Epidemiology and Transmission of HIV-2
Why There Is No HIV-2 Pandemic
- Kevin M. De Cock, MD, MRCP, DTM&H;
- Georgette Adjorlolo, MD;
- Ehounou Ekpini, MD;
- Toussaint Sibailly, MD;
- Justin Kouadio;
- Matthieu Maran;
- Kari Brattegaard;
- Kathleen M. Vetter, MPH;
- Ronan Doorly;
- Helene D. Gayle, MD, MPH
- From Projet RETRO-CI, Abidjan, Ivory Coast (Drs De Cock, Adjorlolo, Ekpini, and Sibailly, Messrs Kouadio, Maran, and Doorly, and Mss Brattegaard and Vetter); the Division of HIV/AIDS, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Ga (Drs De Cock and Gayle); and Emory University School of Public Health, Atlanta, Ga (Ms Vetter).
Abstract
Although human immunodeficiency virus type 1 (HIV-1) and HIV-2 share modes of transmission, their epidemiologic characteristics differ and international spread of HIV-2 has been very limited. Recently, the prevalence of infection with HIV-1 but not HIV-2 has increased rapidly in different West African countries, where HIV-2 was probably present earlier. Among 19 701 women of reproductive age tested in Abidjan, Ivory Coast, between 1988 and 1992, the prevalence of HIV-1 infection increased from 5.0% to 9.2%, while that of HIV-2 declined from 2.6% to 1.5%. Differences in viral load may be responsible: reported results of virus culture and polymerase chain reaction assays suggest that at high CD4+ T-lymphocyte counts viral load is lower in HIV-2—infected than in HIV-1—infected persons; the efficacy of heterosexual and perinatal transmission of HIV-2 is less efficient than that of HIV-1 at this stage. At low (<0.20×109/L [<200/μL]) CD4+ T-lymphocyte counts, virus isolation is equally successful for both viruses, and the efficacy of heterosexual transmission is similar. Differences in HIV-1 and HIV-2 natural history are reflected in differences in viral load, that for HIV-2 being lower until immunodeficiency is severe. Differences in viral load throughout most of the natural history of infection appear to correlate with lower transmissibility of HIV-2 than HIV-1 and are the likeliest explanation for their markedly different global epidemiology.
(JAMA. 1993;270:2083-2086)
Footnotes
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Reprint requests to Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, Keppel Street, London, England WC1E 7HT (Dr De Cock).








