• Myron S Cohen, Ying Q Chen, Marybeth McCauley, Theresa Gamble, Mina C Hosseinipour, Nagalingeswaran Kumarasamy, James G Hakim, Johnstone Kumwenda, Beatriz Grinsztejn, Jose H S Pilotto, Sheela V Godbole, Suwat Chariyalertsak, Breno R Santos, Kenneth H Mayer, Irving F Hoffman, Susan H Eshleman, Estelle Piwowar-Manning, Leslie Cottle, Xinyi C Zhang, Joseph Makhema, Lisa A Mills, Ravindre Panchia, Sharlaa Faesen, Joseph Eron, Joel Gallant, Diane Havlir, Susan Swindells, Vanessa Elharrar, David Burns, Taha E Taha, Karin Nielsen-Saines, David D Celentano, Max Essex, Sarah E Hudelson, Andrew D Redd, Thomas R Fleming, and HPTN 052 Study Team.
• From the Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill (M.S.C., M.C.H., I.F.H., J.E.); the Divisions of Vaccine and Infectious Disease (Y.Q.C., X.C.Z.) and Public Health Science (Y.Q.C.) and the Statistical Center for HIV/AIDS Research and Prevention (L.C.), Fred Hutchinson Cancer Research Center, and the Department of Biostatistics, University of Washington (T.R.F.) - both in Seattle; FHI 360, Washington, DC (M.M.), and Durham, NC (T.G.); Y.R. Gaitonde Center for AIDS Research and Education, Chennai (N.K.), and National AIDS Research Institute, Pune (S.V.G.) - both in India; University of Zimbabwe, Harare (J.G.H.); College of Medicine-Johns Hopkins Project, Blantyre, Malawi (J.K.); Instituto de Pesquisa Clinica Evandro Chagas (B.G.) and Hospital Geral de Nova Iguacu and Laboratorio de AIDS e Imunologia Molecular-IOC/Fiocruz (J.H.S.P.), Rio de Janeiro, and Servico de Infectologia, Hospital Nossa Senhora da Conceicao/GHC, Porto Alegre (B.R.S.) - both in Brazil; Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand (S.C.); Fenway Institute (K.H.M.) and Harvard School of Public Health (M.E.) - both in Boston; the Departments of Pathology (S.H.E., E.P.-M., S.E.H.) and Medicine (A.D.R.), Johns Hopkins University School of Medicine, the Department of Epidemiology, Bloomberg School of Public Health (T.E.T.), and Johns Hopkins Bloomberg School of Public Health (D.D.C.), Baltimore, and the Division of AIDS (V.E., D.B.) and Laboratory of Immunoregulation (A.D.R.), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda - both in Maryland; Botswana Harvard AIDS Institute, Gaborone (J.M.); Centers for Disease Control and Prevention (CDC) Division of HIV/AIDS Prevention/KEMRI-CDC Research and Public Health Collaboration HIV Research Branch, Kisumu, Kenya (L.A.M.); Perinatal HIV Research Unit (R.P.) and Clinical HIV Research Unit, Department of Medicine, Faculty of Health Scien
• N. Engl. J. Med. 2016 Sep 1; 375 (9): 830-9.

BackgroundAn interim analysis of data from the HIV Prevention Trials Network (HPTN) 052 trial showed that antiretroviral therapy (ART) prevented more than 96% of genetically linked infections caused by human immunodeficiency virus type 1 (HIV-1) in serodiscordant couples. ART was then offered to all patients with HIV-1 infection (index participants). The study included more than 5 years of follow-up to assess the durability of such therapy for the prevention of HIV-1 transmission.MethodsWe randomly assigned 1763 index participants to receive either early or delayed ART. In the early-ART group, 886 participants started therapy at enrollment (CD4+ count, 350 to 550 cells per cubic millimeter). In the delayed-ART group, 877 participants started therapy after two consecutive CD4+ counts fell below 250 cells per cubic millimeter or if an illness indicative of the acquired immunodeficiency syndrome (i.e., an AIDS-defining illness) developed. The primary study end point was the diagnosis of genetically linked HIV-1 infection in the previously HIV-1-negative partner in an intention-to-treat analysis.ResultsIndex participants were followed for 10,031 person-years; partners were followed for 8509 person-years. Among partners, 78 HIV-1 infections were observed during the trial (annual incidence, 0.9%; 95% confidence interval [CI], 0.7 to 1.1). Viral-linkage status was determined for 72 (92%) of the partner infections. Of these infections, 46 were linked (3 in the early-ART group and 43 in the delayed-ART group; incidence, 0.5%; 95% CI, 0.4 to 0.7) and 26 were unlinked (14 in the early-ART group and 12 in the delayed-ART group; incidence, 0.3%; 95% CI, 0.2 to 0.4). Early ART was associated with a 93% lower risk of linked partner infection than was delayed ART (hazard ratio, 0.07; 95% CI, 0.02 to 0.22). No linked infections were observed when HIV-1 infection was stably suppressed by ART in the index participant.ConclusionsThe early initiation of ART led to a sustained decrease in genetically linked HIV-1 infections in sexual partners. (Funded by the National Institute of Allergy and Infectious Diseases; HPTN 052 ClinicalTrials.gov number, NCT00074581 .).

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