Veterinary microbiology最新文献

{"title":"Pathobiological characterization and estimation of the basic reproduction number of a recombinant african swine fever virus in contact-exposed pigs in Vietnam","authors":"The Viet Hoang Nguyen ,&nbsp;Ngoc Duong Vu ,&nbsp;Viet Dung Nguyen ,&nbsp;Thi Tam Than ,&nbsp;Thuy Nga Dang ,&nbsp;Huu Thien Nguyen ,&nbsp;Thi Chau Giang Tran ,&nbsp;Hoai Thuong Nguyen ,&nbsp;Phuong Anh Nguyen ,&nbsp;Ki-Hyun Cho ,&nbsp;Seong-Keun Hong ,&nbsp;Aruna Ambagala ,&nbsp;Yeon-Hee Kim ,&nbsp;Van Phan Le","doi":"10.1016/j.vetmic.2026.110961","DOIUrl":"10.1016/j.vetmic.2026.110961","url":null,"abstract":"<div><div>African swine fever virus (ASFV) causes a highly lethal disease in domestic pigs, resulting in severe economic losses. This study examined the clinical course, viral dynamics, immune response, and pathological changes in pigs infected with a recombinant ASFV strain of p72 genotypes I/II (rASFV I/II) via direct inoculation or natural contact. The directly infected pig developed persistent fever (&gt; 40 °C), anorexia, lethargy, and respiratory distress soon after the onset of viremia, and died six days post-inoculation (dpi). Contact-exposed pigs showed similar clinical signs and died between 12 and 21 days post-exposure (dpe). Real-time PCR revealed rapid viral replication in blood and secretions, with peak viral loads detected at or just before death. No detectable antibody response was observed in either group, indicating acute disease progression and high virulence. Gross pathological examination revealed severe lesions in the spleen, lymph nodes, gastrointestinal tract, and lungs. Epidemiological analysis using the susceptible–infectious–removed (SIR) model estimated the generation time (mean ± SD) as 1.101 ± 0.507 days. The basic reproduction number (<em>R₀</em>) was 1.201 (95% CI: 0.628–2.302) using the exponential growth method and 1.248 (95% CI: 0.310–3.236) using the maximum likelihood method. These findings demonstrate the high virulence and transmission potential of the rASFV I/II strain, highlighting the need for early detection and rapid containment measures.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110961"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative RNA-seq analysis of Bovine parainfluenza virus type 3 and its V gene-deleted variant reveals that deletion of the V gene affects autophagy signaling","authors":"Yu Han ,&nbsp;Ao Wang ,&nbsp;Yan Gao ,&nbsp;Chongsheng Bai ,&nbsp;Minying Ju ,&nbsp;Bin Han ,&nbsp;Xiaoqi Jing ,&nbsp;Chongyang Wang ,&nbsp;Shanhui Ren","doi":"10.1016/j.vetmic.2026.110966","DOIUrl":"10.1016/j.vetmic.2026.110966","url":null,"abstract":"<div><div>Bovine parainfluenza virus type 3 (BPIV3) is a major respiratory pathogen in cattle, with a substantial economic impact on the global livestock industry. The V protein, a nonstructural accessory protein expressed via RNA editing of the P gene, antagonizes canonical antiviral signaling. However, its additional role in promoting viral replication remains poorly defined. Here, we demonstrate that the BPIV3 V protein significantly enhances viral replication via a novel autophagy-dependent mechanism. Using a reverse genetics system, we generated a V-gene deletion mutant (rBPIV3-ΔV). Comparative transcriptomic (RNA-seq) analysis of cells infected with wild-type BPIV3 and rBPIV3-ΔV revealed that the V protein specifically modulates host autophagy signaling. We confirmed key differentially expressed genes using real-time quantitative PCR and identified the V protein as the essential viral factor driving BPIV3-induced autophagy. Collectively, our transcriptomic data delineate the molecular differences underlying the attenuated replication of rBPIV3-ΔV and establish that the V protein exploits the autophagy pathway to facilitate viral propagation <em>in vitro</em>. This finding provides a crucial theoretical advance in understanding BPIV3 pathogenesis and reveals potential targets for the development of novel antivirals and vaccines.