New studies and meta-analyses confirm the association of HIV acquisition and transmission with recent STI, although there is considerable heterogeneity between organisms and populations. Much of the recent evidence relates to HSV-, where the population attributable risk (PAR) percent for HSV- is between  andin Africa. Mathematical models show how transmission attributable to STI varies with HIV epidemic phase, and HSV- becomes increasingly important as the epidemic matures. HSV- suppressive therapy reduces HIV concentrations in plasma and the genital tract in people co-infected with HSV, in part due to direct inhibition of HIV reverse transcriptase. Recent trials of HSV- suppressive therapy have not shown an impact on the risk of HIV acquisition, nor in controlling transmission from dually infected people to their sero-discordant heterosexual partners.

Although there is a plausible link between STI and HIV risk, intervention studies continue to be disappointing. This does not disprove a causal link, but mechanisms of action and the design and implementation of interventions need to be better understood. There is a strong association between bacterial and viral sexually transmitted pep hiv infections and both the acquisition and transmission of HIV infection. This was first demonstrated in case series and retrospective studies that showed an association between previous sexually transmitted infections (STI) and human immunodeficiency virus (HIV). Prospective studies strengthened this observation by showing a link between STI and incident HIV infection, with the strongest relative risks for genital ulcer disease but potentially large attributable risks from more common inflammatory conditions such as trichomoniasis.  Such evidence has continued to accumulate over the decades, but has remained difficult to interpret because of confounding due to shared risk factors, particularly sexual behaviour, and difficulties in determining temporal relationships.

In addition to the epidemiological evidence, biological findings support the mechanisms for STI increasing HIV acquisition and transmission through direct mucosal disruption, recruitment of HIV target cells to the genital tract, and by increased HIV load in plasma and genital secretions. Further synergies are described whereby HIV can alter the natural history of some STI.  These observations, together with the fact that HIV itself is a sexually transmitted infection, have underpinned calls for STI management to be an essential part of HIV control programmes. However, results of intervention studies have been disappointing. Several large, well conducted trials of enhanced STI treatment and care have failed to show a consistent impact on HIV incidence. The Mwanza study in Tanzania in the early s showed a reduction in HIV incidence of  with enhanced syndromic management of STI, but others have not.  Interpretation of these results rests on an understanding of different epidemic type and phase, Mwanza was conducted in a period of concentrated epidemic while the others were generalised, and whether the interventions were appropriate for the STI with the largest attributable risk fraction.

In this article we review evidence about the link between STI and HIV transmission and consider implications for control programmes. We start with a summary of recent epidemiological and modelling studies that cast light on the association of HIV with a number of STI, including those concerning mechanisms and biological plausibility. We then focus on evidence concerning the role of herpes simplex virus type  in sexual transmission of HIV, which has been thought to be key to understanding some of the disparity between earlier observational and interventional studies. New studies and meta-analyses confirm the association of HIV acquisition and transmission with recent STI, although there is considerable heterogeneity between organisms and populations as peviously described. Evidence of the association comes from ecological, cross sectional, case control and cohort studies. Most of these designs, with the exception of cohort studies, are unable to distinguish between causation, reverse causation and confounding due to a common causal pathway,  although some have tried to do this through using innovative designs.

The ecological association between HIV and STI has been reported in the USA, where higher rates of HIV occur in African American than white or Hispanic populations , which is thought to be in part due to the disproportionate burden of STI in this group. In Belgium there are also overlapping epidemics in men who have sex with men (MSM) where there are high numbers of HIV diagnoses and of incident STI. Such associations are subject to ecological fallacy, but similar findings are reproduced in individual-based cross sectional studies, including in African American drug using women in the USA and clients of female sex workers in Mexico. Braunstein and colleagues reviewed data around HIV incidence in sub-Saharan Africa;  studies looking at the impact of current or recent STI found an increased HIV risk, the remaining  found no association. The highest STI risk was found for HSV-seropositivity. A retrospective study of acute HIV infection in one part of the USA measured the association with having had an STI in the previous month. ]MSM were far less likely to have had an STI than heterosexual men or women, and most co-infections were in non-whites suggesting the importance of the overlapping HIV and STI epidemics in the black population in North Carolina.

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