APOBEC3B deletion and risk of HIV-1 acquisition

Ping An*, Randall Johnson, John Phair, Gregory D. Kirk, Xiao Fang Yu, Sharyne Donfield, Susan Buchbinder, James J. Goedert, Cheryl A. Winkler

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations

Abstract

The human AFOBEC3 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 APOBEC3B may increase host susceptibility to HIV-1 acquisition and progression to AIDS and warrant further study.

Original languageEnglish (US)
Pages (from-to)1054-1058
Number of pages5
JournalJournal of Infectious Diseases
Volume200
Issue number7
DOIs
StatePublished - Oct 1 2009

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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