Abstract

Objectives: Previous studies have found that recurrent or persistent co-infectionsmay increase HIV viral load (VL) in plasma and genital secretions. This elevation in HIV VLmay increase the risk of HIV transmission, thus increasing HIV incidence. We evaluated the association between malaria, herpes simplex type 2 (HSV-2) and tuberculosis (TB) co-infections and their treatment on HIV VL. Design: Systematic review andmeta-analysis of the association of malaria, HSV-2 and TB co-infections and their treatment on HIV VL. Methods: PubMed and Embase databases were searched to February 10th 2010 for studies in adults that reported HIV plasma and/or genital VL by co-infection status or treatment. Studies that adjusted for CD4 count or time since infectionwere included.Metaanalyses were conducted using random-effects models. Results: Forty-fiveeligible articleswere identified (6malaria, 20 HSV-2 and19 tuberculosis). Therewas strong evidence of increased HIVVLwith acutemalaria (0.67 log10 copies/mL, 95%CI: 0.15, 1.19) and decreased VL following treatment (-0.37 log10 copies/mL, 95% CI: -0.70, -0.04). HSV-2 infectionwas also associatedwith increased HIV VL (0.18 log10 copies/mL, 95% CI: 0.01, 0.34), which decreased withHSVsuppressive therapy (-0.28 log10copies/mL, 95%CI: -0.36, -0.19). Active tuberculosis was associated with increased HIV VL (log10 copies/mL 0.40, 95% CI: 0.13-0.67), but there was no association between tuberculosis treatment and VL reduction (log10 copies/mL -0.02, 95% CI -0.19, 0.15). Conclusions: Co-infections may increase HIV VL in populations where they are prevalent, thereby facilitating HIV transmission. Treatment or co-infection prophylaxis could reverse the effect of co-infections. However, to limit HIV trajectory and optimize positive prevention for HIV-infected individuals pre-ART, we must better understand the mechanisms responsible for augmented VL and the magnitude of VL reduction required, and retune treatment regimens accordingly.

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