More De COCK AND BULL stuff and nonsense

In the face of undeniable facts about HIV/AIDS, cognitive dissonance and passionate defense of vested interests are eliciting from official sources statements that call for the talents of comedians in the tradition of Mort Sahl, Tom Lehrer, Jon Stewart, Stephen Colbert, for appropriate commentary.

Kevin De Cock, for example, chief white-coated HIV/AIDS guru at the World Health Organization, said that “Ten years ago a lot of people were saying there would be a generalised epidemic in Asia . . .  That doesn’t look likely” [emphasis added] (Jeremy Laurence, “Threat of world Aids pandemic among heterosexuals is over, report admits”, Independent.co.uk, 8 June 2008 ).

What’s comical here is that De Cock and his cohorts at WHO and UNAIDS were themselves this “lot of people”, and that they were not only saying it but strenuously insisting on it, trumpeting it, repeating it incessantly and brooking no contradiction.

De Cock’s mention that Swaziland suffers an infection rate of  40% also deserves at least a snigger if not a belly laugh. He bemoans that fewer than one third of people in those African countries are getting the antiretroviral drugs they need. Of course even fewer were getting them until quite recently. Since Swaziland and other sub-Saharan countries have had these high rates for a decade or more in absence of treatment, there should by now be few people left alive there. Where then are all the corpses? Rian Malan (1) looked and couldn’t find them. And how did Africa’s population manage to continue to grow at a few percent per year despite all this carnage?

De Cock’s admission that HIV/AIDS is not going to spread outside Africa might have reflected his encounter with reality as co-author of the review article featured in HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008. A colored graph in that article incorporates the assertion that HIV is disseminated by quite different means in different parts of the world. In sub-Saharan Africa, marital sex is indicted for more than 50% of the spread while commercial sex is responsible for only about 10%, whereas in Eastern Europe about 85% of transmission is owing to injection by drug addicts and only about 10% is ascribed to each of “casual sex” and sex between men—no noticeable amount from marital sex or from commercial sex, which latter is indicted in other parts of the world for between 10% and 20% of transmission. Aren’t some of the drug addicts in the former Warsaw pact countries married? Don’t they have sex with their wives? Are there no sex workers there? Don’t the injecting drug addicts there ever have sex with anyone, or do they have only homo-sex?

In both Latin American and the Caribbean, sex between men is supposed to be responsible for about 60% of the spread—but the overall rate in Latin America is twice that in the Caribbean. Is the proportion of gay men in the Latin American population twice that in the Caribbean?

One shouldn’t in any case speak of any spread at all in those regions, given that there has been no reported increase for at least a decade. UNAIDS in its Global Reports and Updates reported for HIV in Latin America, 0.5% for both 1997 and 2007; in the Caribbean, 1.9% in 1997 and only 1.0% for 2007.

Mother-to-child transmission, according to that review article, accounts for 15% of all transmission in sub-Saharan Africa but is barely noticeable in Latin America and the Caribbean and is not even mentioned for Asia and Eastern Europe. Yet in Asia, 25% of transmission is supposed to be via marital sex. How does it come about that all those married women infected via marital sex never pass their infection on to their newborns?

Someone like De Cock who collaborated in authorship of this review article would, I suggest, find unbidden doubts making themselves felt about the whole business of HIV/AIDS epidemics; albeit those doubts might express themselves only in dreams—or nightmares.

Expressing such doubts in the light of day, and from within the World Health Organization, is tantamount to treason. No surprise, then, that WHO and UNAIDS quickly issued a joint “correction” (“Correction to AIDS story in Independent article 8 June 2008; Joint Note for the Media WHO/UNAIDS - Wed, 11 Jun 2008”).

This correction reiterates that “the global HIV epidemic is by no means over. . . . AIDS remains the leading cause of death in Africa. . . . Worldwide, HIV is still largely driven by heterosexual transmission. The majority of new infections in sub-Saharan Africa occur through heterosexual transmission. We have also seen a number of generalized epidemics outside of Africa, such as in Haiti and Papua New Guinea.”

