatory Western blot analysis or similar test) or viral cultures as high quality evidence of infection. The absence of infection is more difficult to establish. Only studies that used serial testing or follow-up to establish the absence of HIV infection received the highest ratings for study design.” (This is further confirmed in Table 1, where they also disclose that they used different GS criteria for “diseased and nondiseased participants” (???). No definition of “diseased” or “nondiseased” is given. This strikes me as patently absurd: the GS should not vary based on whether one is presumed to be “diseased” or “nondiseased”.)

    Here they are claiming that conventional WB tests or viral cultures are a GS. Remarkably, they claim that “absence of infection is more difficult to establish”, a very strange statement to make. With any GS defining “infection”, “absence of infection” is simply defined as not getting a positive result. (This is disregarding the case of so-called “indeterminate” results.)

    But then they also write (these quotes are not in “chronological order” from the paper):

    “To put the diagnostic performance of PCR in context, the conventional antibody test sequence of an enzyme immunoassay followed by confirmatory Western blot analysis has a sensitivity that exceeds 99% and a specificity greater than 99.5% (corresponding to a false-positive rate less than equals 0.5%) in high-quality screening programs.”

    So, at one point, they claim WB is a “GS”, and at another point, they claim WB has “a sensitivity that exceeds 99% and a specificity greater than 99.5%… in high quality screening programs.” These two statements are mutually contradictory. By definition, every GS has perfect 100% sensitivity and 100% specificity. This is a matter of logic.

    “Because PCR directly amplifies proviral HIV DNA and does not depend on HIV antibody formation, it is a potentially attractive alternative to conventional antibody tests… Typically, a new test is compared with a superior reference (or gold standard) test, but PCR is an example of a class of diagnostic technologies (including, for example, genetic screening tests) that have the potential to outperform and displace existing tests. At least in certain clinical circumstances, PCR may be more sensitive or more specific than the current reference tests (enzyme immunoassay followed by confirmatory Western blot analysis). The lack of an appropriate reference test substantially complicates evaluation. A successful approach to the evaluation of such technologies would be broadly useful.” [my emphasis]


    “We sought to critically and systematically examine the many published studies that have reported on the use of PCR for the diagnosis of HIV infection in adults. If it is sufficiently accurate and inexpensive, PCR could supplant standard antibody tests for diagnosis and screening.” [my emphasis]

    This is very convoluted and confused thinking. First, they say WB test is a GS (“reference test”) for determining sensitivity and specificity of PCR testing. (See Table 1.) Then, they claim “in certain clinical circumstances, PCR may be more sensitive or more specific than… [confirmatory WB]…” And that “if… sufficiently accurate and inexpensive, PCR could supplant standard antibody tests for diagnosis…”

    So, to sum up, they are using one criterion as a GS to test the accuracy of a second criterion. Then they are saying that based on these results, the latter criterion might actually be more accurate and could supplant the former. Completely circular logic.

    Do they realize, the existence of a GS distinct from both WB and PCR is implicit in this chain of reasoning?? Actually they do, as they continue “The lack of an appropriate reference test [i.e. GS] substantially complicates evaluation.” Yet they blithely go on with the following contorted reasoning:

    “Whenever possible, studies of the performance of a diagnostic test should use reference tests [GS] that unequivocally establish the true state of disease or health. Because PCR can detect HIV infection before antibodies have developed, a positive PCR test result in a person with negative results on an HIV enzyme immunoassay could represent either a false-positive PCR result or a false-negative enzyme immunoassay result….”

    Depending on whether you choose WB or PCR as your “GS”!

    “…Evaluation of PCR is challenging because no single diagnostic test can resolve this dilemma with certainty…”

    This is an unequivocal admission that there does not exist a GS for HIV infection.

    How do they rescue themselves? You guessed it: “clinical diagnosis”.

    “…For current studies of HIV infection, the discrepancy can be resolved by serially testing seronegative persons with enzyme immunoassay and Western blot analysis and doing clinical follow-up for a period long enough to exclude acute infection. If a person is truly infected with HIV, then eventually peripheral blood mononuclear cell culture or plasma culture should become positive, the enzyme immunoassay and Western blot analysis should become reactive, or clinical illness should ensue…. Studies of other diagnostic tests for HIV have successfully used serial testing and clinical follow-up to determine true infection status [118]. In high-risk populations, however, the value of long-term serial testing may be attenuated by incident infections. In many of the studies that we reviewed, longer follow-up would have enabled the investigators to convincingly establish the disease status of antibody test-negative participants.” [my emphasis] Currently, interpretation of PCR test results for the diagnosis of HIV infection should be combined with careful consideration of the clinical circumstances and with the use of confirmatory tests and clinical follow-up whenever possible.

    This paper leaves me speechless.

  30. On further inspection, I don’t think the last statement directly contradicts that clinical status claims above it. They are saying that researchers determining PCR status should be blind to clinical status, which is not really the same thing.

    However, I did find this, even more confirmation that “clinical status” is being used as a GS:

    “Currently, interpretation of PCR test results for the diagnosis of HIV infection should be combined with careful consideration of the clinical circumstances and with the use of confirmatory tests and clinical follow-up whenever possible.”

