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MICA and recovery from hepatitis C virus and hepatitis B virus infections

  1. Author:
    Karacki, P. S.
    Gao, X.
    Thio, C. L.
    Thomas, D. L.
    Goedert, J. J.
    Vlahov, D.
    Kaslow, R.
    Strathdee, S.
    Hilgartner, M. W.
    O'Brien, S. J.
    Carrington, M.

  2. Author Address

    Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Dept Epidemiol, Baltimore, MD 21205 USA. SAIC Frederick, Basic Res Program, Intramural Res Support Program, Frederick, MD USA. NCI, Viral Epidemiol Branch, Rockville, MD USA. New York Acad Med, New York, NY USA. Univ Alabama, Dept Epidemiol, Birmingham, AL USA. New York Presbyterian Hosp, Cornell Med Ctr, Dept Pediat, New York, NY USA. NCI, Lab Genom Divers, Frederick, MD 21701 USA. Thomas, DL, Johns Hopkins Univ, Sch Med, Viral Hepatitis Lab, 1503 E Jefferson St, Baltimore, MD 21231 USA
    1. Year: 2004
  2. Journal: Genes and Immunity
    1. 5
    2. 4
    3. Pages: 261-266
  4. Type of Article: Article
  1. Abstract:

    The polymorphic MHC class I chain-related A (MICA) gene encodes a ligand that has different binding affinities for the NKG2D activating receptor of CD8+ T cells and natural killer (NK) cells. We hypothesized that MICA heterogeneity would affect recovery from hepatitis C virus (HCV) and hepatitis B virus (HBV) infections. To test the hypothesis, we initially typed known MICA polymorphisms for 228 persons who cleared HCV infection and 442 persons with persistent hepatitis C matched on other factors affecting viral persistence. Although MICA*015 was detected more than two-fold more often in persons with viral clearance (odds ratio 0.36, 95% confidence interval = 0.19, 0.80), it occurred in fewer than 5% of the study population. In a similar analysis of 442 persons with chronic hepatitis B and 768 matched controls who recovered, MICA*015 was detected in 2.0% of persons with chronic hepatitis B and only 0.9% of controls. No significant associations were detected with other MICA polymorphisms. While further investigation may reveal a structural basis of the MICA*015 associations, these data provide little support for the hypothesis that differential distribution of MICA alleles substantially affects recovery from HCV and HBV infections

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