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Science 4 December 1998:
Vol. 282. no. 5395, pp. 1907 - 1911
DOI: 10.1126/science.282.5395.1907
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Reports

Genetic Acceleration of AIDS Progression by a Promoter Variant of CCR5

Maureen P. Martin, Michael Dean, Michael W. Smith, Cheryl Winkler, Bernard Gerrard, Nelson L. Michael, Benhur Lee, Robert W. Doms, Joseph Margolick, * Susan Buchbinder, dagger James J. Goedert, ddagger Thomas R. O'Brien, ddagger Margaret W. Hilgartner, § David Vlahov, parallel Stephen J. O'Brien, Mary Carrington

The CCR5 gene encodes a cell surface chemokine receptor molecule that serves as the principal coreceptor, with CD4, for macrophage-tropic (R5) strains of human immunodeficiency virus-type 1 (HIV-1). Genetic association analysis of five cohorts of people with acquired immunodeficiency syndrome (AIDS) revealed that infected individuals homozygous for a multisite haplotype of the CCR5 regulatory region containing the promoter allele, CCR5P1, progress to AIDS more rapidly than those with other CCR5 promoter genotypes, particularly in the early years after infection. Composite genetic epidemiologic analyses of genotypes bearing CCR5P1, CCR5-Delta 32, CCR2-64I, and SDF1-3'A affirmed distinct regulatory influences for each gene on AIDS progression. An estimated 10 to 17 percent of patients who develop AIDS within 3.5 years of HIV-1 infection do so because they are homozygous for CCR5P1/P1, and 7 to 13 percent of all people carry this susceptible genotype. The cumulative and interactive influence of these AIDS restriction genes illustrates the multigenic nature of host factors limiting AIDS disease progression.

M. P. Martin, M. W. Smith, C. Winkler, B. Gerrard, M. Carrington, Science Applications International Corporation (SAIC), National Cancer Institute, Frederick MD 21702, USA. M. Dean and S. J. O'Brien, Laboratory of Genomic Diversity, National Cancer Institute, Frederick, MD 21702, USA. N. L. Michael, Division of Retrovirology, Walter Reed Army Institute of Research, 1600 East Gude Drive, Rockville, MD 20850, USA. B. Lee and R. W. Doms, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. J. Margolick and D. Vlahov, Department of Epidemiology, Johns Hopkins School of Hygiene and Public Health, Baltimore, MD 21205, USA. S. Buchbinder, San Francisco Department of Public Health, San Francisco, CA 94102, USA. J. J. Goedert and T. R. O'Brien, Viral Epidemiology Branch, National Cancer Institute, 6130 Executive Boulevard, Bethesda, MD 20892, USA. M. W. Hilgartner, Division of Pediatric Hematology and Oncology, New York Hospital-Cornell Medical Center, New York, NY 10021, USA.
*   For the Multicenter AIDS Cohort Study (MACS).

dagger    For the San Francisco City Cohort.

ddagger    For the Multicenter Hemophilia Cohort Study (MHCS).

§   For the Hemophilia Growth and Development Study.

parallel    For the AIDS Link to Intravenous Experience (ALIVE) Study.

   To whom correspondence should be addressed. E-mail: obrien{at}ncifcrf.gov

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