    I’m still left speechless, though.

  31. Dave said

    Simple question:

    Do Doctors use PCR to evaluate whether you have a bad case of the flu? Or Herpes? Or chicken pox?

    PCR use in the clinical setting of AIDS smacks of Ad Hockery — the failure to measure sufficient viral titer, forces them to resort to PCR to detect DNA/RNA fragments (of something) to let us know whether we are sick or not.

    Quite a Rube Goldberg system of medicine set up by the AIDS establishment.

  32. Dave said

    However, I’ve just refused to accept another comment from Noble that contains nothing new but does contain more ad hominem remarks despite my private e-mail to him reminding him to avoid it.

    Why is it so hard for Chris Noble and other proponents of AIDS orthodoxy to avoid ad hominem attacks and simply address the merits of ideas?

    In Physics, some people think String theory is a sound idea, some don’t. Why the big fuss?

    Even more on point: Eminent Astro-Physicist, Dr. Robert Jastrow, recalled that a vast majority of great physicists simply could not accept the Big Bang Theory when propounded by Hubble, despite the forceful data: (“Irritating,” said Einstein; “Repugnant,” said the great British astronomer Eddington; “I would like to reject it,” said MIT physicist Philip Morrison)

    So, a few talented, scholarly folks like Dr. Henry Bauer, have written a book, supported by data in the peer-reviewed literature, which suggests that the HIV test is measuring something other than infectious virus and misleads a lot of people into thinking they have a deadly disease, when they do not. If ever there were a need for a sober discusion of the issues with life-affirming consequences, this should be it.

    Heck, even Dr. Anthony Fauci is quoted after the recent vaccine failure: “There is not an immediate solution to the problem….. [e]verything is on the table.”

    Why can’t Chris Noble simply address this on the merits? It defies logic and reason. Perhaps, Brian Foley could grace us with some intelligible responses to these critiques.

  33. heja said

    I guess one simple question that needs to be addressed regarding the value of the PCRs is whether, at their development stages, the parameters of these tests have been set to maximize specificity and sensitivity as measured by the ability to replicate the results (infection / no infection) of antibody tests. From what Darin Brown contributed I strongly suspect this to be the case!

  34. Frank said


    Your mention of the physics Orthodoxy brings to mind my favorite signatory to the Mbeki petition, the great American astronomer Halton Arp. When his research turned up data which seemed to call into question some of astronomy’s bedrock assumptions, the Orthodoxy didn’t argue with the data, they attempted to destroy his career. Your question as to why can’t they just address the merits of the data is perhaps partially answered in Reinhold Niebuhr’s quote:

    “Frantic orthodoxy is never rooted in faith but in doubt. It is when we are unsure that we are doubly sure.”

    I think the operative word here is “frantic”. The High Priests dispatch their terriers to rend us heretics and, well, by that time dispassionate argumentation is long forgotten.

  35. MacDonald said


    It is the case that the PCR tests were developed with WB, p24 or some other antigen/antibody test as gold standard.

    In terms of viral load, the PCR tests are measured against each other as well. Take a look at this from the Parenzee case: Prof. Gordon is telling Parenzee’s lawyer that a PCR viral-load test-result is not reproducible by another PCR viral-oad test: (pp. 1074, line 26 – 1075, line 34 (pp. 66-67))

    If a PCR test kit doesn’t pick up on a certain strain of HIV which has been detected on the WB, it will be modified so that it can pick it up in the future. This simple fact is arguably what’s behind the magical near-100% correlation between the antibody and the PCR or nucleic-acid tests.

    If you debate the technically well-grounded HIV-apologists, and you come up with a paper like the one Darin just analyzed from the 1990s, they will invariably say, “That was back then; the technology has improved. Look at this 99.99% correlation in the newest, much more accurate tests”.

    This may or may not be so, who can tell, since that means they have had another 10 years to ‘improve’(modify and correlate) all the tests with each other?

    For this point, see Gordon again, p. 1067 (p.59) lines 17-36.

  36. Cee said

    I didn’t know whether to put the post here under “HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE” or “RACIAL DISPARITIES IN TESTING ‘HIV-positive’: IS THERE A NON-RACIST EXPLANATION?” because there is a race card to the post.

    How can a PCR DNA come back as (0) zero for three times in twelve months, and then out of curiosity a PCR RNA was run and the viral load was was positive around 25,000?

    Can someone explain?

  37. Evelcyclops said

    Martin: I saw this and felt compelled to comment…

    “Those “researchers” (if you want to call them that) are nothing but acolytes with scientific degrees.”

    Perhaps a little more respect is due . . . [to] scientists . . . [who are not all] unscrupulous, blind and unprofessional . . .
    [[Edited by moderator]]

  38. hhbauer said


    The point Martin was making is that anyone who questions the orthodox view is soon out of a grant, or a job, etc. So researchers have to toe the line OR be willing to be (mis)treated like whistle-blowers, and in practice there are very few who choose scientific truth or integrity over career. The circumstances that have progressively led to this are described in my essay,

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