THERE IS NO DISPUTE that in the United States HIV has hit African Americans harder than whites and Americans of other ethnicities. According to the CDC, among the 34 states with long term HIV/AIDS reporting, an estimated 48% of people living with HIV in the US in 2007 were black, compared to 33% who were non-Hispanic white.
Furthermore, among new (incident) HIV diagnoses notified to the CDC in 2007, 51% were among blacks compared to 29% among whites.
Given that African Americans comprise only 12.4% of the US population compared to non-Hispanic whites who are around 66%, the rate of new (incident) HIV diagnoses in 2007 was nine times higher for blacks than whites, and the estimated prevalence of diagnosed HIV was over seven and a half times higher among blacks as compared to whites.
This racial discrepancy in HIV seroprevalence is used by Henry Bauer to argue that HIV cannot be the cause of AIDS, and nor can what is diagnosed using HIV testing algorithms be a sexually transmissible agent. Bauer goes one step further, and argues that "racist" stereotypes are inherent in HIV/AIDS theory. See: http://hivskeptic.wordpress.com/2010/02/08/racist-stereotypes-are-inherent-in-hivaids-theory/
Bauer’s race argument boils down to his assertion that the higher HIV seroprevalence among African Americans could only be explained by proportionately higher rates of "promiscuity" and drug use, if what is detected by HIV tests were a sexually transmitted and blood borne infection. He argues that evidence is lacking for such behavioural differences generalisable to the African American community as a whole, and that therefore positive HIV tests cannot indicate such an infection (see chapters 5 to 7 in The Origin, Persistence and Failings of HIV/AIDS Theory).
Instead, he hypothesises that African Americans are more likely to test HIV positive because of supposed racially-determined genetic variations that result in an extremely high rate of false positive HIV diagnoses. What precisely these variations might be and how they cause clinicians to make false diagnoses - well, he's more than a little vague on this, possibly because he seems to be clueless about the details of how HIV diagnoses are in fact made. Bauer ignores other factors that can result in a relatively higher seroprevalence such as levels of undiagnosed infection (which results in a greater probability of secondary transmission) and the fact that infectious epidemics spread exponentially - very small and localised subepidemics within a community can spread to larger and more generalised ones over time, depending on the relative effectiveness of control efforts, particularly early on.
Remember that HIV has been in the US for well over 30 years. This is plenty of time for even the slowest spreading epidemic to accumulate substantial differences in prevalence rates in different subpopulations: you only need very small differences in the reproduction number (the average number of secondary infections per single infected case) to result in very large and exponentially increasing differences in prevalence and incidence after multiple generations of transmission. There can be numerous factors affecting the reproduction number, but one of the most important is the rate of infections that are undiagnosed.
To put it simply, people who are not aware they have HIV are much more likely to pass it on than people who are.
It is not necessary to posit substantial differences in rates of unprotected sex, "promiscuity", or needle sharing as the only way to account for the substantially higher HIV seroprevalence rates we see among African Americans in the late 2000s. Bauer appears to favor this explanation not only because of his almost complete ignorance of basic epidemiology, but also because of its rhetorical value in dog whistling anxieties about racial stereotyping - anxieties which perhaps lie close to the surface in the audience he is targeting with his pseudo-scholarship.
But even more obviously, Bauer ignores evidence that African Americans diagnosed with HIV progress to AIDS at much the same rates as HIV positive people of other ethnicities: 47% of incident AIDS diagnoses in 2007 and 49% of AIDS deaths were among blacks, compared to 28% of AIDS diagnoses and 29% of AIDS deaths which occurred in non-Hispanic whites.
Per capita, then, African Americans are not only seven to nine times more likely to be diagnosed with HIV, but in 2007 were nine times more likely to be diagnosed with AIDS or to die with AIDS than their white countrymen. If, as Bauer claims, the relatively high HIV seroprevalence among US blacks is because the overwhelming majority of HIV diagnoses are false positives due to cross reactions to race-specific antibodies, he is then left with the problem of explaining how it is that US blacks get otherwise rare AIDS-defining opportunistic diseases and die with AIDS at almost exactly the same ninefold higher rates that they supposedly test “false positive” to HIV.
What is arguably "racist", then, is to deliberately ignore or deny the excessive mortality and suffering of African Americans due to HIV/AIDS, and furthermore to seek for ignorant ideological reasons to undermine competent efforts to address the causes of the problem (such as efforts to reduce the rates of undiagnosed HIV). It might not be deliberate "racism" on Henry Bauer's part, but it sure is dumb.
A SECOND CENTRAL ELEMENT of Henry’s thesis is his “analysis” of the ratio in the US between blacks and whites of AIDS incidence over time, comparing that with HIV incidence.
Here the argument is that the ratio between blacks and whites for rates of incident AIDS does not match that of incident HIV infection. In the earliest years of the epidemic, rates of AIDS per black person and per white person were fairly similar. However, the impact of AIDS has increased over the course of the epidemic much faster for African Americans than for whites: by 2000, black people were six times as likely to be diagnosed with AIDS as whites (and as mentioned above, by 2007 they were nine times more likely to develop AIDS).
