ZCCHC3 inhibits PEDV proliferation by degrading nuclear coat proteins via the proteasome pathway

IF 2.4 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2025-03-06 DOI:10.1016/j.vetmic.2025.110449

Zuyao Zhang , Shuangyang Wang , Huihui Sun , Jie Li , Jun Wang , Yangfan Li , Haichen Lin , Xuan Wang , Ruimin Bi , Zongyi Bo , Haixiao Shen , Liang Li , Pei Sun

{"title":"ZCCHC3 inhibits PEDV proliferation by degrading nuclear coat proteins via the proteasome pathway","authors":"Zuyao Zhang , Shuangyang Wang , Huihui Sun , Jie Li , Jun Wang , Yangfan Li , Haichen Lin , Xuan Wang , Ruimin Bi , Zongyi Bo , Haixiao Shen , Liang Li , Pei Sun","doi":"10.1016/j.vetmic.2025.110449","DOIUrl":null,"url":null,"abstract":"<div><div>Porcine epidemic diarrhea virus (PEDV) infection in pigs is characterized by vomiting, dehydration, and diarrhoea. The structural proteins of PEDV play crucial roles in viral entry, release, assembly, outgrowth, and host immune regulation. Similar to other viruses, PEDV primarily relies on host cellular mechanisms for productive infection. However, the host factors associated with PEDV infection remain undefined. Therefore, an in-depth understanding of the pathogenic mechanisms of PEDV is essential for comprehending this disease. Zinc-containing finger CCHC-type protein 3 (ZCCHC3) is an antiviral factor known to interact with RIG-I and cGAS, inhibiting the replication of pseudorabies virus (PRV). In this study, we investigated the role of porcine ZCCHC3 in PEDV proliferation. We first demonstrated that the expression of ZCCHC3 in LLC-PK1 cells is downregulated upon PEDV infection. Overexpression of ZCCHC3 inhibited PEDV replication, whereas knockdown of ZCCHC3 increased viral titer and N protein levels. Further studies revealed that ZCCHC3 interacts and co-localizes with N proteins, and that ZCCHC3-mediated antiviral effects depend on its zinc finger protease activity. Taken together, these findings provide valuable insights into the role of ZCCHC3 in PEDV proliferation and enhance our understanding of host-virus interactions.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"304 ","pages":"Article 110449"},"PeriodicalIF":2.4000,"publicationDate":"2025-03-06","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/S0378113525000847","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

Porcine epidemic diarrhea virus (PEDV) infection in pigs is characterized by vomiting, dehydration, and diarrhoea. The structural proteins of PEDV play crucial roles in viral entry, release, assembly, outgrowth, and host immune regulation. Similar to other viruses, PEDV primarily relies on host cellular mechanisms for productive infection. However, the host factors associated with PEDV infection remain undefined. Therefore, an in-depth understanding of the pathogenic mechanisms of PEDV is essential for comprehending this disease. Zinc-containing finger CCHC-type protein 3 (ZCCHC3) is an antiviral factor known to interact with RIG-I and cGAS, inhibiting the replication of pseudorabies virus (PRV). In this study, we investigated the role of porcine ZCCHC3 in PEDV proliferation. We first demonstrated that the expression of ZCCHC3 in LLC-PK1 cells is downregulated upon PEDV infection. Overexpression of ZCCHC3 inhibited PEDV replication, whereas knockdown of ZCCHC3 increased viral titer and N protein levels. Further studies revealed that ZCCHC3 interacts and co-localizes with N proteins, and that ZCCHC3-mediated antiviral effects depend on its zinc finger protease activity. Taken together, these findings provide valuable insights into the role of ZCCHC3 in PEDV proliferation and enhance our understanding of host-virus interactions.

查看原文本刊更多论文

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.