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110966"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of immune response in calves vaccinated with baculovirus vectored inactivated vaccine expressing 2.3.4.4b H5 protein of highly pathogenic Avian Influenza virus","authors":"Chang-Won Lee ,&nbsp;Sherry Glover ,&nbsp;Timothy Olivier ,&nbsp;Youngsub Lee ,&nbsp;Sara Erickson ,&nbsp;Bradley Gustafson ,&nbsp;Bishwas Sharma ,&nbsp;Alan J. Young ,&nbsp;Amber Schueler","doi":"10.1016/j.vetmic.2026.110970","DOIUrl":"10.1016/j.vetmic.2026.110970","url":null,"abstract":"<div><div>Clade 2.3.4.4b H5N1 highly pathogenic avian influenza (HPAI) virus is circulating widely in US dairy cattle with significant implications for milk production and cow health. Due to the critical need for intervention strategies for continuing outbreaks of bovine HPAI, a baculovirus vectored inactivated HPAI vaccine expressing the 2.3.4.4b H5 protein (Avian Influenza-H5) was developed utilizing a licensed prescription platform which has been tested and proven safe in multiple species. The immunogenicity of recombinant Avian Influenza-H5 vaccine was tested in 5-month-old calves. The subcutaneously vaccinated animals showed minor post-injection site swelling that resolved without further affect (or compromise). The vaccine induced a measurable immune response by ELISA 3 weeks after 1st vaccination although the antibody response was low or undetectable by virus neutralization (VN) or hemagglutination inhibition (HI) tests. Two- and four weeks after a 2nd vaccination, antibody titers greater than &gt; 40, which are typically considered minimum protective titer against HPAI virus challenge, were consistently observed in all the vaccinated animals by both HI and VN tests. Strong correlation between VN and HI titers (Pearson correlation coefficient (r) greater than 0.8) were observed. Because the vaccine only contains the H5 protein of influenza virus, all vaccinated animals were negative against nucleoprotein (NP) and N1 neuraminidase antibody by commercial NP ELISA and N1 specific enzyme linked lectin assay, respectively, which confirm the vaccine is DIVA (differentiation of infected from vaccinated) surveillance compatible. In summary, this study demonstrates that an inactivated baculovirus-vectored vaccine, Avian Influenza-H5, is immunogenic and generates presumed protective antibody levels in calves, although future studies evaluating the vaccine in lactating dairy cattle would determine the induction of local immunity in the mammary gland and milk, and if the vaccine provides field protection against influenza-induced mastitis.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110970"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computation-driven discovery of a next-generation canine monoclonal antibody for canine parvovirus therapy","authors":"Ying Li ,&nbsp;Xiaoyu Zhang ,&nbsp;Zhihao Wang ,&nbsp;Mingqin Lin ,&nbsp;Sheng Wang ,&nbsp;Chengguang Zhang ,&nbsp;Ling Zhao ,&nbsp;Jiahui Zou ,&nbsp;Hongbo Zhou","doi":"10.1016/j.vetmic.2026.110982","DOIUrl":"10.1016/j.vetmic.2026.110982","url":null,"abstract":"<div><div>Canine parvovirus (CPV) is a highly contagious and lethal pathogen that poses a major threat to canine health. Despite widespread vaccination efforts, CPV remains one of the primary causes of hemorrhagic enteritis and myocarditis. Also, current supportive therapy often fails to work well. Therefore, we urgently need to explore alternative or complementary therapeutic strategies. In this study, by integrating single B-cell sequencing technology with antigen-antibody structure prediction, we successfully screened the canine-derived monoclonal antibody (mAb) E9 against CPV. E9 exhibited high affinity and broad neutralizing activity <em>in vitro</em>, and achieved 80% therapeutic efficacy <em>in vivo</em>. This therapeutic effect highlights E9's great potential as a next-generation CPV biologic. In summary, our study offers a more efficient approach for acquiring neutralizing antibodies and provides a promising strategy for combating CPV.