But this in no way speaks to, let alone contradicts, De Cock’s admission that there are not and will not be heterosexual epidemics in the Americas, Asia, Australia, or Europe. That takes all the wind out of the sails of this “correction”; and the last assertion in this press release deserves to be laughed off the stage:
“AIDS remains the leading infectious disease challenge in global health. To suggest otherwise is irresponsible and misleading.”

As already pointed out in our earlier post (WHO SAYS that WE’VE BEEN VERY WRONG about HIV and AIDS? (Clue: WHO = World Health Organization), 10 June 2008 ), numerous official sources have presented evidence over and over again that more people even in Africa die of malaria and other scourges traditionally present there, than die of AIDS.

Peter Piot, collaborator with de Cock in creating “the Belgian disease” of HIV/AIDS in Africa, seems to have acted with better self-preservation instincts than De Cock: “In a little noticed statement in April, Piot said he would step down when his term ended at the end of this year” (“June 11, 2008: First shoe at UN drops: Peter Piot resigns”  and “Liam Scheff at GNN: The Aids machine grinds to a halt” ). When a Director of UNAIDS and Under-Secretary of the United Nations steps down with a “little noticed statement”, something is awry. Why not the traditional press-release citing his desire to spend more time with his family after having accomplished all that he had aimed to accomplish? That no successor was announced amplifies the smell of fish here, in  its indication of haste and confusion rather than orderly transition at the normal end of a term of service.

The cat is out of the bag. HIV is not fueling heterosexually transmitted epidemics—at least not in most of the world. Outside sub-Saharan Africa, heterosexual epidemics are apparent only among other dark-skinned people, according to WHO/UNAIDS in Haiti and Papua New Guinea. It’s just shameful what those black people do in the way of sex—particularly those married ones in sub-Saharan Africa, see TO AVOID HIV INFECTION, DON’T GET MARRIED, 18 November; HIV/AIDS ABSURDITIES AND WORSE, 9 DECEMBER 2007; B***S*** about HIV from ACADEME via THE PRESS, 4 March 2008.
———————-

Citation:
(1) Rian Malan, “AIDS in Africa: In search of the truth” Rolling Stone Magazine, 22 November 2001; “Africa isn’t dying of Aids”, The Spectator (London), 14 December 2003.

WHO SAYS that WE’VE BEEN VERY WRONG about HIV and AIDS? (Clue: WHO = World Health Organization)

“A 25-year health campaign was misplaced. . . . there will be no generalised epidemic of AIDS in the heterosexual population outside Africa. . . . outside sub-Saharan Africa [the threat of AIDS] . . . was confined to high-risk groups including men who have sex with men, injecting drug users, and sex workers and their clients.

… the threat of a global heterosexual pandemic has disappeared. . .

Ten years ago a lot of people were saying there would be a generalised epidemic in Asia . . . That doesn’t look likely. . . .

In 2006, the Global Fund for HIV, Malaria and Tuberculosis . . . warned that Russia was on the cusp of a catastrophe. . . . it is unlikely there will be extensive heterosexual spread in Russia. . . .

the factors driving HIV [are] still not fully understood. . . .

In the US , the rate of infection among men in Washington DC is well over 100 times higher than in North Dakota, the region with the lowest rate. . . . How do you explain such differences?”

No, these are not statements and questions from “deniers”, “dissidents”, “denialists”, rethinkers, or other outsiders. They are from Dr. Kevin De Cock, head of the World Health Organization’s department of HIV/AIDS (Jeremy Laurance, “Threat of world Aids pandemic among heterosexuals is over, report admits”, Independent.co.uk, 8 June 2008 [’ve changed the British usage, “aids”, to “AIDS” throughout]).

Not only does De Cock hold that authoritative position at WHO, he has been in the forefront of HIV/AIDS research from the very beginning. Indeed, he is at the forefront of those who are demonstrably culpable for promulgating a notion that underpins the whole HIV/AIDS house of cards, namely, the notion of a “virus out of Africa” which was created on the basis of zero evidence as well as high implausibility.

As the Chirimuutas* pointed out long ago, the conceit that 1980s outbreaks in a few American cities stemmed from a virus brought back to the United States by tourists ignores the fact that Africans had been transported to the United States long before that; that people from many parts of Africa had been visiting and residing in the United States for many decades; that the back-and-forth people traffic between Africa and colonial European powers had been far more intense, and had gone on far longer, than between Africa and America, so that an imported-from-Africa virus would have done its first damage in Europe, not America. And, after all, none of the early 1980s AIDS victims had ever been to Africa.

