Goila-Gaur Ritu, Khan Mohammad A, Miyagi Eri, Strebel Klaus
Laboratory of Molecular Microbiology, Viral Biochemistry Section, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892-0460, USA.
J Virol. 2009 Jan;83(2):1156-60. doi: 10.1128/JVI.01734-08. Epub 2008 Nov 12.
HIV-1 Vif counteracts the antiviral activity of APOBEC3G by inhibiting its encapsidation into virions. Here, we compared the relative sensitivity to Vif of APOBEC3G in stable HeLa cells containing APOBEC3G (HeLa-A3G cells) versus that of newly synthesized APOBEC3G. We observed that newly synthesized APOBEC3G was more sensitive to degradation than preexisting APOBEC3G. Nevertheless, preexisting and transiently expressed APOBEC3G were packaged with similar efficiencies into vif-deficient human immunodeficiency virus type 1 (HIV-1) virions, and Vif inhibited the encapsidation of both forms of APOBEC3G into HIV particles equally well. Our results suggest that HIV-1 Vif preferentially induces degradation of newly synthesized APOBEC3G but indiscriminately inhibits encapsidation of "old" and "new" APOBEC3G.
HIV-1病毒感染因子（Vif）通过抑制载脂蛋白B mRNA编辑酶催化多肽样3G（APOBEC3G）包裹进病毒粒子来对抗其抗病毒活性。在此，我们比较了稳定表达APOBEC3G的HeLa细胞（HeLa-A3G细胞）中APOBEC3G对Vif的相对敏感性与新合成的APOBEC3G对Vif的相对敏感性。我们观察到新合成的APOBEC3G比已存在的APOBEC3G对降解更敏感。然而，已存在的和瞬时表达的APOBEC3G以相似的效率被包装进缺乏Vif的1型人类免疫缺陷病毒（HIV-1）病毒粒子中，并且Vif同样有效地抑制这两种形式的APOBEC3G包裹进HIV颗粒。我们的结果表明，HIV-1 Vif优先诱导新合成的APOBEC3G降解，但不加区分地抑制“旧的”和“新的”APOBEC3G的包裹。