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110982"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147387730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isolation of reassortant H5N1 and H5N8 avian influenza viruses from co-infections and their host-dependent replication dynamics","authors":"Yuwei Wu ,&nbsp;Nuo Xu ,&nbsp;Zhifan Li ,&nbsp;Zijun Lu ,&nbsp;Yurui Dong ,&nbsp;Yijie Guo ,&nbsp;Ying Bian ,&nbsp;Kunlin Li ,&nbsp;Chenzhi Huo ,&nbsp;Tao Qin ,&nbsp;Sujuan Chen ,&nbsp;Hui Yang ,&nbsp;Daxin Peng ,&nbsp;Xiufan Liu","doi":"10.1016/j.vetmic.2026.110971","DOIUrl":"10.1016/j.vetmic.2026.110971","url":null,"abstract":"<div><div>Co-infection with avian influenza virus (AIV) is common in poultry populations, primarily due to the diversity of viral subtypes and the practice of mixed-species farming. However, the replication dynamics of different AIV subtypes within distinct avian host-species remain unclear. In this study, we isolated and identified H5N1 and H5N8 AIVs from a naturally co-infected duck and characterized their biological characteristic regarding co-infection under both <em>in vitro</em> and <em>in vivo</em> conditions. Phylogenetic analysis revealed the HA genes of both H5 subtype AIVs belonged to clade 2.3.2.1d, sharing identical segments excluding differences in the M and NA genes. The H5N1 virus exhibited significantly higher infectivity and replication than the H5N8 virus in chicken embryo fibroblasts (CEF) and duck embryo fibroblasts (DEF). Serial passages of co-infection <em>in vitro</em> revealed that H5N1 virus became dominant in the first passage in both CEF and DEF cells. <em>In vivo</em>, both viruses caused high mortality in SPF chickens, while nonlethal in SPF ducks. In co-infected SPF chickens, H5N1 virus exhibited a pronounced replication advantage and higher viral loads. However, compared with single infections, co-infection delayed death time and reduced replication capacity. Conversely, in co-infected SPF ducks, H5N8 virus exhibited a significant replication advantage; however, compared to single infections, the replication capacity of H5N8 virus was reduced while H5N1 virus was maintained. These findings suggest that host-species influence the replication fitness and dominance of AIVs during co-infection, highlighting the importance of enhanced epidemiological surveillance and reducing mixed-species farming to minimize reassortment and evolution of high-risk AIVs.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110971"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-2-aminoadipic acid inhibits porcine epidemic diarrhea virus replication by targeting and reducing cellular autophagy","authors":"Xiao Ma ,&nbsp;Hongbo Cui ,&nbsp;Runze Song ,&nbsp;Yanfei Huang ,&nbsp;Yilei Li ,&nbsp;Junxing Ma ,&nbsp;Hongying Chen ,&nbsp;Shijie Ma ,&nbsp;Zhanyong Wei","doi":"10.1016/j.vetmic.2026.110967","DOIUrl":"10.1016/j.vetmic.2026.110967","url":null,"abstract":"<div><div>Porcine epidemic diarrhea caused by porcine epidemic diarrhea virus (PEDV) is an acute and highly contagious intestinal infectious disease. The metabolic alterations during PEDV infection remain largely unexplored. In this study, LLC-PK1 cells infected with PEDV were subjected to non-targeted metabolomics analysis. Notably, the amino acid metabolite L-2-aminoadipic acid (L-2AA) was significantly upregulated, while indole-3-acetic acid (3-IAA) exhibited a marked downregulation following PEDV infection. Subsequent investigations revealed that both L-2AA and 3-IAA significantly hindered the late stage of viral propagation. Mechanistically, aldehyde dehydrogenase 7A1 (ALDH7A1), a key enzyme involved in the biosynthesis of L-2AA, mediates the PEDV-induced upregulation of L-2AA and functions to negatively regulate viral replication. Detailed analysis indicated that L-2AA mitigates PEDV infection via reducing autophagic activity. These data support a novel mechanism used by L-2AA to downregulate autophagic activity to block viral replication and provide potential anti-PEDV drug targets.