Mayaud P., Legoff J., Weiss H.A., Grésenguet G., Nzambi K., Bouhlal H., Frost E., Pépin J., Malkin J.-E., Hayes R.J., Mabey D.C.W., Bélec L.
Clinical Research Unit, Department of Infectious and Tropical Diseases, Paris, France; Infectious Disease Epidemiology Unit, Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, United Kingdom; Université Paris Descartes, Equipe Immunité et Biothérapie Muqueuse, Hôpital Européen Georges Pompidou, Paris, France; Université Paris Diderot, Laboratoire de Microbiologie, Hôpital Saint-Louis, Paris, France; Centre Médical, Institut Pasteur, Paris, France; Centre National de Reference des Maladies Sexuellement Transmissibles et du SIDA de Bangui, Unité de Recherches et d'Intervention sur les Maladies Sexuellement Transmissibles et du SIDA, Central African Republic, Accra, Ghana; West African Project to Combat AIDS and STIs, Accra, Ghana; Centre for International Health, University of Sherbrooke, Sherbrooke, QC, Canada; Clinical Research Unit, School of Hygiene and Tropical Medicine, Keppel St, London WC1E 7HT, United Kingdom
Mayaud, P., Clinical Research Unit, Department of Infectious and Tropical Diseases, Paris, France, Clinical Research Unit, School of Hygiene and Tropical Medicine, Keppel St, London WC1E 7HT, United Kingdom; Legoff, J., Université Paris Descartes, Equipe Immunité et Biothérapie Muqueuse, Hôpital Européen Georges Pompidou, Paris, France, Université Paris Diderot, Laboratoire de Microbiologie, Hôpital Saint-Louis, Paris, France; Weiss, H.A., Infectious Disease Epidemiology Unit, Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, United Kingdom; Grésenguet, G., Centre National de Reference des Maladies Sexuellement Transmissibles et du SIDA de Bangui, Unité de Recherches et d'Intervention sur les Maladies Sexuellement Transmissibles et du SIDA, Central African Republic, Accra, Ghana; Nzambi, K., West African Project to Combat AIDS and STIs, Accra, Ghana; Bouhlal, H., Université Paris Descartes, Equipe Immunité et Biothérapie Muqueuse, Hôpital Européen Georges Pompidou, Paris, France; Frost, E., Centre for International Health, University of Sherbrooke, Sherbrooke, QC, Canada; Pépin, J., Centre for International Health, University of Sherbrooke, Sherbrooke, QC, Canada; Malkin, J.-E., Centre Médical, Institut Pasteur, Paris, France; Hayes, R.J., Infectious Disease Epidemiology Unit, Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, United Kingdom; Mabey, D.C.W., Clinical Research Unit, Department of Infectious and Tropical Diseases, Paris, France; Bélec, L., Université Paris Descartes, Equipe Immunité et Biothérapie Muqueuse, Hôpital Européen Georges Pompidou, Paris, France
Background. Little is known about the impact of episodic treatment of herpes on human immunodeficiency virus type 1 (HIV-1). Methods. Women from Ghana and the Central African Republic who had genital ulcers were enrolled in a randomized, double-blind, placebo-controlled trial of acyclovir plus antibacterials and were monitored for 28 days. Ulcer etiologies and detection of lesionai HIV-1 RNA were determined by polymerase chain reaction (PCR). Cervicovaginal HIV-1 RNA and herpes simplex virus type 2 (HSV-2) DNA and plasma HIV-1 RNA were quantitated by real-time PCR. Primary analyses included 118 HIV-1-infected women with HSV-2 ulcers (54 of whom were given acyclovir and 64 of whom were given placebo). Results. Acyclovir had little impact on (1) detection of cervicovaginal HIV-1 RNA (risk ratio [RR], 0.96; 95% confidence interval [CI], 0.8-1.2) at day 7 of treatment, (2) the mean cervicovaginal HIV-1 RNA load (-0.06 log10 copies/mL; 95% CI, -0.4 to 0.3 log10 copies/mL) at day 7 of treatment, or (3) the plasma HIV-1 RNA load (+0.09 log10 copies/mL; 95% CI, -0.1 to 0.3 log10 copies/mL) at day 14 of treatment. At day 7, women receiving acyclovir were less likely to have detectable lesionai HIV-1 RNA (RR, 0.70; 95% CI, 0.4-1.2) or cervicovaginal HSV-2 DNA (RR, 0.69; 95% CI, 0.4-1.3), had a lower quantity of HSV-2 DNA (-0.99 log10 copies/mL; 95% CI, -1.8 to -0.2 log10 copies/mL), and were more likely to have a healed ulcer (RR, 1.26; 95% CI, 0.9-1.9). Conclusion. Episodic therapy for herpes reduced the quantity of cervicovaginal HSV-2 DNA and slightly improved ulcer healing, but it did not decrease genital and plasma HIV-1 RNA loads. Trial registration. ClinicalTrials.gov identifier NCT00158483. © 2009 by the Infectious Diseases Society of America. All rights reserved.