Furthermore, De Cock’s explanation, for why AIDS was not noticed or identified in Africa before it traveled to the United States, ignorantly indicted African medicine for incompetence in diagnosis of even such endemic diseases as malaria. De Cock also suggested that Africans had adjusted physiologically in some way to cope with the disease better than Americans could, which hardly explains why AIDS supposedly devastates Africa but not America or Europe.

The book by the Chirimuutas, chock-full of citations of peer-reviewed literature, is a stunning exposé of how early Belgian researchers in Africa—Peter Piot as well as De Cock—laid the groundwork for decades of misguided research through their thoroughly incompetent activities. More recent articles make many of the same points: “Is AIDS African?” (1997); “AIDS and Africa: A case of racism vs. science? AIDS in Africa and the Caribbean 1997”

Piot has been Executive Director of UNAIDS since its creation in 1995 as well as Under-Secretary-General of the United Nations. Given his and De Cock’s role in creating it, perhaps HIV/AIDS should be known as “the Belgian disease”.

————————————

Reality has now intruded so forcibly that De Cock can no longer avoid the fact that AIDS epidemics have not happened, those epidemics that he and his cohorts prophesied with such overweening confidence for more than two decades. But— cognitive dissonance once again!—he also cannot recognize that this fact undermines the whole HIV/AIDS scenario. De Cock describes as “four malignant arguments” some certifiable truths cited by critics: that official data have inflated all HIV/AIDS estimates and that HIV/AIDS has diverted funds from such obvious needs as malaria prevention and the provision of clean water and food, building infrastructure, and sensible public-health programs; even then, plain reality forces De Cock to admit that there are “elements of truth” in these criticisms.

Nevertheless—recall what cognitive dissonance involves, HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008 —De Cock still asserts that AIDS “remains the leading infectious disease challenge in public health” , even as he knows that it is no threat outside Africa and in the face of at least equally authoritative assertions by others that malaria and malnutrition kill far more Africans than “AIDS” does (A SMALL HITCH IN THE BANDWAGON?, 29 May 2008; WHY UNAIDS SHOULD BE DISBANDED, 31 May 2008 ).

De Cock’s muddled state of mind manages only to recognize that something doesn’t fit:

“The biggest puzzle was what had caused heterosexual spread of the disease in sub-Saharan Africa—with infection rates exceeding 40 per cent of adults in Swaziland, the worst-affected country—but nowhere else. . . . Sexual behaviour . . . doesn’t seem to explain [all] the differences between populations.”

Yet having acknowledged that sexual behavior isn’t the explanation, he resorts to sexual behavior as an explanation:

“more commercial sex workers, more ulcerative sexually transmitted diseases, a young population and concurrent sexual partnerships. . . . Even if the total number of sexual partners [in sub-Saharan Africa] is no greater than in the UK, there seems to be a higher frequency of overlapping sexual partnerships”.

Regarding that shibboleth about multiple concurrent overlapping partnerships, not only is there no evidence for such multiple overlapping concurrencies, there is strong evidence against the assumption; see earlier posts, in particular RACE and SEXUAL BEHAVIOR: STEREOTYPE vs. FACT, 27 May 2008.

——————————

The epidemiology is so clear that even such insiders as James Chin++ and Kevin De Cock can’t make it jibe with HIV/AIDS theory. And since— remember, cognitive dissonance—they cannot admit to themselves that they have been utterly and entirely wrong, so too can they not find a way to admit publicly that they have been utterly and entirely wrong. But their attempts to cope with the evidence inevitably become more and more absurd, and the whole enterprise begins to crumble, as insiders from specialties that compete with them for funds begin to raise their voices (A SMALL HITCH IN THE BANDWAGON?, 29 May 2008; WHY UNAIDS SHOULD BE DISBANDED, 31 May 2008 ).