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110967"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modification of N-glycosylation site in the spike protein enhances the neutralizing antibody response against PEDV","authors":"Shuonan Pan ,&nbsp;Liping Wei ,&nbsp;Yingjie Xiang ,&nbsp;Chunxiao Mou ,&nbsp;Huili Liu ,&nbsp;Zhenhai Chen","doi":"10.1016/j.vetmic.2026.110972","DOIUrl":"10.1016/j.vetmic.2026.110972","url":null,"abstract":"<div><div>Porcine epidemic diarrhea virus (PEDV) is a pathogenic enteric coronavirus of swine that causes severe diarrhea and high mortality in neonatal piglets. The extensively glycosylated spike (S) protein is essential for viral entry and vaccine design. For comprehensively characterizing N-glycosylation modifications of S protein, we analyzed the S proteins of 152 PEDV strains, revealing that the average number of N-glycosylation sites per S protein ranged from 27.5 to 30. To elucidate the function of N-glycosylation in the S protein, we generated 26 recombinant PEDV GX4/2021 strains harboring single-point mutations at individual N-glycosylation sites. The N873 glycosylation site of S protein was essential for viral viability, while mutations at N351, N264, N324, N688, N118, N425, N787, N726, N1249, N1261, N1273, N1278, and N1308 significantly reduced viral titers. In vivo mouse studies demonstrated that a PEDV mutant harboring the N324 mutation in S protein increased neutralizing antibody titers against PEDV, positioning it as a promising candidate for inactivated vaccine. Additionally, single-site mutations at the N324 or N873 site of S protein enhanced the capacity of recombinant Sendai virus (SeV) encoding the PEDV S protein to induce neutralizing antibodies against PEDV, suggesting that S proteins containing these mutations are promising candidate immunogens for engineered vector-based vaccines against PEDV. This study demonstrates that S protein N-glycosylation is critical for PEDV replication and immunogenicity, providing a foundation for novel vaccine design.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110972"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Japanese encephalitis virus envelope protein activates the TLR4/NF‑κB pathway to induce testicular inflammation","authors":"Yan Gao ,&nbsp;Qi Sheng ,&nbsp;Xinxin Shi ,&nbsp;Xiangshu Qiu ,&nbsp;Jiaqi Zhang ,&nbsp;Xu Gao ,&nbsp;He Zhang ,&nbsp;Huijun Lu","doi":"10.1016/j.vetmic.2026.110969","DOIUrl":"10.1016/j.vetmic.2026.110969","url":null,"abstract":"<div><div>Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, remains a leading cause of viral encephalitis in Asia and poses serious threats to reproductive health. However, the molecular mechanisms underlying JEV-induced testicular inflammation remain incompletely understood. In this study, an integrated approach involving proteomic, cellular, and animal experiments was used to investigate the role of Toll-like receptor 4 (TLR4) in JEV-triggered inflammatory responses. Proteomic analysis and in vitro assays revealed that JEV infection upregulated TLR4 expression and activated the NF‑κB signaling cascade, resulting in enhanced secretion of inflammatory cytokines, including TNF-α, IL-1β, and IL-6. Among the viral proteins examined, only the envelope (E) protein significantly increased endogenous TLR4 levels in a dose-dependent manner. Direct interaction between the E protein and TLR4 was confirmed by co-immunoprecipitation and immunofluorescence. In a mouse model of JEV infection, the virus induced severe testicular inflammation, characterized by tissue disruption, TLR4 upregulation, and activation of the TLR4/NF-κB pathway, consistent with the in vitro observations. Collectively, these findings identify the JEV E protein as a key inducer of TLR4-mediated inflammation and provide mechanistic insights into JEV-associated testicular pathology.