APOBEC3G genetic variants and their influence on the progression to AIDS

Ping An, Gabriela Bleiber, Priya Duggal, George Nelson, Margaret May, Bastien Mangeat, Irene Alobwede, Didier Trono, David Vlahov, Sharyne Donfield, James J. Goedert, John Phair, Susan Buchbinder, Stephen J. O'Brien, Amalio Telenti, Cheryl A. Winkler*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

166 Scopus citations


The cytosine deaminase APOBEC3G, in the absence of the human immunodeficiency virus type 1 (HIV-1) accessory gene HIV-I viral infectivity factor (vif), inhibits viral replication by introducing G→A hypermutation in the newly synthesized HIV-1 DNA negative strand. We tested the hypothesis that genetic variants of APOBEC3G may modify HIV-1 transmission and disease progression. Single nucleotide polymorphisms were identified in the promoter region (three), introns (two), and exons (two). Genotypes were determined for 3,073 study participants enrolled in six HIV-AIDS prospective cohorts. One codon-changing variant, H186R in exon 4, was polymorphic in African Americans (AA) (f = 37%) and rare in European Americans (f < 3%) or Europeans (f = 5%). For AA, the variant allele 186R was strongly associated with decline in CD4 T cells (CD4 slope on square root scale: -1.86, P = 0.009), The 186R allele was also associated with accelerated progression to AIDS-defining conditions in AA. The in vitro antiviral activity of the 186R enzyme was not inferior to that of the common H186 variant. These studies suggest that there may be a modifying role of variants of APOBEC3G on HIV-1 disease progression that warrants further investigation.

Original languageEnglish (US)
Pages (from-to)11070-11076
Number of pages7
JournalJournal of virology
Issue number20
StatePublished - Oct 2004

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology


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