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1 May 2005

Volume 191, Number 9
The Journal of Infectious Diseases 2005;191:1460–1467
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19109-0012$15.00
DOI: 10.1086/429409
MAJOR ARTICLE

Viral Dynamics of Primary HIV‐1 Infection in Senegal, West Africa

Abdoulaye Dieng Sarr,1

Geoffrey Eisen,1

Aïssatou Guèye‐Ndiaye,2

Christopher Mullins,1

Ibrahima Traoré,2

Mamadou Ciré Dia,2

Jean‐Louis Sankalé,1

Diegane Faye,2

Souleymane Mboup,2 and

Phyllis Kanki1

1Department of Immunology and Infectious Diseases, Harvard AIDS Institute, Harvard School of Public Health, Boston, Massachusetts; 2Department of Bacteriology and Virology, Cheikh Anta Diop University, Dakar, Senegal

Background.Few studies have addressed primary human immunodeficiency virus (HIV) type 1 infection in sub‐Saharan Africa, where the epidemic is of a predominantly heterosexual character and is caused by different subtypes. The present study examines the dynamics of viral replication in subjects infected with various HIV‐1 subtypes.

Methods.Seven hundred fifty‐two HIV‐negative Senegalese women at high risk for infection were monitored every 3 months for acute/early HIV infection; 26 infections were identified (23 HIV‐1 and 3 HIV‐2), with an HIV‐1 incidence rate of 3.23 cases/person‐years observation. Multiple viral‐load measurements were taken for all seroconverters.

Results.The mean ± standard deviation viral load for all subjects during the early stage of infection was log10 copies/mL, with an overall decrease of 0.22 log10 copies/mL after the early stage; the viral set point was reached after 12 months of infection. Most subjects had relatively low viral loads during the early stage of infection. HIV‐1 CRF02_AG–infected women had a significantly higher mean viral load during the early stage of infection (mean ± SD, log10 copies/mL) than did non–HIV‐1 CRF02_AG–infected women (mean ± SD, log10 copies/mL) ( ). None of the subjects reported symptoms consistent with primary HIV‐1 infection.

Conclusion.Our findings in Senegalese women differ from what have been described for primary HIV‐1 infection. Further investigations of primary infections with non‐B subtypes are warranted, to better characterize their differences with primary infections with subtype B.

Received 25 February 2004; accepted 9 December 2004; electronically published 25 March 2005.

Reprints or correspondence: Dr. Phyllis Kanki, Harvard AIDS Institute, Harvard School of Public Health, 651 Huntington Ave., Boston, MA 02115 ().

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  • Presented in part: 13th International Conference on AIDS and STIs in Africa, Nairobi, Kenya, September 2003 (abstract 124792).

    Financial support: National Institutes of Health (grant 5 R01 AI43879‐05 to P.K.). A.D.S., A.G.‐N., and J.‐L.S. are Fogarty International Fellows (grant 5D43 TW00004).

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