Avian coronavirus infectious bronchitis virus Beaudette strain NSP9 interacts with STAT1 and inhibits its phosphorylation to facilitate viral replication

被引：1

作者：

Xia, Ting ^{[1
]}

Xu, Shengkui ^{[1
]}

Li, Xueyan ^{[1
]}

Ruan, Wenke ^{[1
]}

机构：

[1] Beijing Univ Agr, Coll Anim Sci & Technol, Beijing 102206, Peoples R China

来源：

VIROLOGY | 2024年 / 590卷

基金：

中国国家自然科学基金;

关键词：

Infectious bronchitis virus; Coronavirus; Nonstructural protein 9; STAT1; Viral replication; DIMERIZATION; PROTEINS; BLOCKING; PATHWAY; CELLS;

D O I：

10.1016/j.virol.2023.109944

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Avian coronavirus, known as infectious bronchitis virus (IBV), is the causative agent of infectious bronchitis (IB). Viral nonstructural proteins play important roles in viral replication and immune modulation. IBV NSP9 is a component of the RNA replication complex for viral replication. In this study, we uncovered a function of NSP9 in immune regulation. First, the host proteins that interacted with NSP9 were screened. The immune-related protein signal transducer and activator of transcription 1 (STAT1) was identified and the interaction between NSP9 and STAT1 was further confirmed. Furthermore, IBV replication was inhibited in STAT1-overexpressing cells but inversely affected in STAT1 knock-down cells. Importantly, NSP9 inhibited STAT1 phosphorylation. Finally, the expression of JAK/STAT pathway downstream genes IRF7 and ISG20 was significantly decreased in NSP9-overexpressing cells. These results showed the important role of IBV NSP9 in immunosuppression.

引用

页数：7