Anywhere and everywhere, people of African ancestry test HIV-positive more often than others—including members of other “minority” groups in the United States, notably Native Americans and Asians. The dilemma for HIV/AIDS dogmatists is that this well established fact sits very uneasily with the claim that HIV is chiefly transmitted sexually, through risky and widely deplored behavior: that conjunction mirrors racist stereotypes about the sexual behavior of blacks [ANTHONY FAUCI EXPLAINS RACIAL DISPARITIES IN “HIV/AIDS”, 3 June 2008; RACE and SEXUAL BEHAVIOR: STEREOTYPE vs. FACT, 27 May 2008; HIV/AIDS THEORY IS INESCAPABLY RACIST, 19 May 2008; SEX, RACE, and “HIV”, 14 May 2008; RACIAL DISPARITIES IN TESTING “HIV-positive”: IS THERE A NON-RACIST EXPLANATION?, 4 May 2008; DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008; HIV: A RACE-DISCRIMINATING SEXUALLY TRANSMITTED VIRUS!, 16 April 2008; HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008].
A just-published article seemed to promise delivery from this dilemma (“Duffy antigen receptor . . . mediates trans-infection of HIV-1 . . . and affects HIV-AIDS susceptibility”, Weijuing He et al., Cell Host & Microbe 4  52-62). The significance and authoritativeness of this revelation was underscored by the fact that one of the members of the “international team” is “renowned virologist Robin Weiss” [Sabin Russell, San Francisco Chronicle, 16 July 2008]:
“An international team of AIDS scientists has discovered a gene variant common in blacks that protects against certain types of malaria but increases susceptibility to HIV infection by 40 percent. Researchers, keen to find some biological clues to explain why people of African descent are bearing a disproportionate share of the world’s AIDS cases, suspect this subtle genetic trait — found in 60 percent of American blacks and 90 percent of Africans — might partly explain the difference. Ten percent of the world’s population lives in Sub-Saharan Africa, but that region accounts for 70 percent of the men, women and children living with HIV infection today. In the United States, African Americans make up 12 percent of the population, but account for half of newly diagnosed HIV infections. ‘The cause of this imbalance is not necessarily driven by behavior,’ said Phill Wilson, founder of the Black AIDS Institute in Los Angeles. ‘Gay black men do not engage in riskier behavior than gay white men, for example. African people with this gene may have a higher vulnerability’. . . .
The researchers compared 814 African American military personal who were HIV negative with 470 who were infected with HIV. Out of this comparison popped the surprising number: A 40 percent higher risk of HIV among those whose genes suppressed the Duffy protein.”
At first sight, I was less than overwhelmed. A 40% increased risk doesn’t seem all that much help in explaining why African-American men are about 7 times more often “HIV-positive” than white American men, and African-American women about 21 times more often “HIV-positive” than white American women; nor that certain countries in sub-Saharan Africa report an “HIV-positive” rate of between 5 and 35% whereas no other region in the world, with the exception of the Caribbean, reports anything as high even as 1%. Still, HIV/AIDS dogmatists have proven their ability to explain anything, forget about plausibility; one could easily enough conjure some amplification effect.
I was impressed, however—though still not quite overwhelmed—by another aspect of this study:
“The researchers also made another remarkable finding — once a person with the African gene became infected, the same genetic trait appears to prolong survival. One of the Duffy protein’s natural roles appears to be to ramp up the immune system. It attracts a number of chemical signals that promote inflammation — a defensive mechanism that normally protects the body, but lays out a banquet of white blood cells for HIV to infect and destroy. So the same genetic mutation that raises the risk of HIV infection provides some protection to those who become infected. Similarly, those who carry the normal Duffy protein may be somewhat shielded from HIV infection, but once infected may sicken and die sooner without treatment.”
This counter-intuitive claim struck me hard because I had suggested elsewhere on the incongruity that blacks do in fact survive “HIV disease” to greater ages than members of other races, even as they are also “infected” by “HIV” to a far greater extent than are members of other races [HOW TO TEST THEORIES (HIV/AIDS THEORY FLUNKS), 7 January 2008]. I had taken this as further confirmation of my view that testing “HIV-positive” is an entirely non-specific indication of an immune-system response and that racial disparities reflect differences in genetic patterns relevant to immune-system function; now here was a generic explanation that was consistent with the data AND with the mainstream HIV/AIDS theory!
