Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 92, Issue 3, Pages 560-572Publisher
WILEY
DOI: 10.1002/jcb.20082
Keywords
APOBEC3G; HIV-1; innate immunity
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Funding
- NIAID NIH HHS [R01 AI043913] Funding Source: Medline
- NINDS NIH HHS [R01 NS043110] Funding Source: Medline
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The viral protein, Vif, is essential for the production of infectious progeny virions in natural target cells of human immunodeficiency virus type 1 (HIV-1). Several recent reports indicate that Vif acts byantagonizing the activity of an endogenous human antiviral protein, APOBEC3G. To investigate this route to restrict HIV-1 infection, we employed mutagenesis to assess APOBEC3G function during HIV-1 infection including interaction with Vif, localization, and activity in virions. We found that APOBEC3G binds Vif in infected cells and the C'-terminal region is required for this interaction. APOBEC3G was only incorporated into virions in the absence of Vif and deletion of either the N'-terminal or C'-terminal regions of APOBEC3G abrogated virion localization. Assaying endogenous reverse transcription we found that APOBEC3G and its C'-terminal deletion mutant inhibited full-length cDNA synthesis, possibly through binding to viral RNA, a function revealed through gel-shift assays. Taken together, our studies suggest that APOBEC3G inhibits HIV-1 infection through interference with reverse transcription and that Vif counteracts APOBEC3G by impeding its entry into virions. (C) 2004 Wiley-Liss, Inc.
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