* Richard and Rosalind Chirimuuta, AIDS, Africa and Racism, Free Association Books (London), 1989 (2nd ed., revised). Rosalind Harrison (Chirimuuta) is a diplomate in Tropical Medicine and Hygiene, specialized in ophthalmology, and presently a consultant with the British Health Service

++ Re Chin, see for example B***S*** about HIV from ACADEME via THE PRESS, 4 March 2008

Acknowledgment: Many thanks to the several people who alerted me to the article in the Independent.

ANTHONY FAUCI EXPLAINS RACIAL DISPARITIES IN “HIV/AIDS”

(Several references below — euphemism, minority, macacas — are more fully explained in the earlier post, HIV/AIDS IS INESCAPABLY RACIST, 19 May 2008 ).

Anthony Fauci, Director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, has appeared often on the public-radio Diane Rehm show. For example, on 27 November 2007, he was introduced thus (“HIV/AIDS Worldwide”, transcript by Soft Scribe LLC):

“Racial and ethnic minorities continue to be disproportionately affected by the HIV/AIDS epidemic here in the U.S. New figures show that African Americans are among those who are most at risk. Here in Washington, D.C. 1 in 20 residents is thought to have the HIV, and 1 in 50 to have AIDS.”

Once again (see HIV/AIDS IS INESCAPABLY RACIST), that euphemism “minority”. Already the following sentence shows that actually meant is black. (In Washington, DC, blacks comprise a majority of the population.)

Fauci said that “in the District, about 37 - 39 percent [of ‘HIV-positive’ results from] heterosexual transmission, 20-some-odd percent men who have sex with men, and about 14 percent injection-drug users. . . . [This] resembles in some respects . . . what we see in third world countries. And the confluence of an inner city area with poverty, lack of healthcare access, injection-drug use which keeps a core of infection in the city, and then that’s spread heterosexually and then from there you get secondary and tertiary heterosexual spread” [emphasis added].

Once more: “complex social mixing patterns” (see HIV/AIDS IS INESCAPABLY RACIST) are postulated in these “minority” communities whose conditions happen to resemble those in Third-World countries (euphemism for sub-Saharan Africa).

Another remark by Fauci illustrates how content the mainstream is to assert as fact what cannot be known: “there is a disproportional amount of transmission from people who do not know that they are infected”.
STOP.
THINK.
They don’t know they’re infected. No one told them. Why not? Because no one else knows, either.
What Fauci asserts could only be assumed, not actually known; and it is also and first assumed that there’s a short period of undetectable infection but high infectivity just after being infected; because that’s the only way to cope with the undeniable fact that the average probability of apparently transmitting the “HIV-positive” condition is only about 1 per 1000 acts of unprotected intercourse, far too low a probability to sustain any sort of epidemic (14 May 2008, SEX, RACE, and “HIV”).

(”Don’t know they’re infected” reminded me of the study that found “Nine in 10 students who experienced hazing . . . did not think they had been hazed”; Chronicle of Higher Education 21 March 2008, p. A21)

Fauci again: “disproportional amount, more of poverty, lack of access to medical care, a lack of access to counseling for prevention, proximity in locations in inner city for example where there are pockets of injection-drug use . . . . among blacks … being gay and having gay sex is not as accepted … as it is in the society as a whole”.

Again: it’s so but it ain’t “their” fault.

More Fauci: “a misconception that because women get infected in this community that they are leading promiscuous lives. That’s certainly not the case in general. Very often it’s someone who is being monogamous with someone who happens to be infected”.

“Very often”: How often must a monogamous woman have sex with an infected partner to become positive, when the probability is about 1 per 1000? James Chin, epidemiologist, says the contrary. To produce the alleged levels and rapidity of spread, 20-40% of people must be engaged in multiple concurrent relationships with frequent partner change (4 March 2008, B***S*** about HIV from ACADEME via THE PRESS). Doesn’t that qualify as quite promiscuous?

Over and again, Fauci pretends to believe that it’s not their fault, it’s their culture — “very often women want their male sexual partner to use a condom, but they won’t do it. And in certain cultures it is not easy for a woman to assert herself and say, ‘No, this is the way it’s going to be. We don’t have a condom, I’m not having sex.’ They can wind up getting abused as it were. Those are the kind of cultural barriers that we need to overcome” (emphasis added).
(1) How does Fauci know that this happens “very often”?
(2) Again it’s those macaca cultures, which are apparently ensconced just as powerfully in Washington, DC, among people whose ancestors left Africa many generations ago, as among those still now living in Africa.

