Chemokine-receptor genes and AIDS risk
Patricia A. Ramaley,
Neil French,
Pontiano Kaleebu,
Charles Gilks,
James Whitworth and
Adrian V. S. Hill ()
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Patricia A. Ramaley: Wellcome Trust Centre for Human Genetics, University of Oxford
Neil French: Liverpool School of Tropical Medicine
Pontiano Kaleebu: Uganda Virus Research Institute/Medical Research Council (UK) Programme on HIV/AIDS
Charles Gilks: Liverpool School of Tropical Medicine
James Whitworth: Uganda Virus Research Institute/Medical Research Council (UK) Programme on HIV/AIDS
Adrian V. S. Hill: Wellcome Trust Centre for Human Genetics, University of Oxford
Nature, 2002, vol. 417, issue 6885, 140-140
Abstract:
Abstract Schliekelman et al.1 have provided a model to quantify the speed at which HIV-resistance haplotypes can become enriched in a susceptible population through a delay in the onset of AIDS, permitting greater lifetime reproduction and the selection of AIDS-delaying haplotypes. But we question their conclusion1 that there could be a rapid evolution of resistance to AIDS onset in some African populations if the current HIV epidemic persists, as this depends on an untested assumption: that variant forms of the chemokine-receptor-5 (CCR5) gene impart selective advantages or disadvantages in Africa that are comparable to those reported for African Americans2,3,4,5,6. Here we test this premise in a large Ugandan population, and find that CCR5 variants are not associated with HIV/AIDS disease risk in Africa — the origin and centre of the current AIDS pandemic. This gene may therefore not be subject to rapid evolutionary change as a result of the HIV epidemic in Africa.
Date: 2002
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DOI: 10.1038/417140a
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