Feline Panleucopenia Virus NS2 Suppresses the Host IFN-beta Induction by Disrupting the Interaction between TBK1 and STING

文献类型： 外文期刊

第一作者： Kang, Hongtao

作者： Kang, Hongtao;Liu, Dafei;Tian, Jin;Hu, Xiaoliang;Zhang, Xiaozhan;Wu, Hongxia;Liu, Chunguo;Guo, Dongchun;Li, Zhijie;Jiang, Qian;Liu, Jiasen;Qu, Liandong;Yin, Hang

作者机构：

关键词： Feline panleucopenia virus (FPV);Nonstructural protein 2 (NS2);interferon beta (IFN-beta)

期刊名称：VIRUSES-BASEL （ 影响因子：5.048； 五年影响因子：5.127 ）

ISSN： 1999-4915

年卷期： 2017 年 9 卷 1 期

页码：

收录情况： SCI

摘要： Feline panleucopenia virus (FPV) is a highly infectious pathogen that causes severe diseases in pets, economically important animals and wildlife in China. Although FPV was identified several years ago, little is known about how it overcomes the host innate immunity. In the present study, we demonstrated that infection with the FPV strain Philips-Roxane failed to activate the interferon beta (IFN-beta) pathway but could antagonize the induction of IFN stimulated by Sendai virus (SeV) in F81 cells. Subsequently, by screening FPV nonstructural and structural proteins, we found that only nonstructural protein 2 (NS2) significantly suppressed IFN expression. We demonstrated that the inhibition of SeV-induced IFN-beta production by FPV NS2 depended on the obstruction of the IFN regulatory factor 3 (IRF3) signaling pathway. Further, we verified that NS2 was able to target the serine/threonine-protein kinase TBK1 and prevent it from being recruited by stimulator of interferon genes (STING) protein, which disrupted the phosphorylation of the downstream protein IRF3. Finally, we identified that the C-terminus plus the coiled coil domain are the key domains of NS2 that are required for inhibiting the IFN pathway. Our study has yielded strong evidence for the FPV mechanisms that counteract the host innate immunity.

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