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A tumor necrosis factor-alpha-inducible promoter variant of interferon-gamma accelerates CD4(+) T cell depletion in human immunodeficiency virus-1-infected individuals

  1. Author:
    An, P.
    Vlahov, D.
    Margolick, J. B.
    Phair, J.
    O'Brien, T. R.
    Lautenberger, J.
    O'Brien, S. J.
    Winkler, C. A.

  2. Author Address

    NCI, Frederick Canc Res & Dev Ctr, Basic Res Program, SAIC Frederick Inc, Bldg 560, Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA NCI, Lab Genom Divers, Frederick, MD 21702 USA Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA NCI, Viral Epidemiol Branch, DCEG, Bethesda, MD 20892 USA Northwestern Univ, Sch Med, Comprehens AIDS Ctr, Chicago, IL USA Winkler CA NCI, Frederick Canc Res & Dev Ctr, Basic Res Program, SAIC Frederick Inc, Bldg 560, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Journal of Infectious Diseases
    1. 188
    2. 2
    3. Pages: 228-231
  4. Type of Article: Article
  1. Abstract:

    A polymorphism, - 179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. The rarer allele, -179T, but not -179G, is inducible by TNF-alpha. We investigated the effects of IFNG - 179G/T on AIDS pathogenesis. In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG - 179G/T genotype was associated with accelerated progression to CD4 < 200 and AIDS- 1993, a finding suggesting that IFNG - 179T is a risk factor for AIDS progression, as measured by CD4 cell count. It is possible that increased IFN-γ production induced by TNF- α when - 179T is present causes CD4 cell depletion by apoptosis.

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