Laboratory of Molecular Microbiology, Viral Biochemistry Section, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892-0460, United States.
Curr Opin Virol. 2013 Dec;3(6):692-9. doi: 10.1016/j.coviro.2013.08.004. Epub 2013 Nov 15.
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,其特征在于存在辅助基因,如 vif、vpr、vpx、vpu 和 nef。目前的知识表明,灵长类慢病毒的辅助蛋白都没有酶活性。相反,这些蛋白质与细胞配体相互作用,要么作为衔接分子,将宿主因子的正常功能重定向到病毒特异性目的,要么通过介导降解或导致相关因子的细胞内定位/隔离来抑制正常的宿主功能。这篇综述旨在提供最新的信息,说明 Vif、Vpu 和 Vpx 分别如何控制细胞限制因子 APOBEC3G、BST-2 和 SAMHD1。