Fauci: “68 percent of the infections in the world occur in southern Africa. . . . it has to do with cultural and other factors. Poverty, dissolution of the family units, post-colonization where people would leave the family and go and work in mines, go on the trucking routes, get exposed to commercial sex workers, bring the infection back to their family, infect their wives, lack of prevention modalities. . . . some very good studies about sexual activities that in certain cultures, including those in Southern Africa there is what’s called overlapping concurrent multiple sexual partners. If you have a society that has sequential sexual partners, it is much less likely to have explosive transmission than when you have people who have simultaneously multiple sexual partners that you share.
…
there is a degree of disenfranchisement . . . There is discrimination . . . communities in which there is crime, there is murder . . . .”

Once more, it’s those other cultures that do sex differently than “we” do; and those cultures in Washington DC and in southern Africa share the common factor of people with dark-hued skin. As documented in my book, The Origin, Persistence and Failings of HIV/AIDS Theory, Native Americans suffer even more than African Americans from violent crime and disenfranchisement and abuse of alcohol and drugs, but their rate of testing “HIV-positive” is far below that of blacks and not much higher than among whites. It’s the biological race that matters, not the “minority” “culture”.

Note once again the asserting, as fact, matters that are speculative. “Overlapping concurrent multiple sexual partners” have been postulated to explain spread of “HIV” among heterosexuals. I await citation of those “very good studies” that actually found that sort of situation which — recall James Chin’s calculations (14 May 2008, SEX, RACE, and “HIV”) — require 20-40% of adults to be behaving in this fashion if “HIV” is to spread. Such a rate of promiscuity would be evident to the most casual observer, yet it has not been reported by any observers.

Fauci virtually confessed his belief that race and cultural determinants of sexual behavior go together:

FAUCI: it’s very difficult when you have societies whose cultural approach to life has been going on for centuries that you are going to all of a sudden change sexual practices.
REHM: But I don’t think we ought to single out sub-Saharan Africa.
FAUCI: No, not, of course not, anywhere.
REHM: I mean, here in Washington –
REHM: — that kind of promiscuous sex –
FAUCI: Right, and –
REHM: — is going on.
FAUCI: Right, exactly.

*************

Anthony Fauci and many others, including those who speak for the Centers for Disease Control and Prevention, appear willing to ascribe racial disparities in “HIV-positive” to “cultural” factors, even though those disparities transcend all social milieus and all geographic boundaries and all age groups and are seen in both sexes. Would they also ascribe to “cultural” factors characteristic of Caucasians that whites always test “HIV-positive” anywhere from 50% to 300% more often than Asians? Could it be that Caucasians are inherently more given to “multiple concurrent sexual relationships” than Asians are?

RACE and SEXUAL BEHAVIOR: STEREOTYPE vs. FACT

Racial disparities in testing “HIV-positive” are explained — by proponents of HIV/AIDS theory, that is — as stemming from the harmful effects of racial discrimination, which mire the discriminated-against in circumstances rife with drug abuse and sexual promiscuity. That runs counter to a goodly body of actual evidence that undercuts this type of explanation; and it also draws on stereotypes not readily distinguishable from racist beliefs (see 19 May, HIV/AIDS THEORY IS INESCAPABLY RACIST).

Some of the evidence confounding the stereotypes is cited in my book (p. 77):

“As a matter of actual fact, research in the context of HIV/AIDS has not revealed any racial differences in sexual behavior. Among drug users, no significant differences in behavior by race were found as to numbers of sexual partners, frequency of intercourse, numbers of sexual partners who were IDUs, numbers of non-IDU sexual partners, prostitution, or intercourse with people then or later diagnosed with AIDS (Friedman et al. 1987). Samuel and Winkelstein (1987) found no significant racial differences in behavior among gay men in San Francisco, and they concluded that the black-to-white ratio of . . . [“HIV-positive”] could not be explained by differences in major risk factors. The San Francisco Department of Health (1986) found no differences between races as to anal intercourse . . . . Bausell et al. (1986) found white Americans less likely than black Americans to take protective measures during sex. Historical data from Zimbabwe records a higher incidence of venereal disease among the white South Africa Police and the British Armed Services than among the Native Police or among Africans in general (McCulloch 1999, 205, 207). Contemporaneous surveys have found that levels of sexual activity in general populations in Africa are comparable to those in North America and Europe (Brewer et al. 2003; Gisselquist 2002).”

