AIDS RESEARCH AND HUMAN RETROVIRUSES Volume 21, Number 4, 2005, pp. 285–291 © Mary Ann Liebert, Inc. Short Communication Viral Dynamics and CD4 + T Cell Counts in Subtype C Human Immunodeficiency Virus Type 1-Infected Individuals from Southern Africa CLIVE M. GRAY, 1 CAROLYN WILLIAMSON, 2 HELBA BREDELL, 3 ADRIAN PUREN, 1 XIAOHUA XIA, 3 RUBEN FILTER, 3 LYNN ZIJENAH, 4 HUYEN CAO, 5 LYNN MORRIS, 1 EFTHYIA VARDAS, 6 MARK COLVIN, 6 GLENDA GRAY, 7 JAMES MCINTYRE, 7 ROSEMARY MUSONDA, 8 SUSAN ALLEN, 8 DAVID KATZENSTEIN, 9 MIKE MBIZO, 4 NEWTON KUMWENDA, 10 TAHA TAHA, 10 SALIM ABDOOL KARIM, 6 JORGE FLORES, 11 and HAYNES W. SHEPPARD 5 ABSTRACT Defining viral dynamics in natural infection is prognostic of disease progression and could prove to be im- portant for vaccine trial design as viremia may be a likely secondary end point in phase III HIV efficacy tri- als. There are limited data available on the early course of plasma viral load in subtype C HIV-1 infection in Africa. Plasma viral load and CD4 T cell counts were monitored in 51 recently infected subjects for 9 months. Individuals were recruited from four southern African countries: Zambia, Malawi, Zimbabwe, and South Africa and the median estimated time from seroconversion was 8.9 months (interquartile range, 5.7–14 months). All were infected with subtype C HIV-1 and median viral loads, measured using branched DNA, ranged from 3.82–4.02 log 10 RNA copies/ml from 2–24 months after seroconversion. Viral loads significantly correlated with CD4 cell counts (r 0.5, p 0.0001; range, 376–364 cells/mm 3 ) and mathematical mod- eling defined a median set point of 4.08 log 10 (12 143 RNA copies/ml), which was attained approximately 17 months after seroconversion. Comparative measurements using three different viral load platforms (bDNA, Amplicor, and NucliSens) confirmed that viremia in subtype C HIV-1-infected individuals within the first 2 years of infection did not significantly differ from that found in early subtype B infection. In conclusion, the course of plasma viremia, as described in this study, will allow a useful baseline comparator for understand- ing disease progression in an African setting and may be useful in the design of HIV-1 vaccine trials in south- ern Africa. 285 1 National Institute for Communicable Diseases, Johannesburg, South Africa. 2 Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, South Africa. 3 Department of Electrical Engineering, Pretoria University, Pretoria, South Africa. 4 Department of Immunology, University of Zimbabwe, Harase, Zimbabwe. 5 Department of Health Services, Richmond, California. 6 HIV Vaccine and Prevention Trials Unit, MRC, Durban, South Africa. 7 Perinatal HIV Research Unit, University of the Witwatersrand, Johannesburg, South Africa. 8 Zambia-UAB HIV Research Project, Lusaka, Zambia. 9 Center for AIDS Research, Stanford University Medical Center, Stanford, California. 10 Johns Hopkins Research Project, Blantyre, Malawi. 11 Division of AIDS, National Institutes of Health, Washington DC.