APOBEC3G与Vif的相互作用及其对HIV复制的影响  

The effect of the interaction between apolipoprotein B mRNA editing enzyme-catalytic polypeptidelike 3G and viral infectivity factor on HIV-1 replication

作　　者：张昱 李敬云 Zhang Yu;Li Jingyun(Institute of Microbiology and Epidemiology, Academy of Military Medical Science, Beijing, 100071, China)

机构地区：[1]军事科学院军事医学研究院微生物流行病研究所,北京100071

出　　处：《中华实验和临床病毒学杂志》2019年第2期221-224,共4页Chinese Journal of Experimental and Clinical Virology

摘　　要：载脂蛋白B mRNA编辑酶3G(apolipoprotein B mRNA-editing enzyme 3G, APOBEC3G)属于载脂蛋白B mRNA编辑酶催化多肽家族(apolipoprotein B mRNA editing enzyme-catalytic polypeptide family, APOBEC family),可以通过胞嘧啶脱氨机制和非胞嘧啶脱氨机制来抑制人类免疫缺陷病毒1型(human immunodeficiency virus type 1, HIV-1)的复制。病毒感染性因子(viral infectivity factor,Vif)为HIV-1的辅助蛋白,可通过泛素-蛋白酶系统(ubiquitin-proteasome system, UPS)降解APOBEC3G,帮助HIV-1的复制。近年来,一些辅助因子如:核心结合因子β亚基(core binding factor β,CBF-β)、组蛋白去乙酰化酶6(histone deacetylase 6, HDAC6)、小鼠双微体2(mouse double minute 2,MDM2)等的发现帮助我们进一步理解APOBEC3G和Vif相互作用的机制,并为抗HIV-1药物的研发提供了新靶点。本研究综述了APOBEC3G和Vif的结构、两者之间的相互作用机制,以及APOBEC3G与Vif相互作用的干扰剂对HIV-1复制影响的研究进展。Apolipoprotein B mRNA editing enzyme-catalytic polypeptidelike 3G (APOBEC3G), which belongs to the APOBEC family, restricts the replication of HIV-1 through the deminase-dependent and deminase-independent antiviral mechanisms. Viral infectivity factor (Vif), an accessory protein edited by vif gene of HIV-1, promotes APOBEC3G ubiquitination and subsequent degradation by the proteasome result ing in the increased replication of HIV-1. Over the past few years, the discovery of some co-factors such as CBF-β, HDAC6 and MDM2 not only raises our awareness of the interaction between APOBEC3G and Vif but also provides new antiviral targets of HIV-1 in addition. Here we review the structure of APOBEC3G and Vif, and the effect of interference agents on HIV-1 replication by interacting with APOBEC3G and Vif.

关 键 词：人类免疫缺陷病毒1型 载脂蛋白BmRNA编辑酶3G 病毒感染性因子 

分 类 号：R512.91[医药卫生—内科学]