Department of Microbiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan.
Microbes Infect. 2010 Feb;12(2):166-71. doi: 10.1016/j.micinf.2009.11.007. Epub 2009 Nov 26.
We examined various HIV-1 Vif mutants for interaction with APOBEC3 proteins (A3G/A3F). All replication-defective proviral mutants were found to carry A3G/A3F in virions, and of these, a replication-defective mutant with Vif that binds to A3G in cells but not in virions was noted. Furthermore, a mutant Vif protein that suppresses A3F activity but does not exclude A3F from virions was identified. We also showed that incorporation of Vif into virions is dependent on its interaction with A3G/A3F. Taken together, we concluded that functional binding of Vif to A3G/A3F in cells and/or virions is critical for viral infectivity.
我们研究了各种 HIV-1 Vif 突变体与 APOBEC3 蛋白（A3G/A3F）的相互作用。所有复制缺陷型前病毒突变体在病毒粒子中均携带 A3G/A3F，其中，一个复制缺陷型突变体的 Vif 在细胞中与 A3G 结合，但在病毒粒子中不结合。此外，还鉴定出一种抑制 A3F 活性但不将 A3F 从病毒粒子中排除的突变体 Vif 蛋白。我们还表明，Vif 掺入病毒粒子依赖于其与 A3G/A3F 的相互作用。综上所述，我们得出结论，Vif 与 A3G/A3F 在细胞和/或病毒粒子中的功能结合对于病毒感染性至关重要。
