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Still Not Understanding the Uneven Spread of HIV Within Africa


Sexually Transmitted Diseases: June 2004 - Volume 31 - Issue 6 - p 365
Letter to the Editor

*Independent Consultant, Colorado Springs, Colorado, †Independent Consultant, Hershey, Pennsylvania, ‡Institute of Medical Psychology and Behavioral Neurobiology, University of Tübingen, Tübingen, Germany

Correspondence: John J. Potterat, 301 S. Union Blvd., Colorado Springs, CO 80910. E-mail:

To the Editor:

Boerma and colleagues recently reported their failure to find differences in sexual variables that could explain why HIV prevalence is higher in Manicaland, Zimbabwe (15.4% in men, 21.1% in women) than in Kisesa, Tanzania (5.3% in men, 8.0% in women). 1 In their words, “there are at least as many factors that point to lower HIV transmission in Manicaland compared to Kisesa”; the variables they considered “did not explain the much higher HIV prevalence found in Manicaland.” This negative finding is important. After 20 years of research to elucidate patterns of HIV transmission in sub-Saharan Africa, epidemiologists have failed to identify even a single sexual variable that is an important personal risk for HIV acquisition and that is consistently higher in communities with higher HIV prevalence. The scope of this failure is staggering when one considers not only the substantial resources that have been expended to this enterprise, but also the large differences between epidemic trajectories in Africa. Whatever is causing these differences should not be so elusive. Failure makes sense if one considers that a substantial proportion of HIV transmission in Africa must not be mediated by sexual contact.

Boerma and colleagues’ analysis neatly complements the recent 4-cities study, which reported that high-risk sexual behaviors (partner change, sex with prostitutes, concurrent partners, and low condom use) and the presence of bacterial sexually transmitted disease (STD) was “not more common in the two high HIV prevalence cities” compared with the 2 cities with low HIV prevalence. 2 The 4-cities team hypothesized that herpes simplex virus 2 (HSV-2) and lack of male circumcision, which were more common in the cities with high prevalence, played a critical role in determining different epidemic trajectories. 3 Boerma and colleagues confirmed these negative findings about sexual behaviors and bacterial STD. They also notably “found little evidence” to support the hypothesis that differences in circumcision and HSV-2 prevalence explain differential HIV trajectories. 1

What next? One option is to continue searching for sexual variables to explain HIV epidemics in Africa. Given results to date, that would be a scientific gamble, with millions of lives at stake. Einstein defined insanity as “doing the same thing over and over again and expecting different results.” 4 We recommend enlarging the list of risk factors 5 to include evaluation of blood exposures in (especially sex-related) health care, 6,7 of scarification, and of other sexual variables, especially anal intercourse. 8

Aside from its unfortunate failure to consider nonsexual transmission, Boerma and colleagues’ study is a credit to their management and scientific skills. We appreciate their negative findings, for they point away from “heterosexual” transmission for “understanding the uneven spread of HIV within Africa.” As for nonsexual risks, we note that surveys conducted in Kisesa in 1994 to 1995 and 1996 to 1997, from which Boerma and colleagues obtained sexual and socioeconomic data, also collected information on medical injections, 9 which have not yet been published. We ask that they report available data on the association of HIV incidence and injections.




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1. Boerma JT, Gregson S, Nyamukapa C, Urassa M. Understanding the uneven spread of HIV within Africa. Sex Transm Dis 2003; 30:779–787.
2. Buve A, Carael M, Hayes RJ, et al. The multicentre study on factors determining the differential spread of HIV in four African cities: Summary and conclusions. AIDS 2001; 15(suppl 4):S127–S131.
3. Auvert B, Buve A, Ferry B, et al. Ecological and individual level analysis of risk factors for HIV infection in four urban populations in sub-Saharan Africa with different levels of HIV infection. AIDS 2001; 15(suppl 4):S15–S30.
4. Albert Einstein. Available at: http.// Accessed November 5, 2003.
5. Brody S, Potterat JJ. Establishing valid AIDS monitoring and research in countries with generalized epidemics. Int J STD AIDS 2004; 15:1–6.
6. Gisselquist D, Potterat JJ, Brody S, Vachon F. Let it be sexual: How health care transmission of AIDS in Africa was ignored. Int J STD AIDS 2003; 14:148–161.
7. Gisselquist D, Rothenberg R, Potterat JJ, Drucker E. HIV infections in sub-Saharan Africa not explained by sexual or vertical transmission. Int J STD AIDS 2002; 13:657–666.
8. Brody S, Potterat JJ. Assessing the role of anal intercourse in the epidemiology of AIDS in Africa. Int J STD AIDS 2003; 14:431–436.
9. Bloom SS, Urassa, Insigo R, Ng’weshemi J, Boerma JT. Community effects on the risk of HIV infection in rural Tanzania. Sex Transm Infect 2002; 78:261–266.
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