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APOBEC3B Deletion and Risk of HIV-1 Acquisition

  1. Author:
    An, P.
    Johnson, R.
    Phair, J.
    Kirk, G. D.
    Yu, X. F.
    Donfield, S.
    Buchbinder, S.
    Goedert, J. J.
    Winkler, C. A.
  2. Author Address

    Winkler, Cheryl A.] NCI, Lab Genom Div, SAIC Frederick, FCRDC, Frederick, MD 21702 USA. [Kirk, Gregory D.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. [Yu, Xiao-Fang] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD USA. [Goedert, James J.] NCI, Infect & Immunoepidemiol Branch, Bethesda, MD 20892 USA. [Phair, John] Northwestern Univ, Chicago, IL 60611 USA. [Donfield, Sharyne] Rho, Chapel Hill, NC USA. [Buchbinder, Susan] San Francisco Dept Publ Hlth, San Francisco, CA USA.
    1. Year: 2009
  1. Journal: Journal of Infectious Diseases
    1. 200
    2. 7
    3. Pages: 1054-1058
  2. Type of Article: Proceedings Paper
  1. Abstract:

    The human APOBEC3 family of cytidine deaminases provides intrinsic immunity to retroviral infection. A naturally occurring 29.5-kb deletion removes the entire APOBEC3B gene. We examined the impact of the APOBEC3B gene deletion in >4000 individuals from 5 human immunodeficiency virus type 1 (HIV-1) natural history cohorts. The hemizygous genotype had no effect on either acquisition of HIV-1 infection or progression to AIDS. However, the homozygous deletion was significantly associated with unfavorable outcomes for HIV-1 acquisition (odds ratio, 7.37, P = .024), progression to AIDS (relative hazard, 4.01, P = .03) and viral set point (P = .04). These findings suggest that the loss of APOPBEC3B may increase host susceptibility to HIV-1 acquisition and progression to AIDS and warrant further study.

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External Sources

  1. DOI: 10.1086/605644
  2. PMID: 19698078

Library Notes

  1. No notes added.
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