Long-term CD4+ lymphocyte response following HAART initiation in a U.S. Military prospective cohort

Alan R. Lifson, Elizabeth M. Krantz, Lynn E. Eberly, Matthew J. Dolan, Vincent C. Marconi, Amy C. Weintrob, Nancy F. Crum-Cianflone, Anuradha Ganesan, Patricia L. Grambsch, Brian K. Agan

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33 Scopus citations

Abstract

Background: Among HIV-infected persons initiating highly active antiretroviral therapy (HAART), early CD4+ lymphocyte count increases are well described. However, whether CD4+ levels continue to increase or plateau after 4-6 years is controversial.Methods: To address this question and identify other determinants of CD4+ response, we analyzed data for 1,846 persons from a prospective HIV military cohort study who initiated HAART, who had post-HAART CD4+ measurements, and for whom HIV seroconversion (SC) date was estimated.Results: CD4+ count at HAART initiation was ≤ 200 cells/mm3 for 23%, 201-349 for 31%, 350-499 for 27%, and ≥500 for 19%. The first 6 months post-HAART, the greatest CD4+ increases (93-151 cells) occurred, with lesser increases (22-36 cells/year) through the first four years. Although CD4+ changes for the entire cohort were relatively flat thereafter, HIV viral load (VL) suppressors showed continued increases of 12-16 cells/year. In multivariate analysis adjusting for baseline CD4+ and post-HAART time interval, CD4+ responses were poorer in those with: longer time from HIV SC to HAART start, lower pre-HAART CD4+ nadir, higher pre-HAART VL, and clinical AIDS before HAART (P < 0.05).Conclusions: Small but positive long-term increases in CD4+ count in virally suppressed patients were observed. CD4+ response to HAART is influenced by multiple factors including duration of preceding HIV infection, and optimized if treatment is started with virally suppressive therapy as early as possible.

Original languageEnglish (US)
Article number2
JournalAIDS Research and Therapy
Volume8
DOIs
StatePublished - Jan 18 2011

Bibliographical note

Funding Information:
Support for this work (IDCRP-000-03) was provided by the Infectious Disease Clinical Research Program (IDCRP), a Department of Defense program executed through the Uniformed Services University of the Health Sciences. This project has been funded in whole, or in part, with federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, under Inter-Agency Agreement Y1-AI-5072. Additional members of the IDCRP HIV/STI Working Group include Susan Banks, Mary Bavaro, Helen Chun, Cathy Decker, Connor Eggleston, Susan Fraser, Joshua Hartzell, Gunther Hsue, Arthur Johnson, Mark Kortepeter, Michael Landrum, Tahaniyat Lalani, Michelle Linfesty, Grace Macalino, Scott Merritt, Robert O’Connell, Jason Okulicz, Shiela Peel, Michael Polis, John Powers, Roseanne Ressner, Edmund Tramont, Tyler Warkentien, Paige Waterman, Timothy Whitman, Ken Wilkins, Glenn Wortmann, and Michael Zapor. The content and views expressed in this publication is the sole responsibility of the authors and does not necessarily reflect the views or policies of the NIH or the Department of Health and Human Services, the DoD or the Departments of the Army, Navy, Air Force, Department of Defense, nor the U.S. Government. Mention of trade names, commercial products, or organizations does not imply endorsement by the U.S. Government.

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