中文摘要：

载脂蛋白BmRNA编辑酶催化多肽样蛋白3G（apolipoprotein B mRNA—editing enzyme catalytic polypeptide 3 protein G，APOBEC3G）属于固有免疫家族成员，具有胞嘧啶脱氨酶活性，在HIV-1复制过程中通过与HIV-1的Gag蛋白相互作用，选择性包装进入病毒毒粒。在HIV-1的逆转录过程中，APOBEC3G通过催化病毒负链cDNA中的dc脱氨为dU，在病毒基因组中引入广泛的超突变，从而发挥抗病毒作用。除了胞嘧啶脱氨机制外，APOBEC3G还能通过某些非脱氨机制抑制HIV-1的活性，但具体机制尚需深入研究。HIV-1编码的Vif蛋白可以通过泛素-蛋白酶体的降解途径来拮抗APOBEC3G的抗病毒活性。APOBEC3G具有广谱的抗病毒活性，可显著抑制多种逆转录病毒，逆转录转座子和乙型肝炎病毒（HBV）等的活性。上调APOBEC3G的表达水平或抑制Vif对APOBEC3G的拮抗可能成为治疗HIV-1感染的新的有效方法。

英文摘要：

Apolipoprotein B mRNA-editing enzyme catalytic polypeptide 3 protein G （APOBEC3 G） is part of the innate immune system of host cells and has cytidine deaminase activity. It specifically incorporates into the virion during HIV-1 replication. The incorporation of APOBEC3G needs its interaction with HIV-1 Gag. In the HIV-1 reverse transcription process, APOBEC3G deaminates dC to dU in the first minus strand cDNA, and then induces extensive hypermutation in the viral genome. Besides deamination, APOBEC3G also inhibits HIV-1 by some kinds of non-deamination mechanisms which need to be further elucidated. HIV-1 Vif counteracts the activity of APOBEC3G by an ubiquitin-proteasome-mediated degradation of APOBEC3G. As a broad spectrum inhibitor of viruses, APOBEC3G also inhibits various retroviruses, retrotransposons and other viruses like HBV. Upregulating the expression of APOBEC3G or blocking the Vif-mediated degradation of APOBEC3G might be novel strategies to treat HIV-1 infection in the future.