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Cytotoxic T-lymphocyte antigen 4 gene and recovery from hepatitis B virus infection

  1. Author:
    Thio, C. L.
    Mosbruger, T. L.
    Kaslow, R. A.
    Karp, C. L.
    Strathdee, S. A.
    Vlahov, D.
    O'Brien, S. J.
    Astemborski, J.
    Thomas, D. L.

  2. Author Address

    Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Dept Epidemiol, Baltimore, MD 21205 USA. NCI, Lab Genomic Divers, Frederick, MD 21701 USA. Univ Alabama, Dept Epidemiol, Birmingham, AL USA. Cincinnati Childrens Hosp, Med Ctr, Div Mol Immunol, Cincinnati, OH USA. New York Acad Med, New York, NY USA Thio, CL, 1503 E Jefferson St, Baltimore, MD 21231 USA
    1. Year: 2004
    2. Date: OCT
  2. Journal: Journal of Virology
    1. 78
    2. 20
    3. Pages: 11258-11262
  4. Type of Article: Article
  1. Abstract:

    Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is an inhibitory T-cell receptor expressed by activated and regulatory T cells. We hypothesized that single-nucleotide polymorphisms (SNPs) in the gene encoding CTLA-4 may affect the vigor of the T-cell response to hepatitis B virus (HBV) infection, thus influencing viral persistence. To test this hypothesis, we genotyped six CTLA4 SNPs, from which all frequent haplotypes can be determined, using a large, matched panel of subjects with known HBV outcomes. Haplotypes with these SNPs were constructed for each subject using PHASE software. The haplotype distribution differed between those with viral persistence and those with clearance. Two haplotypes were associated with clearance of HBV infection, which was most likely due to associations with the SNPs - 1722C (odds ratio [OR] = 0.60, P = 0.06) and +49G (OR = 0.73, P = 0.02). The wild-type haplotype, which contains an SNP leading to a decreased T-cell response (+6230A), was associated with viral persistence (OR = 1.32, P = 0.04). These data suggest that CTLA4 influences recovery from HBV infection, which is consistent with the emerging role of T regulatory cells in the pathogenesis of disease

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External Sources

  1. View record in Web of Science®
  2. WOS: 000224229000041

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