Admittedly, this explanation of how the Duffy protein could both increase and decrease susceptibility to “HIV” made my head swim. It ramps up the immune system, that should be good. But those extra cells whose job it is to defend the body are thereby exposed to the predations of “HIV”! That fits with the Ho view of frantic rapid turnover, but Ho’s math was discredited as soon as it was published. The explanation is also reminiscent of attempts to invoke immune (hyper)- activation or auto-immune reactions to explain how HIV destroys the immune system—but those had also been found wanting. Just too technically sophisticated for a lay person to understand. Anyway, wouldn’t this mean that anything that ramps up the immune system also makes it easier for HIV to destroy it? Beware vaccination! No wonder all attempts to make an anti-HIV vaccine have failed, indeed have sometimes increased susceptibility!
I was totally confused, so it was some comfort to find that technically sophisticated people could also find this explanation difficult: “The researchers offer an explanation that they concede is far from straightforward. ‘If you found the paper plain sailing, most of my students didn’t,’ Dr. Weiss said.”
Still, that didn’t erase my concern that here was a shred of evidence to support a mainstream explanation. Fortunately, alleviation came from several sources. Nick Wade in the New York Times cited certain reservations [17 July 2008; Gene variation may raise risk of H.I.V., study finds]: “David B. Goldstein, geneticist who studies H.I.V. at Duke University, said that the new result ‘would be pretty exciting if it holds up’” [emphasis added]; and he remarked that the techniques used to avoid effects of chance correlation “might not have been adequate”.
The crucial point seems to be that the Duffy gene in question is characteristic of—closely associated with—African ancestry. The tendency to test “HIV-positive” is also strongly associated with African ancestry. Therefore the Duffy gene and testing “HIV-positive” will inevitably show an association, a correlation, whether or not the gene has any causative role as to “HIV”. It’s the same old correlation-doesn’t-prove-causation fallacy that HIV/AIDS researchers—and innumerable others too, of course—often commit (for example, about “HIV” and excess deaths in Africa, see p.194 in The Origin, Persistence and Failings of HIV/AIDS Theory).
Two blogs concerned with genetics give a full explanation of why the attempts by this “international team of AIDS scientists” to rule out chance correlation were flawed. Some of the gene bits (SNPs) used as “tests” were not independent of the Duffy gene; others were poor discriminators between European and African ancestry, and therefore unsatisfactory for gauging the proportional ancestry of African Americans; and the choice of SNPs raised the suspicion that they had initially been looked at for possible correlations with “HIV” and only later for ancestry-indicating tests; see “DARC and HIV: a false positive due to population structure?” and “Duffy-HIV association: an odd choice of ancestry markers”.
An HIV-gene claim analogous to the Duffy one was made some years ago about the supposedly protective properties of CCR5 genes with a particular deletion (Δ32), because that is found in European but not in African populations. But it’s present in only a small proportion of Europeans, and moreover its distribution varies enormously from north to south. It’s also present to a negligible extent in North Africa, whereas HIV is as uncommon in North Africa as it is in Europe.
For comparison, “HIV” rates, with North African countries in bold; “HIV” should increase from red to pale yellow regions if CCR5delta32 protects against it:
Albania, Algeria, Bosnia/Herzegovina, Bulgaria, Croatia, Cyprus, Czech Republic, Egypt, Libya, Romania, Slovakia, Slovenia, Turkey <0.2%; Finland, Germany, Hungary, Malta, Morocco, Norway, Poland, Tunisia 0.1; Denmark, Greece, Iceland, Ireland, Netherlands, Serbia/Montenegro, Sweden, United Kingdom 0.2; Austria, Belgium 0.3; France, Portugal, Switzerland 0.4; Italy 0.5, Spain 0.6 (UNAIDS 2006 report on the global AIDS epidemic)
These quite typical episodes illustrate something that science writers and journalists do not usually know but should know—indeed, that it would be good for everyone to know:
REAL SCIENCE ISN’T NEWS
“Real science”, the stuff that is almost universally regarded as reliable, trustworthy, in fact true, is not and cannot be the latest, newest “breakthrough”, because it takes time and the critiquing and testing by other investigators to determine how much validity any new claim has. The real, reliable science is what’s been around long enough to have been thoroughly tested. Science is made trustworthy not by any formulaic “scientific method” but by a knowledge filter of the criticisms and repetitions and modifications and disproofs rendered by other researchers and peer reviewers.
Those who cover science for the media should learn to be as cautiously suspicious of “scientists” and “scientific” institutions as they mostly are of politicians, political institutions, business executives, and corporations. Scientists are no less human than other people, and they are no less capable of being corrupted by career ambitions and pressures, by “the system”, by taking goodies “because it doesn’t hurt anyone” “because everybody does it” and “If I didn’t do it, someone else would”.
Modern-day “Big Science” does not fit the traditional view of a quasi-religious vocation attracting disinterested truth-seekers who form an intellectual free market in which an invisible hand safeguards against error; modern-day “Big Science” is an array of bureaucracies that produce knowledge monopolies and research cartels.