Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway

被引：13

作者：

Chen, Cancan ^{[1
,2
,3
]}

Ma, Xiaocao ^{[1
,2
]}

Hu, Qifei ^{[1
,2
]}

Li, Xinghua ^{[4
]}

Huang, Feng ^{[1
,2
]}

Zhang, Junsong ^{[1
,2
]}

Pan, Ting ^{[1
,2
]}

Xia, Jinyu ^{[4
]}

Liu, Chao ^{[1
,2
]}

Zhang, Hui ^{[1
,2
]}

机构：

[1] Sun Yat Sen Univ, Inst Human Virol, Zhongshan Sch Med, Guangzhou 510080, Guangdong, Peoples R China

[2] Sun Yat Sen Univ, Zhongshan Sch Med, Key Lab Trop Dis Control, Minist Educ, Guangzhou 510080, Guangdong, Peoples R China

[3] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Pathol, Guangzhou 510080, Guangdong, Peoples R China

[4] Sun Yat Sen Univ, Affiliated Hosp 5, Dept Infect Dis, Zhuhai 519000, Peoples R China

来源：

RETROVIROLOGY | 2017年 / 14卷

基金：

中国国家自然科学基金;

关键词：

MOV10; A3G; Vif; HIV-1; Ubiquitin-proteasome system (UPS); HIV-1; VIF; CBF-BETA; ANTIVIRAL ACTIVITY; ENZYME APOBEC3G; LIGASE COMPLEX; HOST RESTRICTION; E3; LIGASE; PROTEIN; IDENTIFICATION; BINDING;

D O I：

10.1186/s12977-017-0382-1

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Background: MOV10 protein has ATP-dependent 5'-3' RNA helicase activity and belongs to the UPF1p superfamily. It can inhibit human immunodeficiency virus type 1 (HIV-1) replication at multiple stages and interact with apolipoprotein-B-mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G or A3G), a member of the cytidine deaminase family that exerts potent inhibitory effects against HIV-1 infection. However, HIV-1-encoded virion infectivity factor (Vif) protein specifically mediates the degradation of A3G via the ubiquitin-proteasome system (UPS). Results: We demonstrate that MOV10 counteracts Vif-mediated degradation of A3G by inhibiting the assembly of the Vif-CBF-beta-Cullin 5-ElonginB-ElonginC complex. Through interference with UPS, MOV10 enhances the level of A3G in HIV-1-infected cells and virions, and synergistically inhibits the replication and infectivity of HIV-1. In addition, the DEAG-box of MOV10 is required for inhibition of Vif-mediated A3G degradation as the DEAG-box mutant significantly loses this ability. Conclusions: Our results demonstrate a novel mechanism involved in the anti-HIV-1 function of MOV10. Given that both MOV10 and A3G belong to the interferon antiviral system, their synergistic inhibition of HIV-1 suggests that these proteins may play complicated roles in antiviral functions.

引用

页数：19

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