Sus scrofa RNase L通过激活I型IFN信号通路和细胞凋亡抑制PRRSV复制。

IF 2.4 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2025-01-13 DOI:10.1016/j.vetmic.2025.110392

Xiangju Wu , Xiaoyan Cong , Ping Jiang , Mingming Zhou , Ying Yu , Dandan Jiang , Yue Hu , Juntong Li , Jinxia Zhang , Ying Cao , Haowen Zhang , Yijun Du , Jing Qi

{"title":"Sus scrofa RNase L通过激活I型IFN信号通路和细胞凋亡抑制PRRSV复制。","authors":"Xiangju Wu , Xiaoyan Cong , Ping Jiang , Mingming Zhou , Ying Yu , Dandan Jiang , Yue Hu , Juntong Li , Jinxia Zhang , Ying Cao , Haowen Zhang , Yijun Du , Jing Qi","doi":"10.1016/j.vetmic.2025.110392","DOIUrl":null,"url":null,"abstract":"<div><div>Porcine reproductive and respiratory syndrome virus (PRRSV) has become one of the most economically important diseases to the global pig industry. RNase L is a ubiquitous cellular endoribonuclease that is activated upon the binding of a specific ligand, 2′,5′-linked oligoadenylates (2–5 A), which is synthesized by oligoadenylate synthetases (OASs). However, whether Sus scrofa RNase L (sRNase L) could inhibit PRRSV replication and its mechanism have not been fully elucidated. In this study, sRNase L was cloned and characterized in homology and structure firstly. Then the antiviral activity of sRNase L against PRRSV was explored. Overexpression of sRNase L significantly inhibited the propagation of PRRSV when treated with 2–5 A or poly(I: C) or mock treated. Furthermore, sRNase L induced degradation of cellular and viral ssRNAs, enhanced the activation of IFN-β promoter and IFN-β expression, and induced apoptosis to inhibit PRRSV replication. Taken together, we have first elucidated the anti-PRRSV function and the underlying mechanism of sRNase L, which may provide a new strategy for preventing PRRSV infection.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"302 ","pages":"Article 110392"},"PeriodicalIF":2.4000,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Sus scrofa RNase L inhibits PRRSV replication by activation of type I IFN signaling pathway and apoptosis\",\"authors\":\"Xiangju Wu , Xiaoyan Cong , Ping Jiang , Mingming Zhou , Ying Yu , Dandan Jiang , Yue Hu , Juntong Li , Jinxia Zhang , Ying Cao , Haowen Zhang , Yijun Du , Jing Qi\",\"doi\":\"10.1016/j.vetmic.2025.110392\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Porcine reproductive and respiratory syndrome virus (PRRSV) has become one of the most economically important diseases to the global pig industry. RNase L is a ubiquitous cellular endoribonuclease that is activated upon the binding of a specific ligand, 2′,5′-linked oligoadenylates (2–5 A), which is synthesized by oligoadenylate synthetases (OASs). However, whether Sus scrofa RNase L (sRNase L) could inhibit PRRSV replication and its mechanism have not been fully elucidated. In this study, sRNase L was cloned and characterized in homology and structure firstly. Then the antiviral activity of sRNase L against PRRSV was explored. Overexpression of sRNase L significantly inhibited the propagation of PRRSV when treated with 2–5 A or poly(I: C) or mock treated. Furthermore, sRNase L induced degradation of cellular and viral ssRNAs, enhanced the activation of IFN-β promoter and IFN-β expression, and induced apoptosis to inhibit PRRSV replication. Taken together, we have first elucidated the anti-PRRSV function and the underlying mechanism of sRNase L, which may provide a new strategy for preventing PRRSV infection.</div></div>\",\"PeriodicalId\":23551,\"journal\":{\"name\":\"Veterinary microbiology\",\"volume\":\"302 \",\"pages\":\"Article 110392\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-01-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Veterinary microbiology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0378113525000276\",\"RegionNum\":2,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Veterinary microbiology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0378113525000276","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MICROBIOLOGY","Score":null,"Total":0}

引用次数: 0

摘要

猪繁殖与呼吸综合征病毒（PRRSV）已成为全球养猪业最重要的经济疾病之一。RNase L是一种普遍存在的细胞核糖核酸内切酶，在与特定配体结合时被激活，2',5'-连接的低聚腺苷酸（2-5 a），由低聚腺苷酸合成酶（OASs）合成。然而，sRNase L是否能够抑制PRRSV的复制及其机制尚未完全阐明。本研究首次克隆了sRNase L，并对其同源性和结构进行了鉴定。探讨sRNase L对PRRSV的抗病毒活性。sRNase L的过表达在2-5 A或poly（I: C）或mock处理下显著抑制PRRSV的繁殖。此外，sRNase L诱导细胞和病毒的ssrna降解，增强IFN-β启动子的激活和IFN-β的表达，诱导细胞凋亡，从而抑制PRRSV的复制。综上所述，我们首次阐明了sRNase L的抗PRRSV功能及其潜在机制，这可能为预防PRRSV感染提供新的策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Sus scrofa RNase L inhibits PRRSV replication by activation of type I IFN signaling pathway and apoptosis

Porcine reproductive and respiratory syndrome virus (PRRSV) has become one of the most economically important diseases to the global pig industry. RNase L is a ubiquitous cellular endoribonuclease that is activated upon the binding of a specific ligand, 2′,5′-linked oligoadenylates (2–5 A), which is synthesized by oligoadenylate synthetases (OASs). However, whether Sus scrofa RNase L (sRNase L) could inhibit PRRSV replication and its mechanism have not been fully elucidated. In this study, sRNase L was cloned and characterized in homology and structure firstly. Then the antiviral activity of sRNase L against PRRSV was explored. Overexpression of sRNase L significantly inhibited the propagation of PRRSV when treated with 2–5 A or poly(I: C) or mock treated. Furthermore, sRNase L induced degradation of cellular and viral ssRNAs, enhanced the activation of IFN-β promoter and IFN-β expression, and induced apoptosis to inhibit PRRSV replication. Taken together, we have first elucidated the anti-PRRSV function and the underlying mechanism of sRNase L, which may provide a new strategy for preventing PRRSV infection.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

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.