Screening interferon antagonists from accessory proteins encoded by P gene for immune escape of Caprine parainfluenza virus 3
文献类型： 外文期刊
作者： Sun, Min 1 ; Li, Wenliang 1 ; Zhang, Wenwen 1 ; Yang, Leilei 1 ; Hao, Fei 1 ; Li, Jizong 1 ; Mao, Li 1 ; Jiang, Jieyuan 1 ;
作者机构： 1.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing 210014, Peoples R China
2.Jiangsu Univ, Sch Food & Biol Engn, Zhenjiang 212013, Jiangsu, Peoples R China
关键词： Caprine parainfluenza virus 3; JAK; STAT signaling; Accessory protein; Interferon antagonist; STAT1
期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.03； 五年影响因子：2.923 ）
ISSN： 0378-1135
年卷期： 2021 年 254 卷
页码：
收录情况： SCI
摘要： The Caprine parainfluenza virus 3 (CPIV3) is a novel Paramyxovirus that is isolated from goats suffering from respiratory diseases. Presently, the pathogenesis of CPIV3 infection has not yet been fully characterized. The Type I interferon (IFN) is a key mediator of innate antiviral responses, as many viruses have developed strategies to circumvent IFN response, whether or how CPIV3 antagonizes type I IFN antiviral effects have not yet been characterized. This study observed that CPIV3 was resistant to IFN-? treatment and antagonized IFN-? antiviral responses on MDBK and goat tracheal epithelial (GTE) cell models. Western blot analysis showed that CPIV3 infection reduced STAT1 expression and phosphorylation, which inhibited IFN-? signal transduction on GTE cells. By screening and utilizing specific monoclonal antibodies (mAbs), three CPIV3 accessory proteins C, V and D were identified during the virus infection process on the GTE cell models. Accessory proteins C and V, but not protein D, was identified to antagonize IFN-? antiviral signaling. Furthermore, accessory protein C, but not protein V, reduced the level of IFN-? driven phosphorylated STAT1 (pSTAT1), and then inhibit STAT1 signaling. Genetic variation analysis to the PIV3 accessory protein C has found two highly variable regions (VR), with VR2 (31-70th aa) being involved in for the CPIV3 accessory protein C to hijack the STAT1 signaling activation. The above data indicated that CPIV3 is capable of inhibiting IFN-? signal transduction by reducing STAT1 expression and activation, and that the accessory protein C, plays vital roles in the immune escape process.
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