Delany S., Mlaba N., Clayton T., Akpomiemie G., Capovilla A., Legoff J., Belec L., Stevens W., Rees H., Mayaud P.
Reproductive Health and HIV Research Unit, University of Witwatersrand, Johannesburg, South Africa; Clinical Research Unit and Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom; Department of Molecular Medicine and Haematology, University of Witwatersrand, Johannesburg, South Africa; Laboratoire de Microbiologie, Hôpital Saint-Louis, France; Université Paris V, Centres de Recherches Biomédicales des Cordeliers and Laboratoire de Virologie, Hôpital Européen Georges Pompidou, Paris, France; Reproductive Health and HIV Research Unit, University of the Witwatersrand, PO Box 18512, Hillbrow, Johannesburg 2038, South Africa
Delany, S., Reproductive Health and HIV Research Unit, University of Witwatersrand, Johannesburg, South Africa, Clinical Research Unit and Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom, Reproductive Health and HIV Research Unit, University of the Witwatersrand, PO Box 18512, Hillbrow, Johannesburg 2038, South Africa; Mlaba, N., Reproductive Health and HIV Research Unit, University of Witwatersrand, Johannesburg, South Africa; Clayton, T., Clinical Research Unit and Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom; Akpomiemie, G., Reproductive Health and HIV Research Unit, University of Witwatersrand, Johannesburg, South Africa; Capovilla, A., Department of Molecular Medicine and Haematology, University of Witwatersrand, Johannesburg, South Africa; Legoff, J., Laboratoire de Microbiologie, Hôpital Saint-Louis, France; Belec, L., Université Paris V, Centres de Recherches Biomédicales des Cordeliers and Laboratoire de Virologie, Hôpital Européen Georges Pompidou, Paris, France; Stevens, W., Department of Molecular Medicine and Haematology, University of Witwatersrand, Johannesburg, South Africa; Rees, H., Reproductive Health and HIV Research Unit, University of Witwatersrand, Johannesburg, South Africa; Mayaud, P., Clinical Research Unit and Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom
Background: Several studies suggest that herpes simplex virus type 2 (HSV-2) may enhance HIV-1 transmission and disease progression. Methods: We conducted a randomized, double-blind, placebo-controlled trial of aciclovir 400 mg twice daily for 3 months in 300 HSV-2/HIV-1 co-infected women not yet on highly active antiretroviral therapy (HAART). Participants were evaluated prerandomization and at monthly visits for 3 months. Primary outcomes were the detection and quantity of genital HIV-1 RNA at the month 3 (M3) visit. Analyses were also undertaken using data from all visits. The treatment effects on plasma HIV-1 RNA, CD4 + cell count and genital HSV-2 DNA were also assessed. Results: At M3 fewer women had detectable genital HIV in the aciclovir group compared to placebo, but this was not significant [61/132 (46%) vs. 71/137 (52%), risk ratio (RR) 0.89, 95% confidence interval (CI) 0.70-1.14; P = 0.36]. There was also little difference in quantity of HIV-1 RNA among shedders(+0.13 log 10 copies/ml, 95% CI -0.14 to 0.39) at M3. However, aciclovir significantly decreased the frequency of HIV-1 shedding over all visits [adjusted odds ratio (OR) 0.57, 95% CI 0.36-0.89]. Significant reductions in M3 plasma HIV-1 RNA (-0.34 log 10 copies/ml, 95% CI 0.15-0.54), genital HSV-2 DNA (8 vs. 20%, RR 0.37, 95% CI 0.19-0.73) and genital ulceration (8 vs. 18%, RR 0.43, 95% CI 0.22-0.84) were observed in the aciclovir group. Conclusion: HSV-2 suppressive therapy, by reducing HIV-1 plasma viral load and altering the pattern of genital HIV-1 shedding, may contribute to the reduction in sexual transmission of HIV-1 and may delay the requirement for HAART initiation. © 2009 Wolters Kluwer Health|Lippincott Williams & Wilkins.