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Chemokine-receptor genes and AIDS risk

Author

Listed:
  • 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)

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.

Suggested Citation

  • Patricia A. Ramaley & Neil French & Pontiano Kaleebu & Charles Gilks & James Whitworth & Adrian V. S. Hill, 2002. "Chemokine-receptor genes and AIDS risk," Nature, Nature, vol. 417(6885), pages 140-140, May.
    • Handle: RePEc:nat:nature:v:417:y:2002:i:6885:d:10.1038_417140a
    DOI: 10.1038/417140a
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