Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling

被引：0
|
作者：
Qu, Changbo [1 ,2 ,3 ]
Li, Yang [4 ]
Li, Yunlong [4 ]
Pan, Yihang [1 ]
机构：
[1] Sun Yat Sen Univ, Precis Med Res Ctr, Tomas Lindahl Nobel Laureate Lab, Affiliated Hosp 7, Shenzhen 518107, Peoples R China
[2] Radboud Univ Nijmegen Med Ctr, Radboud Inst Mol Life Sci, Dept Biochem, Nijmegen, Netherlands
[3] Radboud Univ Nijmegen Med Ctr, Radboud Ctr Mitochondrial Med, Nijmegen, Netherlands
[4] Erasmus MC Univ Med Ctr, Dept Gastroenterol & Hepatol, NL-3015 CN Rotterdam, Netherlands
来源：
ARCHIVES OF VIROLOGY | 2022年 / 167卷 / 05期
关键词：
RIG-I; C-VIRUS;
D O I：
10.1007/s00705-022-05415-9
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
Hepatitis E virus (HEV) infection is the leading cause of acute hepatitis worldwide. The mitochondrial antiviral signaling protein (MAVS)-mediated interferon (IFN) response plays a pivotal role in hepatic antiviral immunity. However, little is known about the effect of overexpression of MAVS on HEV infection. Full-length MAVS (FL-MAVS) is the main form of MAVS that increases the production of IFNs. Here, we studied the effect of FL-MAVS on HEV infection. We found that overexpression of FL-MAVS profoundly inhibited HEV replication. Furthermore, we showed that the anti-HEV effect of FL-MAVS is largely dependent on JAK-STAT signaling activation.
引用
收藏
页码：1293 / 1300
页数：8
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