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Author Notes:

Correspondence to Matt A. Price, International AIDS Vaccine Initiative 125 Broad Street, 9th Floor New York, NY 10004, USA. Tel: +1 646 752 0255; e-mail: mprice@iavi.org

The authors are grateful to numerous people, whose contributions have made this study possible: All of the Study Participants, Drs James Tang and Richard Kaslow (University of Alabama at Birmingham for HLA typing), Dr Ed Acosta (University of Alabama at Birmingham School of Medicine for antiretroviral drug testing), staff at the Central Laboratory Services and the Perinatal HIV Research Unit, South Africa; staff at the IAVI Human Immunology Laboratory, Imperial College, London; the Africa-based IAVI staff; Helen Thomson, Marietta Krebs, Leslie Nielsen, Melissa Simek, Lisa Stoll, Paul Sayer, Jan de Bont, Andrea von Lieven, Sarah Yates, Elise van der Elst, Dr Nzeera Ketter, and Dr Chrispin Kambili.

The contents are the responsibility of the study authors and do not necessarily reflect the views of USAID or the United States Government.

This report was published with permission from KEMRI.

There are no conflicts of interest.


Research Funding:

We also thank the study funders: Becton, Dickinson and Company; Bill and Melinda Gates Foundation; Bristol-Meyers Squibb; Canadian International Development Agency; Dutch Product Development Partnership Fund; European Commission South Africa; Foundation for the National Institute of Health; John Evans Foundation; Medical Research Council; Norwegian Agency for Development Corporation; Organization of the Petroleum Exporting Countries (OPEC) Fund for International Development; Pfizer, Inc.; Spain Ministry of Foreign Affairs; Swedish International Development Agency; United Kingdom Department for International Development; United States Agency for International Development (USAID); and World Bank.

Funding source: Primary: United States Agency for International Development (USAID).

This work was made possible in part by the generous support of the American people through the United States Agency for International Development (USAID).


  • Adolescent
  • Adult
  • Africa South of the Sahara
  • CD4 Lymphocyte Count
  • Cohort Studies
  • Disease Progression
  • Female
  • HIV Infections
  • HIV-1
  • Humans
  • Longitudinal Studies
  • Male
  • Middle Aged
  • Prospective Studies
  • Viral Load
  • Young Adult
  • Africa
  • AIDS
  • CD4+ cell count
  • HIV disease progression
  • HIV-1 subtype
  • HIV-serodiscordant couples
  • Men who have sex with men
  • Viral load

Disease progression by infecting HIV-1 subtype in a seroconverter cohort in sub-Saharan Africa

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Journal Title:



Volume 27, Number 17


, Pages 2775-2786

Type of Work:

Article | Final Publisher PDF


Objective: To describe immunologic, virologic, and clinical HIV disease progression by HIV-1 subtype among Africans with well documented estimated dates of HIV infection (EDIs). Design: Prospective cohort. Methods: Adults and youth with documented HIV-1 infection in the past 12 months were recruited from seroincidence cohorts in East and Southern Africa and followed at 3-6 month intervals. Blood for lymphocyte subset and viral load determination was collected at each visit. Pol was sequenced from the first positive specimen to ascertain subtype. Preantiretroviral therapy disease progression was measured by three time-toevent endpoints: CD4 + cell count 350 cells/ml or less, viral load measurement at least 1*105 copies/ml, and clinical AIDS. Results: From 2006 to 2011, 615 participants were enrolled at nine research centers in Kenya, Rwanda, South Africa, Uganda, and Zambia; 579 (94.1%) had viral subtyping completed. Predominant subtypes were C (256, 44.2%), A (209, 36.1%), and D (84, 14.5%). After adjustment for age, sex, and human leukocyte antigen alleles in Cox regression analyses, subtype C-infected participants progressed faster than subtype A to all three endpoints [CD4 + hazard ratio 1.60, 95% (confidence interval) CI 1.16, 2.20; viral load hazard ratio 1.59, 95% CI 1.12, 2.25; and AIDS hazard ratio 1.60, 95% CI 1.11, 2.31). Subtype D-infected participants reached high viral load more rapidly (hazard ratio 1.61, 95% CI 1.01, 2.57) and progressed nearly twice as fast to AIDS compared to subtype A (hazard ratio 1.93, 95% CI 1.21, 3.09). Conclusion: Subtype-specific differences in HIV disease progression suggest that the local subtype distribution be considered when planning HIV programs and designing and defining clinical endpoints for HIV prevention trials.

Copyright information:

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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