Encephalomyocarditis virus non-structural protein 2C induces the degradation of NDP52 autophagy protein to promote its own survival

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2025-05-07 DOI:10.1016/j.vetmic.2025.110549

Rongqian Mo , Rongrong Cheng , Pingan Dong , Tingting Ma , Yaxin Zhang , Jingying Xie , Shasha Li , Huixia Li , Adi Idris , Xiangrong Li , Ruofei Feng

{"title":"Encephalomyocarditis virus non-structural protein 2C induces the degradation of NDP52 autophagy protein to promote its own survival","authors":"Rongqian Mo , Rongrong Cheng , Pingan Dong , Tingting Ma , Yaxin Zhang , Jingying Xie , Shasha Li , Huixia Li , Adi Idris , Xiangrong Li , Ruofei Feng","doi":"10.1016/j.vetmic.2025.110549","DOIUrl":null,"url":null,"abstract":"<div><div>EMCV is a significant zoonotic pathogen that causes severe encephalitis and myocarditis, particularly in pigs, posing substantial economic and public health challenges. Nuclear dot protein (NDP) 52 is an important autophagy adaptor protein known to target microbial pathogens, including viruses into autophagosomes to facilitate the selective autophagy process. Here, we investigated the interaction between EMCV and NDP52. We found that NDP52 negatively regulates the entry and replication phases of EMCV and interacts with EMCV VP1/VP2 proteins to mediate its autophagic degradation. Moreover, we show that EMCV 2C protein interacts with NDP52 through its N-terminal region to trigger the autophagic degradation of NDP52 via the involvement of the late endosomal molecules, Rab7 and Rab9. Our study reveals a novel mechanism by which EMCV uses its non-structural protein 2C to hijack the autophagy pathway, evading host antiviral responses and promoting survival.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110549"},"PeriodicalIF":2.7000,"publicationDate":"2025-05-07","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/S0378113525001841","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

Abstract

EMCV is a significant zoonotic pathogen that causes severe encephalitis and myocarditis, particularly in pigs, posing substantial economic and public health challenges. Nuclear dot protein (NDP) 52 is an important autophagy adaptor protein known to target microbial pathogens, including viruses into autophagosomes to facilitate the selective autophagy process. Here, we investigated the interaction between EMCV and NDP52. We found that NDP52 negatively regulates the entry and replication phases of EMCV and interacts with EMCV VP1/VP2 proteins to mediate its autophagic degradation. Moreover, we show that EMCV 2C protein interacts with NDP52 through its N-terminal region to trigger the autophagic degradation of NDP52 via the involvement of the late endosomal molecules, Rab7 and Rab9. Our study reveals a novel mechanism by which EMCV uses its non-structural protein 2C to hijack the autophagy pathway, evading host antiviral responses and promoting survival.

查看原文本刊更多论文

脑心肌炎病毒非结构蛋白2C诱导NDP52自噬蛋白降解，促进自身存活

EMCV是一种重要的人畜共患病原体，可引起严重脑炎和心肌炎，特别是在猪中，对经济和公共卫生构成重大挑战。核点蛋白（Nuclear dot protein， NDP） 52是一种重要的自噬适配蛋白，可将包括病毒在内的微生物病原体靶向自噬体，促进选择性自噬过程。在这里，我们研究了EMCV和NDP52之间的相互作用。我们发现NDP52负调控EMCV的进入和复制阶段，并与EMCV VP1/VP2蛋白相互作用，介导其自噬降解。此外，我们发现EMCV 2C蛋白通过其n端区域与NDP52相互作用，通过后期内体分子Rab7和Rab9的参与触发NDP52的自噬降解。我们的研究揭示了EMCV利用其非结构蛋白2C劫持自噬途径，逃避宿主抗病毒反应并促进存活的新机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

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.