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猪细小病毒 3C 抑制 I 型干扰素的产生。

Porcine Sapelovirus 3C Inhibits the Production of Type I Interferon.

机构信息

State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.

Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, China.

出版信息

Front Cell Infect Microbiol. 2022 Jun 15;12:852473. doi: 10.3389/fcimb.2022.852473. eCollection 2022.

DOI:10.3389/fcimb.2022.852473
PMID:35782136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9240219/
Abstract

Porcine sapelovirus (PSV) is the causative pathogen of reproductive obstacles, acute diarrhea, respiratory distress, or severe polioencephalomyelitis in swine. Nevertheless, the pathogenicity and pathogenic mechanism of PSV infection are not fully understood, which hinders disease prevention and control. In this study, we found that PSV was sensitive to type I interferon (IFN-β). However, PSV could not activate the IFN-β promoter and induce IFN-β mRNA expression, indicating that PSV has evolved an effective mechanism to block IFN-β production. Further study showed that PSV inhibited the production of IFN-β by cleaving mitochondrial antiviral signaling (MAVS) and degrading melanoma differentiation-associated gene 5 (MDA5) and TANK-binding kinase 1 (TBK1) through viral 3C. In addition, our study demonstrated that PSV 3C degrades MDA5 and TBK1 through its protease activity and cleaves MAVS through the caspase pathway. Collectively, our results revealed that PSV inhibits the production of type I interferon to escape host antiviral immunity through cleaving and degrading the adaptor molecules.

摘要

猪传染性脑脊髓炎病毒（PSV）是引起猪繁殖障碍、急性腹泻、呼吸窘迫或严重脑脊髓灰质炎的病原体。然而，PSV 感染的致病性和发病机制尚不完全清楚，这阻碍了疾病的预防和控制。在本研究中，我们发现 PSV 对 I 型干扰素（IFN-β）敏感。然而，PSV 不能激活 IFN-β启动子并诱导 IFN-βmRNA 表达，这表明 PSV 已经进化出一种有效的机制来阻断 IFN-β的产生。进一步的研究表明，PSV 通过病毒 3C 切割线粒体抗病毒信号（MAVS）并降解黑色素瘤分化相关基因 5（MDA5）和 TANK 结合激酶 1（TBK1）来抑制 IFN-β的产生。此外，我们的研究表明 PSV3C 通过其蛋白酶活性降解 MDA5 和 TBK1，并通过半胱天冬酶途径切割 MAVS。总之，我们的研究结果表明，PSV 通过切割和降解衔接分子来抑制 I 型干扰素的产生，从而逃避宿主抗病毒免疫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/4b94cf6a0524/fcimb-12-852473-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/50e7ebf8b033/fcimb-12-852473-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/18bb911ba0f8/fcimb-12-852473-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/5b3d2d12d107/fcimb-12-852473-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/0ae2ee2e563d/fcimb-12-852473-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/282880432edc/fcimb-12-852473-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/b6bc528fe9c1/fcimb-12-852473-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/4b94cf6a0524/fcimb-12-852473-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/50e7ebf8b033/fcimb-12-852473-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/18bb911ba0f8/fcimb-12-852473-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/5b3d2d12d107/fcimb-12-852473-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/0ae2ee2e563d/fcimb-12-852473-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/282880432edc/fcimb-12-852473-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/b6bc528fe9c1/fcimb-12-852473-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/456f/9240219/4b94cf6a0524/fcimb-12-852473-g007.jpg

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