State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth Diseases Reference Laboratory, Key Laboratory of Animal Virology of Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China.
Department of Pathology, Basic Medical College, Lanzhou University, Lanzhou 730000, China.
Virology. 2018 May;518:1-7. doi: 10.1016/j.virol.2018.01.028. Epub 2018 Feb 7.
Seneca Valley Virus (SVV) is a newly emerged virus belonging to the family Picornaviridae. Basic knowledge of the immunological response to SVV is limited. To date, one study has demonstrated that SVV 3C mediates the cleavage of host MAVS, TRIF, and TANK at specific sites and consequently escapes the host's antiviral innate immunity. In this study, we show that SVV 3C reduces IRF3 and IRF7 protein expression level and phosphorylation. SVV infection also reduces expression of IRF3 and IRF7 protein. The degradation of IRF3 and IRF7 is dependent on the 3C protease activity. We also identify interactions between 3C and IRF3 and IRF7 in PK-15 cells. A detailed analysis revealed that the degradation of IRF3 and IRF7 blocks the transcription of IFN-β, IFN-α1, IFN-α4, and ISG54. Together, our results demonstrate a novel mechanism developed by SVV 3C to allow the virus to escape the host's intrinsic innate immune system.
森那病毒（SVV）是一种新出现的病毒，属于小核糖核酸病毒科。目前对 SVV 免疫反应的基本知识知之甚少。迄今为止，有一项研究表明，SVV 3C 在特定部位介导宿主 MAVS、TRIF 和 TANK 的切割，从而逃避宿主的抗病毒先天免疫。在这项研究中，我们表明 SVV 3C 降低了 IRF3 和 IRF7 蛋白表达水平和磷酸化。SVV 感染也降低了 IRF3 和 IRF7 蛋白的表达。IRF3 和 IRF7 的降解依赖于 3C 蛋白酶活性。我们还在 PK-15 细胞中鉴定了 3C 和 IRF3 和 IRF7 之间的相互作用。详细分析表明，IRF3 和 IRF7 的降解阻断了 IFN-β、IFN-α1、IFN-α4 和 ISG54 的转录。总之，我们的研究结果表明，SVV 3C 开发了一种新的机制，使病毒能够逃避宿主的固有先天免疫系统。
