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APOBEC3G genetic variants and their influence on the progression to AIDS

  1. Author:
    An, P.
    Bleiber, G.
    Duggal, P.
    Nelson, G.
    May, M.
    Mangeat, B.
    Alobwede, I.
    Trono, D.
    Vlahov, D.
    Donfield, S.
    Goedert, J. J.
    Phair, J.
    Buchbinder, S.
    O'Brien, S. J.
    Telenti, A.
    Winkler, C. A.

  2. Author Address

    NCI, Basic Res Program, SAIC Frederick, Canc Res & Dev Ctr, Frederick, MD 21702 USA. NCI, Lab Genom Divers, Frederick, MD 21702 USA. NHGRI, Inherited Dis Res Branch, Baltimore, MD USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21218 USA. NCI, Viral Epidemiol Branch, Bethesda, MD 20892 USA. Rho Inc, Chapel Hill, NC USA. Northwestern Univ, Fineberg Sch Med, Comprehens AIDS Ctr, Chicago, IL 60611 USA. San Francisco Dept Publ Hlth, San Francisco, CA USA. Univ Lausanne, Inst Microbiol, CH-1015 Lausanne, Switzerland. Univ Geneva, Dept Genet & Microbiol, CH-1211 Geneva 4, Switzerland. Univ Hosp Geneva, Div Infect Dis, Geneva, Switzerland. Univ Bristol, Bristol BS8 1TH, Avon, England Winkler, CA, NCI, Basic Res Program, SAIC Frederick, Canc Res & Dev Ctr, Frederick, MD 21702 USA
    1. Year: 2004
    2. Date: OCT
  2. Journal: Journal of Virology
    1. 78
    2. 20
    3. Pages: 11070-11076
  4. Type of Article: Article
  1. Abstract:

    The cytosine deaminase APOBEC3G, in the absence of the human immunodeficiency virus type 1 (HIV-1) accessory gene HIV-1 viral infectivity factor (vif), inhibits viral replication by introducing G-->A hypermutation in the newly synthesized HIV-1 DNA negative strand. We tested the hypothesis that genetic variants of APOBEC3G may modify HIV-1 transmission and disease progression. Single nucleotide polymorphisms were identified in the promoter region (three), introns (two), and exons (two). Genotypes were determined for 3,073 study participants enrolled in six HIV-AIDS prospective cohorts. One codon-changing variant, H186R in exon 4, was polymorphic in African Americans (AA) (f = 37%) and rare in European Americans (f < 3%) or Europeans (f = 5%). For AA, the variant allele 186R was strongly associated with decline in CD4 T cells (CD4 slope on square root scale: -1.86, P = 0.009), The 186R allele was also associated with accelerated progression to AIDS-defining conditions in AA. The in vitro antiviral activity of the 186R enzyme was not inferior to that of the common H186 variant. These studies suggest that there may be a modifying role of variants of APOBEC3G on HIV-1 disease progression that warrants further investigation

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External Sources

  1. View record in Web of Science®
  2. WOS: 000224229000024

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