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The proportion of new HIV infections attributable to HSV- 2 increases over time: simulations of the changing role of sexually transmitted infections in sub-Saharan African HIV epidemics
  1. Esther E Freeman (esther_freeman{at}hms.harvard.edu)
  1. London School of Hygiene and Tropical Medicine/secondarily, Harvard Medical School, United Kingdom
    1. Kate Orroth (korroth{at}adelphia.net)
    1. London School of Hygiene and Tropical Medicine, United Kingdom
      1. Richard White (richard.white{at}lshtm.ac.uk)
      1. London School of Hygiene and Tropical Medicine, United Kingdom
        1. Judith R Glynn
        1. London School of Hygiene and Tropical Medicine, United Kingdom
          1. Roel Bakker
          1. Erasmus MC, University Medical Center Rotterdam, Netherlands
            1. Marie-Claude Boily
            1. Imperial College, United Kingdom
              1. Dik Habbema
              1. Erasmus MC, University Medical Center Rotterdam, Netherlands
                1. Anne Buve (abuve{at}itg.be)
                1. Institute of Tropical Medicine, Belgium
                  1. Richard Hayes
                  1. London School of Hygiene and Tropical Medicine, London, UK, United Kingdom

                    Abstract

                    Objective: To understand the changing impact of HSV-2 and other sexually transmitted infections (STI) on HIV incidence over time in four sub-Saharan African cities using simulation models.

                    Methods: An individual-based stochastic model was fitted to demographic, behavioural and epidemiological data from cross-sectional population-based surveys in four African cities (Kisumu, Kenya; Ndola, Zambia; Yaounde, Cameroon; and Cotonou, Benin) in 1997. To estimate the proportion of new HIV infections attributable to HSV-2 and other STIs over time, HIV incidence in the fitted model was compared to that in model scenarios in which the cofactor effect of the STIs on HIV susceptibility and infectivity were removed 5, 10, 15, 20, and 25 years into the simulated HIV epidemics.

                    Results: The proportion of incident HIV attributable to HSV-2 infection (the model estimated population attributable fraction, PAFM) increased with maturity of the HIV epidemic. In the different cities, the PAFM was 8%-31% 5 years into the epidemic, but rose to 35%-48% 15 years after the introduction of HIV. In contrast, the proportion of incident HIV attributable to chancroid decreased over time with strongest effects 5 years after HIV introduction, falling to no effect 15 years after. Sensitivity analyses showed that, in the model, recurrent HSV-2 ulcers had more of an impact on HIV incidence than did primary HSV-2 ulcers, and that the effect of HSV-2 on HIV infectivity may be more important for HIV spread than the effect on HIV susceptibility, assuming that HSV-2 has similar cofactor effects on HIV susceptibility and infectivity. The overall impact of other curable STIs on HIV spread (syphilis, gonorrhoea, and chlamydia) remained relatively constant over time.

                    Conclusions: Although HSV-2 appears to have a limited impact on HIV incidence in the early stages of sub-Saharan African HIV epidemics, when the epidemic is concentrated in core groups, it has an increasingly large impact as the epidemic progresses. In generalised HIV epidemics where control programs for curable STIs are already in place, interventions against HSV-2 may have a key role in HIV prevention.

                    • Epidemiology
                    • HIV
                    • Herpes (HSV-2)
                    • Mathematical Modelling

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