HIV/AIDS Skepticism

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


Posted by Henry Bauer on 2008/05/04

Whenever people in the United States have been tested for “HIV”, members of the officially recognized racial groups have yielded different results: blacks always test “HIV-positive” more often than others, Asians always test “HIV-positive” less often than others. Whites test “HIV-positive” significantly more often than Asians, Native Americans somewhat more often than whites, and Hispanics significantly more often than Native Americans.

The same racial bias in “HIV” tests is found in other parts of the world: within South Africa (pp. 75-6 in The Origin, Persistence and Failings of HIV/AIDS Theory); between sub-Saharan Africa and northern Africa; within the Caribbean; in Europe (HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008; HIV: A RACE-DISCRIMINATING SEXUALLY TRANSMITTED VIRUS!, 16 April 2008; DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008).

A comprehensive recent review acknowledges the racial bias in testing “HIV-positive”:
“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” (Cohen et al., Journal of Clinical Investigation 118 [2008] 1244-54).

The racial disparities in testing “HIV-positive” are as firmly accepted in mainstream discourse as any aspect of HIV/AIDS is.

WHY? Why are “HIV” tests racially biased?


For reasons that need no reiterating, deep and delicate sensitivities are aroused by any discussion of human differences associated genetically with the commonly used racial designations. One should therefore bear in mind that race is a matter of biology, not at all the same thing as perpetrating racism, which is a matter of social practices and public policy. The eminent anthropologist Ruth Benedict had wise things to say on this score (Race and Racism, first published 1942; page references from 1983 edition, Routledge & Kegan Paul):
—“a student may have at his tongue’s end a hundred racial differences and still be no racist” (p. vii)
—“Race is not ‘the modern superstition,’ as some amateur egalitarians have said. It is a fact. . . . Race . . . is not the modern superstition. But racism is.” (pp. 96, 97)

Benedict makes clear the distinction between race and culture. Race is a biological matter having to do with phenotypes, genotypes, DNA, physiology, colors of eye and hair and skin, and so on. Culture is a matter of learned behavior, and culture and behavior are not determined by race; innumerable cultures have maintained their distinguishing characteristics while the racial composition of the people expressing those cultures changed; and no race has always expressed some unique culture of its own everywhere.

“Race” is a very crude biological classification. There are only half-a-dozen or so human groups in the typical list of “races”, and there is enormous genetic variation among members of any one of these groups. Yet the classification has its uses, particularly perhaps in medicine, in view of significant statistical associations of race with predisposition to such conditions as Tay-Sachs disease or sickle-cell anemia.

But it is rather few predispositions that are significantly linked to this crude classification into half-a-dozen racial groups. That’s what makes the racial disparities in testing HIV-positive so extraordinarily difficult to explain on the basis of HIV/AIDS theory. Testing “HIV-positive” is unquestionably linked to biological race. HIV/AIDS theory ascribes testing “HIV-positive” to behavior. Thus HIV/AIDS theory appears to require that sexual and drug-abusing behavior be determined by biological race to an extent that is seen with rather few other characteristics and that has certainly not been found with any other form of behavior.


If HIV is an infection transmitted predominantly via sex, then racial disparities in its distribution have to be explained in terms of racial disparities in sexual behavior. That is contrary to the evidence, and it is contrary to what anthropology and biology and psychology and sociology know. Is there any way in which racial disparities as to HIV could be explained in non-racist terms?

One would have to postulate that there are racially linked genes that influence how a person reacts when exposed to the virus. Perhaps people with certain genetic traits are more likely to be infected upon exposure? In that case, one would not have to ascribe racial disparities in rates of actual infection to differential rates of exposure, that is, differences in sexual behavior.

Much research has aimed to identify genetic factors that make for resistance to “HIV infection” or resistance to progression to AIDS after “infection” (or seroconversion), by studying so-called “long-term non-progressors” or “elite controllers” or individuals persistently exposed to HIV without seroconverting. These searches have remained unsuccessful. It has become something of a shibboleth that genetic variants of CCR5, a “co-receptor” of HIV, provide resistance, but this does not begin to accommodate the facts as to racial disparities: the pertinent allele is found “at high frequency in European Caucasians (5%-14%, with north-south and east-west clines) but is absent among African, Native American, and East Asian populations”; but non-CCR5-protected Asians resist “HIV” even more strongly than supposedly-CCR5-protected Caucasians, and Africans are affected by “HIV” far more than are Native Americans. Moreover, the CCR5 allele in question appears to have been the subject of neutral evolution over thousands of years and certainly was not selected for under the pressure of supposedly fatal infection by “HIV” (Sabeti et al., PLoS Biology 3 [(#11, 2005] e378.)

The facts as to a putative resistance to infection also speak quite stubbornly against such a phenomenon. The probabilities of apparent transmission are the same for blacks, whites, and south-east Asians, always on the order of 1 per 1000 acts of unprotected intercourse (relatively more for male-to-female and less for female-to-male), according to (at least) three published reports from Africa, one each from Haiti and Thailand, and nine from the United States (individual sources cited at p. 44 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory).

