中文摘要：

病毒感染因子（virion infectivity factor，Vif）是人免疫缺陷病毒（human immunodeficiency virus，HIV）的6个辅助蛋白之一，是病毒进行有效复制所必需的。由于Vif功能的复杂性以及对相应复合物体系的不了解，一直以来，对Vif的研究进展缓墁。直到2002年发现载脂蛋白BmRNA编辑酶催化多肽样蛋白3G（apolipoprotein B mRNA-editingenzyme catalytic polypeptide-like 3G，APOBEC3G）是存在于细胞内的一种天然抗病毒因子后，Vif的功能才被逐步阐明。APOBEC3G主要通过嘧啶脱氨基活性使HIV-1的负链DNA在逆转录过程中发生致死性超突变，从而起到抗病毒作用。HIV-1基因编码Vif来拮抗APOBEC3G，二者在宿主细胞内达到动态平衡。Vif通过介导APOBEC3G降解、减少在胞内的表达、阻碍其向病毒粒子的包装以及促使其装配成无活性的高分子质量复合体等多种途径起到中和作用。对Vif／APOBEC3G相互作用及其调节机制的进一步研究，将为新型抗HIV-1病毒药物的研制与开发提供理论依据。

英文摘要：

The virion infectivity factor （Vif） is one of the six human immunodeficiency virus （HIV） accessory proteins. It is essential for efficient viral replication. For a long time, the progress in Vif function is limited because the complexity of its function and correspondingly complex systems are not clear. Until 2002, some studies have revealed the apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G （APOBEC3G） is a potent intrinsic inhibitor of retroviral replication. Vif-function has been rapidly elucidated. APOBEC3G blocks the produc- tive infection of HIV- 1 mainly through cytidine deaminase activity. APOBEC3G effectively halts HIV replication by lethal dC to dU editing and dG to dA hypermutation during the reverse transcription. Retroviruses have evolved Vif to counter the antiretroviral action of APOBEC3G. Firstly, Vif can directly induce APOBEC3G rapid degradation via the ubiquitin-proteasomal pathway. Secondly, Vif inhibits the translation of APOBEC3G mRNA, further reducing the enzyme within the cell. In addition, Vif might promote the transition of APOBEC3G from low molecular mass （LMM） to high molecular mass （HMM） conformations, thereby defeats the antiviral activity of APOBEC3G. The further research on the reaction of Vif/APOBEC3G will provide the theoretical basis for the antiviral drug development.