It has become fashionable to assert that black women in the United States are at particular risk because of black men “on the down low” (indulging secretly in male-with-male sex), becoming “HIV-positive”, then transmitting that to their female partners. But here again, the evidence doesn’t sustain the speculation:

“The lifestyle referenced by the term the DL is neither new nor limited to blacks, and sufficient data linking it to HIV/AIDS disparities currently are lacking. Common perceptions about the DL reflect social constructions of black sexuality as generally excessive, deviant, diseased, and predatory. [“social construction” means stemming from human interpretation rather than from the objective reality] Research targeting black sexual behavior that ignores these constructions may unwittingly reinforce them” (Ford et al., Ann Epidemiol 17 [2007] 209-16).

An illustration of such unwitting reinforcement is one of the CDC’s statements:
“The phenomenon of men on the down low has gained much attention in recent years; however, there are no data to confirm or refute publicized accounts of HIV risk behavior associated with these men. What is clear is that women, men, and children of minority races and ethnicities are disproportionately affected by HIV and AIDS” (emphasis added; unchanged since at least March 2006; www.cdc.gov/hiv/topics/aa/resources/qa/downlow.htm, accessed 11 May 2008).

Another common and politically correct gambit (attempting to explain away that blacks always test “HIV-positive” more often than others) seizes on the high incarceration rate of young black men, particularly from inner-city regions, and combines that with the shibboleth that prisons are a hotbed of “HIV” transmission (for example, Johnson & Rafael 2006). But once again the speculation goes contrary to fact, because “actual observations in prisons have failed to reveal transmission of HIV there (Brown 2006; Horsburgh et al. 1990; Kelley et al. 1986)” (p. 79 in The Origin, Persistence and Failings of HIV/AIDS Theory).

In South Africa, blood from black donors was, for some time, being destroyed as “unsafe” because it tested “HIV-positive” so much more often than blood from people of mixed race or from South-East Indians or whites (p. 75 in The Origin, Persistence and Failings of HIV/AIDS Theory). However, since testing was available for the blood, this blanket rule surely owed something to underlying and pre-existing racist beliefs. Racist preconceptions in the 1980s among HIV/AIDS workers in Africa — some of whom are still prominent in HIV/AIDS research nowadays — were described, long ago and in detail, by the Chirimuutas (AIDS, Africa and Racism, Free Association Books, London [UK] 1987/89). Konotey-Ahulu, a distinguished Ghanaian physician and medical researcher, also exposed the lack of evidence for an African origin of HIV/AIDS in a book (What is AIDS? 1989/96, ISBN 0-9515442-3-3) I described in a review as “flavored by a traditional attitude toward what constitutes acceptable behavior” and displaying “what used to be called good breeding and proper upbringing”, exploding by personal example all sorts of notions about “those Africans” (Journal of Scientific Exploration 21 [2007] 206-9).

That blacks always test “HIV-positive” more often than others simply cannot be explained by differences in behavior:

“AIDS researchers don’t have a solid explanation for why black women in America have such a shockingly high prevalence of HIV infection. . . . injection drug use, a particularly effective way to spread HIV, is actually lower in black women than in white women” — Jon Cohen, “A silent epidemic”, 27 October 2004, www.slate.com/id/2108724/.

“Black young adults . . . are at high risk even when their behaviors are normative. Factors other than individual risk behaviors and covariates appear to account for racial disparities” — Halfors et al., Sexual and drug behavior patterns and HIV and STD racial disparities: the need for new directions, Am J Public Health 97 [2007] 125-32.

“HIV-positive gay men are more likely than HIV-positive black African heterosexual men and women to engage in sexual behaviour that presents a risk of HIV transmission. . . . There were no significant differences between white gay men and those from other ethnic background in terms of sexual behaviour” (Rod Dawson, 5 January 2007. AIDSmap news, summarizing Elford et al., “Sexual behaviour of people living with HIV in London: implications for HIV transmission”, AIDS 21 [suppl. 1, 2007] S63-70).