Since the apparent probability of transmitting “HIV-positive” displays this remarkably reproducible figure of about 1 per 1000, differences in prevalence of the “HIV-positive” condition can only be ascribed—under HIV/AIDS theory—to differences in frequency of exposure or type of sexual behavior.

There is no way around it. To accept HIV/AIDS theory means to accept that there are characteristic differences in sexual behavior between Asians, Caucasians, Native Americans, Hispanics, and blacks; and, among Hispanics in the United States, characteristic differences in sexual activity between the East and West coasts, differences that happen also to run parallel to differences in racial ancestry. That requires acceptance of a radically extreme version of sociobiology, namely, that sexual behavior is determined genetically and not culturally. Such acceptance also constitutes what Ruth Benedict correctly described as racism and as contrary to fact.


  1. Dave said

    A cruel, cosmic irony: During the midst of a heated presidential campaign, we have a controversial black pastor who has claimed that the U.S. Government created the “AIDS virus” to inflict genocide on the black community, and that pastor was associated with a church attended by a worthy candidate, Barack Obama.

    To suggest that the U.S. Government created the “AIDS virus” is utter hogwash.

    Rather, we have a government scientist (Bob Gallo), who patented an unreliable, surrogate marker test (HIV antibody) that purports to designate numerous more blacks than whites as being infected with a deadly, contagious virus, thereby wrecking sex lives, causing enormous emotional and psychological harm, and if used as the basis for taking AZT and other toxic drugs, often leads to illness and death.

  2. hhbauer said


    Unfortunately, that hogwash theory is widely believed, according to many commentators on the Wright affair who are familiar with sectors of black communities.

    It is indeed ironic that what one might call unwitting genocide is actually being experienced by black people—as also by gay men, and quite likely by people suffering from tuberculosis; because people in all three of those groups test “HIV-positive” much mroe often than other people do, and are therefore more often exposed to the toxic “antiretroviral” treatments.

  3. Martin said

    Hi Dr Bauer, Reverend Wright’s ideas come from a lawyer named Boyd Graves PhD. David Crowe “debated” him (check the Alberta Reappraising AIDS website). It was to me an unsatisfactory debate because the two debaters could not agree on any ground rules or facts. I believe Dr. Graves got it wrong – as he believes that the US gov invented the AIDS virus.

    Did you see the article in the New York Times Magazine on Murder as an infectious disease and an epidemiologist (Slutkin) who thinks he has the answer. He even compared gun violence as a contagious virus to HIV as a contagious virus. I guess epidemiology as a curriculum doesn’t include any courses in statistics and survey research.

  4. hhbauer said


    That epidemiologist’s comparison reminds me of the saying that it takes someone very intelligent to be so stupid 🙂

  5. hhbauer said

    From MacDonald via e-mail:

    One reason why certain population groups — notably Blacks, gays, drug users and any combination thereof — are particularly prone to test positive is found in the circular logic behind the creation of the tests. Neville Hodgkinson:

    “It never proved possible to validate the tests by culturing, purifying and analysing particles of the purported virus from patients who test positive, then demonstrating that these are not present in patients who test negative. This was despite heroic efforts to make the virus reveal itself in patients with Aids or at risk of Aids, in which their immune cells were stimulated for weeks in laboratory cultures using a variety of agents.

    After the cells had been activated in this way, HIV pioneers found some 30 proteins in filtered material that gathered at a density characteristic of retroviruses. They attributed some of these to various parts of the virus. But they never demonstrated that these so-called “HIV antigens” belonged to a new retrovirus.

    So, out of the 30 proteins, how did they select the ones to be defined as being from HIV? The answer is shocking, and goes to the root of what is probably the biggest scandal in medical history. They selected those that were most reactive with antibodies in blood samples from Aids patients and those at risk of Aids.

    This means that “HIV” antigens are defined as such not on the basis of being shown to belong to HIV, but on the basis that they react with antibodies in Aids patients. Aids patients are then diagnosed as being infected with HIV on the basis that they have antibodies which react with those same antigens. The reasoning is circular.

    Gay men leading “fast-track” sex lives, drug addicts, blood product recipients and others whose immune systems are exposed to multiple challenges and who are at risk of Aids are much more likely to have raised levels of the antibodies looked for by the tests than healthy people – because the antigens in the tests were chosen on the basis that they react with antibodies in Aids patients. But this association does not prove the presence of a lethal new virus.

    The tests do discriminate between healthy blood and the blood of patients with Aids or Aids-like conditions, because Aids patients suffer a range of active infections and other blood abnormalities, some of which are transmissible. This is why the tests are useful as a screen for the safety of blood supplies.”

