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Antiretroviral Therapy Initiated During Acute HIV Infection Fails to Prevent Persistent T-Cell Activation

Vinikoor, Michael J. MD*; Cope, Anna MPH*; Gay, Cynthia L. MD*; Ferrari, Guido MD; McGee, Kara S. MSPH; Kuruc, Joann D. BSN*; Lennox, Jeffrey L. MD§; Margolis, David M. MD*; Hicks, Charles B. MD; Eron, Joseph J. MD*

JAIDS Journal of Acquired Immune Deficiency Syndromes: April 15th, 2013 - Volume 62 - Issue 5 - p 505–508
doi: 10.1097/QAI.0b013e318285cd33
Brief Report: Basic and Translational Science

Abstract: Initiation of antiretroviral therapy during acute HIV-1 infection may prevent persistent immune activation. We analyzed longitudinal CD38+HLA-DR+ CD8+ T-cell percentages in 31 acutely infected individuals who started early (median 43 days since infection) and successful antiretroviral therapy, and maintained viral suppression through 96 weeks. Pretherapy a median of 72.6% CD8+ T cells were CD38+HLA-DR+, and although this decreased to 15.6% by 96 weeks, it remained substantially higher than seronegative controls (median 8.9%, P = 0.008). Shorter time to suppression predicted lower activation at 96 weeks. These results support the hypothesis that very early events in HIV-1 pathogenesis may result in prolonged immune dysfunction.

*Department of Medicine, Center for Infectious Diseases, University of North Carolina at Chapel Hill, Chapel Hill, NC;

the Departments of Surgery and

Medicine, Duke University, Durham, NC; and

§Department of Medicine, Emory University, Atlanta, GA.

Correspondence to: Michael J. Vinikoor, MD, Center for Infectious Diseases, University of North Carolina, 130 Mason Farm Road, CB #7030, 2nd Floor Bioinformatics, Chapel Hill NC 27599 (e-mail:

Supported by research contracts from Bristol-Myers Squibb, Gilead Sciences, and Janssen Therapeutics, and the following NIH-funded programs: UNC Center for AIDS Research (CFAR; 1P30 AI 50410-04), Duke CFAR (1P30 AI 64518), NCRR UL1TR000083, 5R01 AI050483, 5R13 AI084562, 2K24 AI01608 award, and 5T32 AI07001-35 award. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the article.

C.L.G. has received research support from Bristol-Myers Squibb, Gilead Sciences, and Janssen Therapeutics. C.B.H. has received grant support and/or consulting/honoraria from Bristol-Myers Squibb, GlaxoSmithKline/Viiv, Merck, Janssen Therapeutics, Gilead Sciences, Myriad, and Koronis. D.M.M. has received research support from Bristol-Myers Squibb, Gilead Sciences, and Merck, and honoraria from Bristol-Myers Squibb, Merck, Chimerix, and Janssen Therapeutics. J.J.E. receives research support from Bristol-Myers Squibb and GlaxoSmithKline and is a consultant to Bristol-Myers Squibb, Merck, GlaxoSmithKline/ViiV Healthcare, and Janssen Therapeutics. M.J.V., A.C., G.F., K.S.M., J.D.K., and J.L.L. have no conflicts of interest to disclose.

Received September 20, 2012

Accepted January 02, 2013

© 2013 Lippincott Williams & Wilkins, Inc.