APOBEC3G expression and hypermutation are inversely associated with human immunodeficiency virus type 1 (HIV-1) burden in vivo

Yordanka Kourteva, MariaPia De Pasquale*, Tara Allos, Chara McMunn, Richard T. D'Aquila

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

APOBEC3G (A3G) and APOBEC3F (A3F) reduce Vif-negative HIV-1 provirus formation and cause disabling provirus G-to-A hypermutation . in vitro. However, evidence conflicts about whether they negatively impact Vif-positive HIV-1, or only enhance virus genetic diversity, . in vivo. We studied peripheral blood mononuclear cells (PBMC) from 19 antiretroviral-naïve, HIV-infected adults: 12 long-term non-progressors (LTNP) and 7 non-controllers (NC). Cells from LTNP had higher A3G and A3F mRNA levels, lower provirus burden, and more A3G-hypermutated positions in provirus sequence than cells from NC. A3G mRNA level was directly associated with its Hypermutation Index (HI) and inversely associated with provirus burden. Plasma HIV-1 RNA levels were inversely associated with A3G expression levels and with HI only among subjects who had HI>1. A3G HI was not associated with provirus burden. These results indicate that A3G deaminase-dependent activity above a threshold level, and its deaminase-independent functions, contribute to decreasing Vif-positive virus replication . in vivo.

Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalVirology
Volume430
Issue number1
DOIs
StatePublished - Aug 15 2012

Keywords

  • APOBEC3F
  • APOBEC3G
  • Cytidine deaminase
  • G-to-A hypermutations
  • HIV-1
  • Long-term non-progressors

ASJC Scopus subject areas

  • Virology

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