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Schliekelman et al. 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 conclusion 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 Americans. 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.

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Acquired Immunodeficiency Syndrome, African Continental Ancestry Group, Alleles, Disease Progression, European Continental Ancestry Group, Evolution, Molecular, Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, HIV-1, Haplotypes, Humans, Linkage Disequilibrium, Models, Genetic, Promoter Regions, Genetic, Receptors, CCR2, Receptors, CCR5, Receptors, Chemokine, Regression Analysis, Selection, Genetic, Uganda