Differential Sensitivity of "Old" versus "New" APOBEC3G to Human Immunodeficiency Virus Type 1 Vif
Differential Sensitivity of "Old" versus "New" APOBEC3G to Human Immunodeficiency Virus Type 1 Vif
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DOI：
10.1128/jvi.01734-08
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发表时间：
2009-01-15
影响因子：
5.4
通讯作者：
Strebel, Klaus
中科院分区：
文献类型：
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作者：
Goila-Gaur, Ritu;Khan, Mohammad A.;Strebel, Klaus
HIV-1 Vif通过抑制APOBEC3G的病毒颗粒包裹而中和其抗病毒活性。在这里，我们比较了APOBEC3G在稳定的含有APOBEC3G的HeLa细胞(HeLa-A3G细胞)和新合成的APOBEC3G对VIF的相对敏感性。我们观察到，新合成的APOBEC3G比现有的APOBEC3G对降解更敏感。然而，预先存在的和瞬时表达的APOBEC3G以相似的效率被包装成病毒缺陷的人类免疫缺陷病毒1型(HIV-1)病毒粒子，而Vif同样很好地抑制了这两种形式的APOBEC3G被包装到HIV颗粒中。我们的结果表明，HIV-1 Vif优先诱导新合成的APOBEC3G的降解，但不分青红皂白地抑制“旧的”和“新的”APOBEC3G的包装。
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.