3C(pro) of FMDV inhibits type II interferon-stimulated JAK-STAT signaling pathway by blocking STAT1 nuclear translocation
文献类型： 外文期刊
作者： Wu, Xiangju 1 ; Chen, Lei 2 ; Sui, Chao 1 ; Hu, Yue 1 ; Jiang, Dandan 1 ; Yang, Fan 3 ; Miller, Laura C. 4 ; Li, Juntong 1 ; Cong, Xiaoyan 1 ; Hrabchenko, Nataliia 1 ; Lee, Changhee 5 ; Du, Yijun 1 ; Qi, Jing 1 ;
作者机构： 1.Shandong Acad Agr Sci, Inst Anim Sci & Vet Med, Shandong Key Lab Anim Dis Control & Breeding, Inst Crop Germplasm Resources,Key Lab Livestock &, Jinan 250100, Peoples R China
2.Shandong Normal Univ, Coll Life Sci, Jinan 250358, Peoples R China
3.Chinese Acad Agr Sci, Lanzhou Vet Res Inst, State Key Lab Vet Etiol Biol, Natl Foot & Mouth Dis Reference Lab, Lanzhou 730050, Peoples R China
4.Kansas State Univ, Coll Vet Med, Dept Diagnost Med & Pathobiol, Manhattan, KS 66506 USA
5.Gyeongsang Natl Univ, Coll Vet Med, Jinju 52828, South Korea
6.Gyeongsang Natl Univ, Virus Vaccine Res Ctr, Jinju 52828, South Korea
关键词： Foot-and-mouth disease virus (FMDV); 3C; IFN-gamma; JAK-STAT signaling pathway; STAT1; KPNA1
期刊名称：VIROLOGICA SINICA （ 影响因子：5.5； 五年影响因子：4.9 ）
ISSN： 1674-0769
年卷期： 2023 年 38 卷 3 期
页码：
收录情况： SCI
摘要： Foot-and-mouth disease virus (FMDV) has developed various strategies to antagonize the host innate immunity. FMDV L-pro and 3C(pro) interfere with type I IFNs through different mechanisms. The structural protein VP3 of FMDV degrades Janus kinase 1 to suppress IFN-gamma signaling transduction. Whether non-structural proteins of FMDV are involved in restraining type II IFN signaling pathways is unknown. In this study, it was shown that FMDV replication was resistant to IFN-gamma treatment after the infection was established and FMDV inhibited type II IFN induced expression of IFN-gamma-stimulated genes (ISGs). We also showed for the first time that FMDV non-structural protein 3C antagonized IFN-gamma-stimulated JAK-STAT signaling pathway by blocking STAT1 nuclear translocation. 3C(pro) expression significantly reduced the ISGs transcript levels and palindromic gamma-activated sequences (GAS) promoter activity, without affecting the protein level, tyrosine phosphorylation, and homodimerization of STAT1. Finally, we provided evidence that 3C protease activity played an essential role in degrading KPNA1 and thus inhibited ISGs mRNA and GAS promoter activities. Our results reveal a novel mechanism by which an FMDV non-structural protein antagonizes host type II IFN signaling.
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