Genital herpes implicated in up to half of all HIV infections in some African countries

Keith Alcorn
Published: 27 August 2007

Up to half of all HIV infections in some African countries with long-standing HIV epidemics may be due to the presence of genital herpes and and its cause, HSV-2, in HIV-positive people or their partners, epidemiologists from the London School of Hygiene and Tropical Medicine estimate.

Their projections, published this month in a supplement to the journal Sexually Transmitted Infections, are drawn from data accumulated during the Four Cities study, which compared trends in HIV prevalence in four African cities in different regions, and from local trends data from each city.

A previous meta-analysis of published studies carried out by the same research group estimated that 38-60% of new HIV infections in African women and 8-49% of new infections in African men could be attributed to HSV-2, depending on HSV-2 prevalences that ranged from 29% to 71% in women and 5% to 53% in men.

The investigators wanted to model the interactions between HIV transmission and sexually transmitted infections over time in order to pinpoint when interventions against HSV-2 and curable sexually transmitted infections would have the greatest relative impact.

They used data on HSV-2, chancroid, syphilis, gonorrhoea and chlamydia infections, as well as modelling HIV incidence. However the main focus was the interaction between HSV-2 and HIV.

Results

The study found that over time, in each city, the proportion of HIV infections attributable to genital herpes rose, and the proportion attributable to other sexually transmitted infections (including chancroid) fell.

Five years after the introduction of HIV, HSV-2 was implicated in between 8% and 30% of infections varying by city. Fifteen years into the epidemic, the proportion had grown to between 35% and 48% of HIV infections varying by city. The highest proportion of infections due to HSV-2 was seen in Cotonou in Benin, where the rate of other STIS fell markedly over time due to intensive STI treatment in commercial sex workers.

In Yaoundé, Cameroon, the proportion of infections attributable to HSV-2 levelled off around 37% after ten years, due in part to strong uptake of condoms in the early 1990s.

Chancroid’s role in amplifying HIV transmission declined; while it had an important role in establishing the HIV epidemic in three of the four cities, its influence declined as syndromic treatment of STIs became established during the 1990s.

The authors observe that, according to their model, “at the current stage of the HIV epidemics, and given the current level of condom use and provision of STI treatment services, further strengthening of treatment services for curable STIs may be expected to produce little additional gain. However, withdrawing those services would most likely result in increased prevalence of curable STIs and increased HIV transmission.”

HSV-2 infection appears to drive up HIV incidence over time, and become responsible for a larger proportion of HIV infections at a population level, the authors suggest, more because of its effect on infectivity, rather than because it makes HIV-negative people more susceptible to HIV infection.

The increased infectivity is more important, they think, because individuals with HSV-2 and HIV may have multiple partners and may have increased levels of HIV in their genital fluids for long periods as a result of HSV-2 infection, whereas genital herpes lesions in an HIV-negative person only make that person vulnerable while the lesions are present.

The authors also point out that trials of HSV-2 interventions need to be designed and interpreted in the light of these findings, since the stage of the HIV epidemic in a location and variables such as condom use and incidence of other sexually transmitted infections clearly modulate the interaction between HIV and HSV-2 and could affect the results of trials.

Recently reported studies of HSV-2 interventions have found that treatment with valaciclovir, a drug that suppresses HSV-2, reduced HIV shedding in HIV-positive women, but the effect of aciclovir (a similar drug) appeared modest in two studies in HIV-positive women. All these studies followed women for a relatively short time.

The only study to look at HIV incidence, in HIV-negative women with HSV-2 infection, found that daily aciclovir therapy did not reduce the risk of HIV infection, possibly due to poor adherence.

Assumptions in the model

  • Primary ulceration lasts three weeks and ulcers recur every two and half to three months for the first two years, and every six to eight months during the following ten years. After the primary infection, ulceration lasts for one week.
  • The per-contact probability of transmission from men to women was 0.30 during the primary infection and 0.20 during later infection if an ulcer was present, with a much lower per-contact probability associated with HSV-2 shedding during latent infection (0.01 per contact during the first two years, and 0.005 subsequently).
  • HIV infection increases ulcer duration and recurrence fourfold.
  • Presence of primary herpetic and chancroid lesions increased the per contact risk of HIV transmission 25-fold
  • Since recurrent ulcers were assumed to last for a shorter period, they were assumed to account for a tenfold increase in the per contact risk of transmission.
  • Syphilis increased the per contact risk of HIV transmission sevenfold, gonorrhoea and chlamydia threefold.

Reference

Freeman EE et al. Proportion of new HIV infections attributable to herpes simplex 2 increases over time: simulations of the changing role sexually transmitted infections in sub-Saharan African HIV epidemics. Sex Transm Infect 83 (suppl 1): i17-i24, 2007.

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