    [End excerpt]

    There are 2 things to note:

    (1) Hodgkinson says, “the tests do discriminate between healthy blood and the blood of patients with Aids or Aids-like conditions”, because the proteins were chosen which reacted best with clinically diagnosed AIDS patients. However, Prof. Bauer’s analysis of the US HIV statistics suggests that the constantly ‘improved’ tests quickly became biased against the specific groups and races where most AIDS patients were found. In other words, because of the practice of identifying ‘HIV’ proteins by their reaction with clinically diagnosed AIDS (or at risk) patients, they singled out both the blood abnormalities of genuinely sick people AND the normal blood (conditions) of the groups and races those people belonged to. This bias is apparently strong enough to produce almost unfailingly the consistent racial patterns observed in the HIV statistics.

    It may also explain the huge variety of more or less geographically determined clades and subtypes of HIV. A US HIV-test biased towards, say, Blacks, gays and drug-abusers may work only poorly on heterosexual Indians or Thai people. As I have shown in my previous Comment under “HIV Illustrates Cognitive Dissonance”, the solution has been to switch antigens (proteins) to ones that react with the genetically and environmentally determined blood (conditions) of those clinically diagnosed with AIDS in the specific geographical regions.

    Because of the lack of a viral gold standard, and because of the supposed endless variability of ‘HIV’, it is possible to modify the tests, so that they pick out any population group or race one wishes to indict. It is quite possible in this way to create heterosexual epidemics on one continent and gay epidemics on another, as long as there exists a real difference either behavioural, genetic or environmental. This is the racist scandal of the HIV tests.

    (2) Hodgkinson says that some of the blood conditions that may trigger a positive HIV-tests are transmissible, which provides part of the explanation why ‘HIV’ occasionally seems to be infectious.

  6. Nick Naylor said

    Thanks MacDonald for reminding us of the circular reasoning problem that’s fundamental in the elaboration of all things HIV-1. Interestingly, it is now conceded that 30+ proteins can present when HIV-1 is “purified” according to the “velocity gradient” technique. Various MHC and immunoglobulin family proteins produced from defined regions of the human genome co-fractionate with “purified” HIV-1 and provide us with an example of a second type of “gold-standard” cognitive dissonance besides the diagnostic one Darin mentioned. If this is a purified preparation, what are recognized cellular proteins doing there? Etc …

    Clearly also detection of MTCT is confounded by the recognized transmission of maternal antibodies through the placenta during pregnancy. But let’s make a feeble attempt to move the discussion forward for the benefit of those who want to heed the advice of Dr Fauci.

    As the good doctor well knows, official status has been granted to “microchimerism” which allows for the MTC transmission of lymphocytes including, of course, the retroviral passengers that constitute 8-9% of the human genome. Does it matter if a small fraction of these retroviruses are exogenous proviruses in terms of a child’s health? If fragments of the child’s retroviral cDNA line up on a “confirmatory” PCR test using HIV-1 primers?

    What “microchimerism” infers (see Scientific American, Feb – 2008, page 72) – i.e., a mechanism for eventual “exogenization” of endogenous retroviral genes and re-infection of the germ-line – has implications for primate evolution and better explains the “variant HIVs”, IMO.

    The orthodox proclaim a “natural history of HIV-1 infection”. This “history” ignores cellular constraints, template switching, etc. on reverse transcriptase reactions and is simply ASSUMED. The pure genius of using mathematical models is the illusion of precision that sweeps all problems under the rug. Furthermore, HOW those biotech computers do maximum (or is it minimum?) parsimony analysis, line up nucleotide sequences, construct phylogenetic trees and calculate molecular clocks can be as mysterious to the uninitiated as the physics of time travel. Thus, when faced with such a construct for a particular HIV-1 clade, what kind of dummy can ignore such an obvious fact as that newly “discovered” clade. But by now it should be obvious that one can invoke GIGO anyway. Since politeness rules here, let’s refrain from that and say that HIV-clade models are way “underdetermined”. This ignorance means other explanations for “HIV-1 variants” are appropriate, NOT exclusively evolution of a unique disease pathogen.

    Finally, quantitation (or lack thereof) bolsters the necessity of alternative arguments. If there is a hyper-multiplication of the HIV genome (swarm) in AIDS patients, evidence would be directly available from peripheral blood cells/plasma ex vivo with a definite number of complete RNA genomes using conventional non-PCR biotech measures. Since this evidence is lacking, one cannot claim that variant HIVs “exist” as quasispecies, subtypes or groups. It is more likely that what’s being measured are polymorphisms in human populations consistent with that quite large HERV number (short of 300 million base pairs) in each human genome. Somatic retrotranspositions increase the number of sequence variant possibilities that could be picked up by long PCR.

    And what’s the connection with protein coding ‘housekeeping genes’ that make monkeys out of all of us (yuk yuk). It’s in the regulatory sequences and yes, there’s a retroviral connection there as well: the LTRs or cis regulatory promoter regions that make it possible for the cell to transcribe protein coding genes. Humans and chimpanzees are differentially regulated – in the genomic/developmental sense the differences that make a difference.

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