The recent paper by Brown and colleagues  concerning the impact of incident and prevalent herpes simplex virus type 2 (HSV-2) on the acquisition of HIV among women in Uganda and Zimbabwe provides further evidence for the role of the former in the spread of the latter and confirms the results of an earlier longitudinal study among female sex workers  and a recent meta-analysis . Of particular importance is the relative contribution of incident and prevalent herpes simplex virus infection. Brown and colleagues  show that incident HSV-2 infection has a greater impact on the risk of HIV acquisition than does prevalent HSV-2 infection. The hazard ratio for the risk of acquiring HIV among individuals with incident and prevalent infection does not, however, quite reach significance at the 5% level in either of their two data sets. In Figure 1 we compare the data given by Brown and colleagues  with the corresponding data from South Africa .
The three estimates do not differ significantly and the weighted average hazard ratio suggests that women with incident HSV-2 infections are 2.46 (1.53–3.95) times more likely to be infected with HIV-1 than women with prevalent HSV-2 infections. These data suggest that the risk of acquiring HIV-1 infections wanes over time after infection with HSV-2, but none of the studies provide sufficient data to measure the rate at which this happens directly. The South African study may tend to give a higher estimate than the studies carried out in Uganda and Zimbabwe because of the much shorter time between visits (one month versus 3 months), which would mean that women were identified as being HSV-2 positive sooner after being infected in South Africa than in Uganda. Furthermore, the South African women were sex workers and at a higher overall risk with an HSV-2 incidence over the course of the study of 35% per year compared with 10 and 9% in Uganda and Zimbabwe, respectively, .
In a study in Carletonville, South Africa, among young adults from the general population  HIV infection was very strongly associated with HSV-2 infection; the odds ratios for HIV infection among those with and without HSV-2 infection was 5.3 (2.7–10.3) for men and 8.4 (4.9–14.2) for women. Furthermore, by the time they reached 24 years of age, 89% of women and 51% of men were infected with HSV-2. The high population prevalence and the very high incidence of HSV-2 among women between the ages of 15 and 25 years adds to the urgency of finding ways to prevent and manage HSV-2 infection.
We fully endorse the conclusions drawn by Brown and colleagues  concerning the need to find ways to control HSV-2 as part of the overall strategy for controlling HIV. If, as seems to be the case, the effect of HSV-2 on HIV acquisition wanes over time then prevention of HSV-2 is likely to be even more effective for HIV prevention than cure or symptomatic treatment of HSV-2. The study in South Africa adds important evidence in support of their arguments, especially in protecting young women from being infected with HIV.
We thank Peter Ghys for helpful comments and suggestions during the preparation of this manuscript.
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