Primate immunodeficiency viruses, including HIV-1, are characterized by the presence of accessory genes such as vif, vpr, vpx, vpu, and nef. Current knowledge indicates that none of the primate lentiviral accessory proteins has enzymatic activity. Instead, these proteins interact with cellular ligands to either act as adapter molecules to redirect the normal function of host factors for virus-specific purposes or to inhibit a normal host function by mediating degradation or causing intracellular mislocalization/sequestration of the factors involved. This review aims at providing an update of our current understanding of how Vif, Vpu, and Vpx control the cellular restriction factors APOBEC3G, BST-2, and SAMHD1, respectively.

灵长类免疫缺陷病毒，包括 HIV-1，其特征是存在辅助基因，例如vif 、 vpr 、 vpx 、 vpu和nef 。目前的知识表明灵长类慢病毒辅助蛋白均不具有酶活性。相反，这些蛋白质与细胞配体相互作用，要么充当衔接分子，以重定向宿主因子的正常功能以达到病毒特异性的目的，要么通过介导降解或引起相关因子的细胞内错误定位/隔离来抑制正常宿主功能。本综述旨在更新我们目前对 Vif、Vpu 和 Vpx 如何分别控制细胞限制因子 APOBEC3G、BST-2 和 SAMHD1 的理解。