That is not in dispute. But what Bauer claims is that the relative incidence of HIV among blacks compared to whites has not changed over that period – and that therefore “HIV and AIDS are not correlated in their relative impact on white and black people”.
“In other words, the racial disparities as to AIDS were appreciably less than the disparities with respect to HIV; that again speaks against a correlation between HIV and AIDS...
...In the United States, the proportion of AIDS victims who are black has increased more than three-fold from the first appearance of AIDS to the present: from 14 percent in 1981 (KSOI 1982), to 25.5 percent for the period 1981-87, to 31.2 percent for 1988-92, to 38 percent during 1993-95, to 44.9 percent for 1996-2000 (MMWR 2001a)... Thus the ratio of black cases of AIDS changed from 0.20 to 0.43 to 0.62 to 0.90 to 1.32 – in other words by a factor of more than 6 over the course of 20 years. By contrast, the black to white ratio of F(HIV) has remained the same with no obvious change, for 20 years (Table 28).” (bold added)
- The Origin Persistence and Failings of HIV/AIDS Theory, p 106.
This of course is also an example of pseudoscholarship. “F(HIV)” is a term of Henry’s own invention which he uses variously and indiscriminately to stand for the incidence or sometimes the prevalence of diagnosed HIV, or specifically for the ratio of positive and negative diagnoses in a given study of a certain selected population at a particular time. Sometimes he uses it to refer not to HIV diagnoses, but the results of the initial antibody screening test – for example in infants born to HIV infected mothers, and in whom the presence of HIV antibodies is not diagnostic (you can’t distinguish between the infant’s own antibodies and those of maternal origin). It is not clear if he understands that these are (at least) four quite different things, and mixing them up botches the analysis and the conclusions you can validly draw.
In this case, he seems to be using the pseudo-term to stand for HIV prevalence (or maybe incidence?) throughout the black and white populations in the US over the period 1981-2000. He’s claiming that the proportion of the HIV positive population who are black has remained constant over that period.
In reality, it is very difficult to accurately estimate HIV seroincidence or seroprevalence over the whole country from early contemporaneous data for the simple reason that unlike AIDS diagnoses, HIV diagnoses were not notifiable on a consistent nationwide basis. They still aren’t: the most recent data on the CDC website estimates HIV diagnoses only for the 34 out of the 50 states that had long term confidential name based reporting.
Instead, what “Table 28” on p 107 of OPFHAT consists of is a collection of various studies performed at various times among disparately selected populations (army recruits, antenatal clinic attenders, gay men, college students) and not surprisingly the black/white ratio of incident diagnoses varies widely between different studies at different times in different populations, from as low as 1.5 in one study to 15.5 in another. There is no discernable pattern over time for the simple reason that each study is measuring completely different populations. They are not validly comparable. But no discernable pattern over time is not the same thing as constant over time.
Even here, though, Henry appears to have been somewhat selective in his choice of studies to support his contention, despite his insistence that “I did not omit any contradictory data about HIV test results, nor am I aware that any exist; I would appreciate being given the citation to any that I had failed to find.”
Not included in "Table 28" is, for example, a study by McNeil et al in 1991 of seroconversions among US military personnel. This is the follow-up study by the same authors of the very first reference of "Table 28", and is readily available in full free text on the net. This study is salient here, because unlike the mish-mash of studies in "Table 28" of OPFHAT which try to compare completely disparate groups in different study settings, McNeil et al compare seroconversions during three different periods between 1985 and 1989 in essentially the same population: soldiers in the US army, who were recurrently tested. And not surprisingly given what we know about changing racial patterns of AIDS diagnoses over time, what they find is that the ratio between white and black HIV diagnoses changes noticeably, even over that 4-5 year period:
Source: McNeil et al: Trends of HIV seroconversion among young adults in the US army, 1985 to 1989: JAMA 1991; 265: 1709-1714.
Of course, you cannot take a single study of the observed change in black/white ratio for seroincidence in the US army over a short period during the 1980s and extrapolate that to the entire US population over the entire course of the epidemic. But what McNeil et al found is at least consistent with the mainstream view that HIV incidence ratios by race have changed significantly over time, and is inconsistent with Henry’s utterly baseless claim that they have remained stable.
In summary, Bauer’s claim that “the black to white ratio of [HIV incidence or prevalence – I’m not sure what F(HIV) is supposed to refer to here] has remained the same with no obvious change, for 20 years” is not sustained by his data. The problem is that while it is almost certain that the disproportionate rates of HIV infection among African Americans has become more marked year by year over the past 30 years or so, there are no reliable notification data about HIV incidence in the US (and the relative proportions of African Americans and whites infected) from the earliest days of the epidemic.
This trick of finding a gap in the reliable surveillance data and then cherry picking studies or making up figures to fit the hypothesis is a common rhetorical strategy among HIV/AIDS denialists. Bauer does it frequently, and it’s the basis of much of Duesberg’s epidemiological argument. It is, for example, the basis of their notorious “1 million constant US seroprevalence ever since 1985” canard – a nonsense argument constructed from the fact that 1980s US HIV prevalence estimates were made not by counting HIV notifications (let alone actual infections in a given year), but were based largely on very rough back calculations from a relatively small number of notified AIDS cases and as a result had huge ranges of error.