Racial disparity in HIV incidence in MSM in the United States: how can it be reduced?

van Griensven, Fritsa,b; Stall, Ronald D.c

doi: 10.1097/QAD.0000000000000097
Editorial Comment
Author Information

aThai Red Cross AIDS Research Center and HIV Netherlands Australia Thailand Research Collaboration (HIVNAT), Bangkok, Thailand

bDivision of Preventive Medicine and Public Health, School of Medicine, University of California at San Francisco, California

cCenter for LGBT Health Research, Department of Behavioral and Community Health Sciences, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Correspondence to Dr Frits van Griensven, Thai Red Cross AIDS Research Center, 104 Ratchadamri Road, Patumwan, Bangkok 10330, Thailand. Tel: +66 900922908; e-mail: fritsvg@trcarc.org

Received 1 September, 2012

Revised 23 September, 2012

Accepted 23 September, 2012

Article Outline

In this issue of the Journal, Beer et al.[1] present the results of their firm study of differences in blood plasma HIV RNA viral load between HIV-infected Black and White MSM in the US, as a proxy for HIV infectiousness possibly explaining (part of) the racial disparity in HIV incidence between these two groups. On the basis of one of the most thorough and detailed analyses of factors driving racial health disparities in the Western world to date, Millet et al.[2–4] hypothesized assortative sexual mixing, higher background prevalence and incidence of sexually transmitted infections (STIs), and lower access, uptake and adherence to antiretroviral therapy (ART) among (HIV-infected) Black MSM as possible explanations for the higher HIV incidence within this subpopulation.

Beer et al.[1] analyzed data from a subpopulation of sexually active Black (n = 314) and White MSM (n = 696) out of 4217 persons (response rate 39%) who consented to interviews and medical file review, from a total sample of 9338 adults attending HIV care facilities throughout the US (The Medical Monitoring Project) [1]. After a process of weighting and adjustment, these 4217 individuals were reported to be representative for the 421 186 HIV-infected adults receiving HIV care in the US between January and May 2009 [1].

From their analyses, it appeared that whereas Black and White MSM did not differ in sexual behavior, Black MSM were less likely to be on ART (effect size 11%), and if on ART, they were less likely to be virally suppressed (effect size 21%). After adjustment for confounders in multivariable analysis, the difference in ART uptake persisted (effect size 7%), but the difference in viral suppression disappeared.

Whereas the differences in ART uptake and HIV viral suppression between Black and White MSM are in the expected direction, the magnitude of the dissimilarities seems to be too minimal to account for a substantial part of the six-fold difference in the rate of new HIV infections between them. This raises the question of what might then be driving these substantial disparities in HIV incidence rates between Black and White MSM. Thus, additional causes, such as sexual mixing patterns and their ramifications for the pool of circulating HIV-infecting viruses, and the role of prevalent and incident STIs as HIV transmission facilitating co-factors among Black and White MSM [2–4], need to be evaluated more in detail to see if they can help unravel the reasons behind the huge difference in HIV incidence. For example, increased intra-racial mixing among Black MSM may be associated with recycling of phenotypic representations of HIV with a successful history of previous transmissions, such as those found clustering or in chains of transmission associated with acute and early HIV infection [5–8]. Disregarding the absence of vast differences in ART uptake and HIV viral expression between Black and White MSM, the choice of blood plasma HIV viral load as a proxy for HIV infectiousness in MSM is less than perfect. This proxy assumption relies for a large part on the results of the HIV Prevention Trials Network 052 study [9], conducted among HIV serodiscordant couples. However, only 3% of couples in that study were nonheterosexual, too few to extend its internal validity to the male homosexual population. In addition, the question of whether it is possible to equate the penile–vaginal heterosexual environment from couples recruited from four different continents with the highly inflammatory challenged and possibly damaged penile rectal environment among MSM in the US deserves a lot more caution than it has received to date. Moreover, in a recent study in 114 MSM with suppressed blood plasma HIV RNA (also from the US), 10% had detectable HIV RNA and 63% had evidence of at least one type of herpes virus in seminal fluid [10]. It should also be mentioned that a trend for an association was observed between cytomegalovirus (CMV) expression, Epstein–Barr virus presence and HIV RNA in seminal fluid, whereas CMV was found predictive of seminal HIV RNA [8]. In addition, it is important to note that mounting phylogenetic and molecular epidemiologic evidence suggests that in rising or ongoing HIV epidemics among MSM, acute HIV infection (AHI) may account for up to 50% or more of new HIV infections [5–8]. And this proportion may further increase in the presence of biological or behavioral co-factors in the index case or host, such as STIs or penile–rectal trauma associated with high-intensity sexual contact with multiple different consecutive sexual partners associated with the use of stimulant and erectile dysfunction agents [11,12]. In this scenario, most new HIV infections will have already occurred before ART for prevention is initiated. Alternatively, early ART can make a substantial difference by interrupting the AHI transmission chain, if it is initiated early enough. Recently, a study among 90 MSM with AHI in Bangkok, Thailand, demonstrated that immediate administration of ART following AHI detection was associated with an instant sharp drop in HIV RNA viral load in blood plasma, seminal fluid and ano-rectal lavage specimens, with 73% of patients having undetectable HIV RNA in seminal plasma at week 4 and close to 100% having undetectable viral load in all compartments by week 12 [13]. By contrast, seminal HIV viral load levels have been shown to peak at 30 days after HIV acquisition in untreated individuals [14]. In addition, HIV transmission risk behavior (unprotected anal intercourse) fell by 70–85% (dependent on partner type) upon learning about AHI, reductions sustained through 48 weeks of follow-up [13]. Furthermore, in these early treated men, HIV disease prognosis improved considerably, with 90% having undetectable cell-integrated HIV RNA in peripheral blood mononuclear cells, commensurate with ‘Elite Controllers’ of HIV infection [15,16]. However, even if such an early combined equipoised curative and preventive intervention could be successfully replicated among MSM in the US, the difference between Black and White MSM may not disappear. These and other types of racial health disparities will only be reduced or eliminated if the structural barriers in timely access to high-quality healthcare for Black people in general and for Black MSM in particular are resolved [2–4].

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Conflicts of interest

There are no conflicts of interest.

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antiretroviral therapy; health status disparities; men who have sex with men; surveillance; viral load

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