APOBEC3G is a restriction factor of EV71 and mediator of IMB-Z antiviral activity

胞苷脱氨酶 生物 病毒学 APOBEC3G公司 病毒复制 RNA干扰 核糖核酸 基因敲除 调解人 病毒 肠道病毒71 细胞生物学 细胞培养 遗传学 基因 肠道病毒 生物化学
作者
Huiqiang Wang,Ming Zhong,Yanping Li,Ké Li,Shuo Wu,Tingting Guo,Shan Cen,Jian–Dong Jiang,Zhuorong Li,Yuhuan Li
出处
期刊:Antiviral Research [Elsevier]
卷期号:165: 23-33 被引量:17
标识
DOI:10.1016/j.antiviral.2019.03.005
摘要

Enterovirus 71 (EV71), a single-stranded positive-sense RNA virus, is the causative agent of hand, foot, and mouth disease (HFMD), for which no effective antiviral therapy is currently available. Apolipoprotein B messenger RNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G or A3G) is a cytidine deaminase that inhibits the replication of several viruses, such as human immunodeficiency virus-1, hepatitis B virus and hepatitis C virus. In our efforts toward understanding the antiviral spectrum and mechanism of A3G, we found that ectopic expression of A3G inhibited EV71 replication, whereas knockdown of endogenous A3G expression promoted EV71 replication. Moreover, inhibition of EV71 replication by IMB-Z, a N-phenylbenzamide derivative, is associated with increased levels of intracellular A3G, but reducing the level of A3G by RNA interference diminished the antiviral activity of IMB-Z. Mechanistically, we obtained evidence suggesting that the cytidine deaminase activity is not required for A3G inhibition of EV71 replication. Instead, we demonstrated that A3G can interact with viral 3D RNA-dependent RNA polymerase (RdRp) and viral RNA and be packaged into progeny virions to reduce its infectivity. Taken together, our results indicate that A3G is a cellular restriction factor of EV71 and mediator of the antiviral activity of IMB-Z. Pharmacological induction and/or stabilization of A3G is a potential therapeutic approach to treat diseases caused by EV71 infection, such as HFMD.
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