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110969"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147387731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Equine neorickettsiosis: A global perspective of the natural habitat of the bacteria and clinical disease","authors":"Luis G. Arroyo ,&nbsp;Alexandre S. Borges ,&nbsp;John D. Baird ,&nbsp;Brian D. Perry ,&nbsp;Yasuko Rikihisa ,&nbsp;Stephen E. Greiman","doi":"10.1016/j.vetmic.2026.110963","DOIUrl":"10.1016/j.vetmic.2026.110963","url":null,"abstract":"<div><div>Equine neorickettsiosis (EN) is an infectious, non-contagious systemic disease of horses caused by the closely related obligatory intracellular bacterial species <em>Neorickettsia risticii</em> and <em>N. findlayensis</em>. Clinical cases are considered endemic in multiple regions across the United States and Canada, as well as in parts of South America, including Uruguay and Brazil. <em>Neorickettsia</em> spp. are obligate endosymbionts of digenean trematodes, which have complex life cycles involving a molluscan first intermediate host, a wide range of invertebrate or vertebrate second intermediate hosts, and a vertebrate definitive host in which sexual reproduction occurs. Horses serve as aberrant hosts following ingestion of aquatic insects parasitized with <em>Neorickettsia-</em>infected trematodes. Horses develop nonspecific clinical signs such as fever, lethargy, and anorexia. Gastrointestinal manifestations including altered intestinal motility, colic, and watery diarrhea are common, and some horses experience acute laminitis and abortions in pregnant mares. Molecular detection of nucleic acids is currently the preferred diagnostic method due to its rapid turnaround time and high analytical sensitivity. Antibiotic treatment is recommended in suspected cases, particularly in endemic areas, even before confirmatory test results is obtained. Early therapy is associated with a favorable prognosis for EN-associated colitis. However, effective long-term disease prevention strategies remain limited, and the development of broadly protective vaccines capable of addressing strain diversity and providing durable immunity represents an important ongoing research priority.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110963"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147387733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GRP78 interacts with the Nsp3 of porcine deltacoronavirus and inhibits viral replication","authors":"Zhengxin Liu ,&nbsp;Ruiming Yu ,&nbsp;Liping Zhang ,&nbsp;Yuhan Wen ,&nbsp;Dongsheng Wang ,&nbsp;Xinru Wang ,&nbsp;Zhongwang Zhang ,&nbsp;Peng Zhou ,&nbsp;Xiaohua Du ,&nbsp;Huichen Guo ,&nbsp;Li Pan ,&nbsp;Xia Liu ,&nbsp;Xinsheng Liu","doi":"10.1016/j.vetmic.2026.110984","DOIUrl":"10.1016/j.vetmic.2026.110984","url":null,"abstract":"<div><div>Porcine deltacoronavirus (PDCoV) is an important intestinal coronavirus, which has caused large economic losses to the global pig industry. Endoplasmic reticulum chaperone protein (GRP78) is involved in viral infection replication and regulates the homeostasis of host cells during pathogen infection. However, the role of GRP78 in PDCoV replication remains unclear. In this study, overexpression or knockdown of GRP78 was used to explore effects on PDCoV replication. The interaction between GRP78 and viral non-structural proteins was determined with co-IP and laser confocal microscopy experiments, and the role of GRP78 in PDCoV replication was further determined. GRP78 overexpression significantly inhibited PDCoV replication. PDCoV infection in LLC-PK1 cells decreased the expression of endogenous GRP78, thus demonstrating an antagonistic effect between them. Co-IP and laser confocal microscopy indicated that GRP78 interacted with PDCoV non-structural protein Nsp3, and GRP78 and Nsp3 antagonized each other, thus activating the unfolded protein response (UPR) and the cellular lysosomal autophagy pathway, and inhibiting PDCoV replication in host cells. These results demonstrate a novel mechanism through which the host protein GRP78 regulates viral replication, thus providing new information for understanding the interaction between PDCoV and the host.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110984"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147387732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}