“According to Robert Janssen, director of CDC’s Division of HIV/AIDS Prevention, blacks do not engage in riskier sexual behavior compared with other groups, but the population’s HIV/AIDS infection rates mean that blacks who have sex with other blacks are more likely to get HIV than people in other ethnic groups” — (emphasis added; Kaiser Daily HIV/AIDS Report, 9 March 2007).
Perhaps Janssen has never heard of the chicken-&-egg conundrum? How did the infection rate in the black community become higher than in others in the first place, given that the first affected groups in the USA were predominantly white gay men?

That ill-founded grasping-at-straws argument is not unique with Janssen:
“racial disparities in seroprevalence were . . . not attributable to disparities in risk factors such as STD, bisexuality, or acceptance of HIV testing. This finding suggests that the observed differences may reflect racial differences in the background seroprevalences” — Torian et al., Sex Transm Dis. 29 [2002] 73-8.
I suppose one must sympathize with people trying desperately to explain the unexplainable. This “explanation” is a tautology: blacks test “HIV-positive” more often than others because blacks already test “HIV-positive” more often than others.

“Paradoxically, potentially risky sex and drug-using behaviors were generally reported most frequently by whites and least frequently by blacks. . . . Understanding racial/ethnic disparities in HIV risk requires information beyond the traditional risk behavior and partnership type distinctions” — Harawa et al., “Associations of race/ethnicity with HIV prevalence and HIV-related behaviors among young men who have sex with men in 7 urban centers in the United States”, JAIDS 35 [2004] 526-36.

The Centers for Disease Control and Prevention found, in one study, that “Black gay and bisexual men . . . [were] more likely to engage in safe-sex practices than their white counterparts. . . . ‘Across all studies, there were no overall differences [by race] in reported unprotected receptive sex or any unprotected anal intercourse . . . among young MSM — those ages 15 to 29 — African-Americans were one third less likely than whites to report in engaging in unprotected anal intercourse’ . . . . Black gay or bisexual men were also ‘36 percent less likely than whites to report having as many sex partners as white MSM’ . . . . Blacks in the study were also less likely to use recreational drugs, such as methamphetamine or cocaine, compared to whites” (“One-third of HIV-infected gay men have unsafe sex: CDC”, HealthDay News, 3 December 2007).

*******************

Black people always test “HIV-positive” more often than others.

Black people do not differ greatly from others in their sexual behavior. Where they do, it is through behaving somewhat more responsibly than white people.

The racial disparities in testing “HIV-positive” cannot be explained by differential behavior: blacks always test positive much more often, but their sexual behavior does not constitute a corresponding risk.

THEREFORE: Testing “HIV-positive” must indicate something other than a sexually acquired condition. Testing “HIV-positive” does not mark infection by a sexually transmitted agent. Rather, testing “HIV-positive” is a very non-specific indication of some sort of physiological stress; see, for example, REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008; “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; UNRAVELING HIV/AIDS, 8 March 2008; HIV DEMOGRAPHICS FURTHER CONFIRMED: HIV IS NOT SEXUALLY TRANSMITTED, 26 February 2008; TWINS ATTRACT THEIR MOTHER’S HIV, 12 January 2008; HOW TO TEST THEORIES (HIV/AIDS THEORY FLUNKS), 7 January 2008.

UPDATE: MORE SPONTANEOUS SEROREVERSION

According to HIV/AIDS dogma, testing “HIV-positive” denotes infection by “HIV” which is permanent and ineradicable. One of several independent proofs that HIV/AIDS theory is wrong is the fact that people do spontaneously revert from “HIV-positive” to “HIV”-negative, perhaps most notably and frequently, babies born “HIV-positive” and reformed drug abusers (p. 96 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory). But whenever spontaneous reversion happens to be noticed, it’s treated as the secular equivalent of a miracle (HIV “INFECTION” DISAPPEARS SPONTANEOUSLY, 22 January 2008). Here are a couple more instances:

“BEIJING, Dec. 3 (Xinhua) — A farmer in northeast China’s Jilin Province has tested HIV negative, six years after being diagnosed as HIV-positive, according to the provincial Center of Disease Control (CDC).
Wen Congcheng . . . first tested HIV positive in 2001 [during testing of blood donors]. . . . Late in 2003, he was re-confirmed to have HIV/AIDS as a result of another test . . . . However, in July this year [2007], Wen received a negative test result at the No. 1 Clinical Hospital of Beihua University in Jilin. Wen decided to seek another opinion and went to the First Hospital of the China Medical University and another three hospitals for HIV tests, which all proved to be negative. The Jilin municipal CDC carried out a follow-up test which confirmed the negative result, and later the provincial CDC also confirmed the result.”

But, of course, the white-coated gurus refuse to accept this, and have questioned the original positive result, while the lab that made the diagnosis sticks by it.

“ ‘I am pretty sure there are no problems with the blood samples and the tests,’ said Liu Baogui, former director of the HIV/AIDS and STD Section of the CDC of Jilin City. . . . Professor Wu Min, a member of the HIV/AIDS experts’ committee under the Ministry of Health, is sceptical about the validity of the original positive test result. ‘I can not believe that such miracle could have really happened,’ he said. ‘Some patients appear to be free of the virus after effective treatment, but the HIV anti-body is always there, so the test result will still be positive.’ Wu said the inaccuracy rate of tests by the provincial CDCs is lower than 0.01 percent. ‘But it is possible that the person’s name and blood sample was mixed up at the Chuanying District CDC where Wen tested HIV positive for the first time,’ he said.
. . .
In 2003, Andrew Stimpson, a 25-year-old Briton, tested HIV-negative 14 months after testing positive in May 2002. The case has never been scientifically explained.”

And here’s more detail about Andrew Stimpson:

“Doctors baffled as HIV man ‘cures’ himself” (Sophie Kirkham, Sunday Times, 13 November 2005)

“A MAN who tested positive for HIV, the virus that causes Aids [sic, British usage], has subsequently shown up negative for the disease in a case that has mystified doctors. It was claimed last night that Andrew Stimpson, 25, may have shaken off the virus with his own immune system after contracting HIV in 2002.
If proved, the NHS has said the case would be ‘medically remarkable’. … The Chelsea and Westminster Healthcare NHS trust, which treated Stimpson, has said he needs to undergo more tests before it can be established how he apparently conquered HIV. ‘These tests were accurate and they were his, but what we don’t know at the moment is why that has happened, and we want him to come back in for more tests… It is potentially a fantastic thing.’ Stimpson was tested three times in August 2002 … and the results showed he was producing HIV antibodies to fight the disease. Stimpson … contracted the virus from his boyfriend, Juan Gomez, 44. He began taking vitamins and other dietary supplements to keep his body healthy in the hopes that this might fend off the development of full-blown Aids. In October 2003, after impressing doctors with his good health, Stimpson was offered a new test, which came back negative. Further tests in December 2003 and March last year also proved negative. … ‘I couldn’t understand how anyone could cure themselves of HIV . . . I thought it had to be wrong because no one can recover from HIV, it just doesn’t happen.’ The tests were re-checked by the Chelsea and Westminster Healthcare NHS Trust when Stimpson threatened litigation believing there must be a mistake, but the results confirmed all the tests had been accurate. In a letter understood to be from the NHS Litigation Authority in October this year, Stimpson was told: ‘The fact you have recovered from a positive antibody result to a negative result is exceptional and medically remarkable.’ The trust said there had been several other cases of claimed ‘spontaneous clearance’ of the virus worldwide, although it is not believed any have been proved. A spokeswoman added that the trust had urged Stimpson to return for tests, but that so far he had not done so.”

If I were Stimpson, I too would decline further tests administered by people who would love to be able to tell me that I do, after all, have an incurable and fatal illness. Stimpson’s case is readily explicable by Tony Lance’s intestinal dysbiosis hypothesis [WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT, 20 February 2008] or by the Perth-Group view that testing HIV-positive merely denotes oxidative stress. It was not that Stimpson “contracted the virus from his boyfriend”, but that they shared a lifestyle conducive in some manner to oxidative stress or intestinal dysbiosis.