The underlying mechanism of Porcine Teschovirus 2 3Cpro antagonizing the NLRP3 inflammasome

IF 2.7 2区农林科学 Q3 MICROBIOLOGY Veterinary microbiology Pub Date : 2025-03-20 DOI:10.1016/j.vetmic.2025.110479

Xin-yu Zhang , Yu-ying Li , Wei Chen , Yi-min Zhou , Lin Zhou , Lu-lu Xie , Yan-Qing Hu , Hai-xin Huang , Chen-chen Zhao , Yan Qin , Tian Lan , Wen-chao Sun

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Abstract

Porcine teschovirus (PTV) can cause diseases such as poliomyelitis, pneumonia, and reproductive disorders in sows, but research on the pathogenesis of PTV infection is limited. In this investigation, we observed that PTV infection inhibits the activation of the NLRP3 inflammasome. PTV 3C^pro inhibits the activation of the NLRP3 inflammasome and pyroptosis by degrading NLRP3, IL-1β, and GSDMD. The degradation mechanism of 3C^pro involves the interaction of NLRP3, IL-1β, and 3C^pro, and 3C^pro degrades IL-1β through the caspase pathway. The mechanism by which PTV 3C^pro degrades GSDMD diverges from other picornavirus, remaining mechanistically elusive. Moreover, 3C^pro cannot degrade target proteins after their protease activity is lost. Our study provides new insights into the mechanism of antagonizing programmed cell death by PTV.

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猪Teschovirus 23cpro拮抗NLRP3炎性体的潜在机制

猪蛲虫病毒（PTV）可引起母猪脊髓灰质炎、肺炎和生殖障碍等疾病，但对PTV感染的发病机制研究有限。在这项研究中，我们观察到PTV感染抑制NLRP3炎性体的激活。PTV 3Cpro通过降解NLRP3、IL-1β和GSDMD抑制NLRP3炎性小体的激活和焦亡。3Cpro的降解机制涉及NLRP3、IL-1β和3Cpro的相互作用，3Cpro通过caspase途径降解IL-1β。PTV 3Cpro降解GSDMD的机制与其他小核糖核酸病毒不同，其机制尚不清楚。此外，3Cpro在失去蛋白酶活性后不能降解靶蛋白。我们的研究为PTV拮抗程序性细胞死亡的机制提供了新的见解。

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来源期刊

Veterinary microbiology 农林科学-兽医学

CiteScore

5.90

自引率

6.10%

发文量

221

审稿时长

52 days

期刊介绍： Veterinary Microbiology is concerned with microbial (bacterial, fungal, viral) diseases of domesticated vertebrate animals (livestock, companion animals, fur-bearing animals, game, poultry, fish) that supply food, other useful products or companionship. In addition, Microbial diseases of wild animals living in captivity, or as members of the feral fauna will also be considered if the infections are of interest because of their interrelation with humans (zoonoses) and/or domestic animals. Studies of antimicrobial resistance are also included, provided that the results represent a substantial advance in knowledge. Authors are strongly encouraged to read - prior to submission - the Editorials (''Scope or cope'' and ''Scope or cope II'') published previously in the journal. The Editors reserve the right to suggest submission to another journal for those papers which they feel would be more appropriate for consideration by that journal. Original research papers of high quality and novelty on aspects of control, host response, molecular biology, pathogenesis, prevention, and treatment of microbial diseases of animals are published. Papers dealing primarily with immunology, epidemiology, molecular biology and antiviral or microbial agents will only be considered if they demonstrate a clear impact on a disease. Papers focusing solely on diagnostic techniques (such as another PCR protocol or ELISA) will not be published - focus should be on a microorganism and not on a particular technique. Papers only reporting microbial sequences, transcriptomics data, or proteomics data will not be considered unless the results represent a substantial advance in knowledge. Drug trial papers will be considered if they have general application or significance. Papers on the identification of microorganisms will also be considered, but detailed taxonomic studies do not fall within the scope of the journal. Case reports will not be published, unless they have general application or contain novel aspects. Papers of geographically limited interest, which repeat what had been established elsewhere will not be considered. The readership of the journal is global.