Veterinary microbiology最新文献

{"title":"SVA virus-like vesicle vaccine based on VEEV-VSVG vector elicits efficient immune responses and protection in swine","authors":"Zhenxiang Rong ,&nbsp;Mingjin Jiao ,&nbsp;Nan Cao ,&nbsp;Mingxing Lu ,&nbsp;Shudan Liu ,&nbsp;Chao Zhang ,&nbsp;Liuqing Wei ,&nbsp;Yamei Li ,&nbsp;Huanchun Chen ,&nbsp;Xiangmin Li ,&nbsp;Ping Qian","doi":"10.1016/j.vetmic.2025.110862","DOIUrl":"10.1016/j.vetmic.2025.110862","url":null,"abstract":"<div><div><em>Seneca Valley virus</em> (SVV), a member of the <em>Picornaviridae</em> family，which is closely associated with porcine idiopathic vesicular disease (PIVD), spread quickly and has posed a potential threat to the swine industry in several countries. Currently, SVA demonstrate persistent genetic evolution, yet no licensed vaccines or effective therapeutics are commercially available for disease containment，which underscores the significance of strategies for preventing and controlling SVA infection. A <em>Venezuelan equine encephalitis virus</em> (VEEV) replicon system expressing <em>Vesicular stomatitis virus</em> glycoprotein (VSVG) was constructed in the preliminary research. In this study, we developed a recombinant virus-like vesicles (rVLVs) vaccine expressed SVA VP1 and VP2 protein based on the VEEV-VSVG system and evaluated the characterization and stability. Subsequently, immunization with rVLVs vaccine elicited robust humoral and cellular immune responses in both mice and swine. In addition, the swine challenge experiment manifested that immunization with rVLVs-SVA-VP2 conferred complete protection, comparable to the inactivated vaccine, whereas rVLVs-SVA-VP1 vaccination demonstrated a 60 % protective efficacy.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110862"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145980512","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":"Transcriptomic profiling reveals that NSDV exploits autophagy as a proviral mechanism to enhance viral replication","authors":"Xue-Lian Zhang ,&nbsp;Xiao-Wen Li ,&nbsp;Wei-Hao Tan ,&nbsp;Jia-Run Yang ,&nbsp;Jie-Yue Liang ,&nbsp;Jian-Wei Shao","doi":"10.1016/j.vetmic.2026.110895","DOIUrl":"10.1016/j.vetmic.2026.110895","url":null,"abstract":"<div><div>Nairobi sheep disease virus (NSDV), a tick-borne orthonairovirus that causes lethal hemorrhagic gastroenteritis in small ruminants, has recently expanded eastward into China. However, its molecular pathogenesis remains poorly understood. In this study, time-course transcriptomic profiling of NSDV-infected BHK-21 cells revealed a progressive reprogramming of the autophagy pathway, characterized by significant up-regulation of autophagy-related genes. Enhanced autophagosome formation and accelerated autophagosome–lysosome fusion were confirmed by electron microscopy and mRFP-GFP-LC3 flux assays. Pharmacological blockade of autophagy with chloroquine markedly reduced viral RNA accumulation and concurrently enhanced type I interferon responses, indicating that NSDV actively exploits autophagy to facilitate replication and dampen innate immunity. These findings identify autophagy as a proviral mechanism essential for optimal NSDV replication and suggest that targeting this pathway could offer a novel therapeutic strategy against emerging nairoviral infections.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110895"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998980","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":"The role of neuraminidase NanH in drug-induced phagocytic resistance of G. parasuis and its targeted intervention","authors":"Yuqing Tan ,&nbsp;Ze Li ,&nbsp;Shijiao Huan ,&nbsp;Yaqin Liu ,&nbsp;Hengming Liu ,&nbsp;Shenglan Liu ,&nbsp;Zhixin Lei","doi":"10.1016/j.vetmic.2026.110905","DOIUrl":"10.1016/j.vetmic.2026.110905","url":null,"abstract":"<div><h3>Background</h3><div><em>Glaesserella parasuis</em> (<em>G. parasuis</em>) is the core pathogen of porcine respiratory disease syndrome (PRDC), and the co-evolution of its drug resistance and virulence has seriously threatened the biosecurity of the global pig farming industry.</div></div><div><h3>Objective</h3><div>This study aims to clarify the core function of neuraminidase (NanH) in the formation and pathogenic mechanism of <em>G. parasuis</em> resistance and explore its feasibility as a novel therapeutic target.</div></div><div><h3>Method</h3><div>Drug-resistant strains were induced by tildipirosin combined with florfenicol (MIC increased to 16 μg/mL), and the mechanism of drug resistance was systematically analyzed by transcriptomics, gene knockout and multi-model infection experiments.</div></div><div><h3>Result</h3><div>The activity of the ABC transport system in drug-resistant strains was enhanced, the virulence genes <em>VapC</em> and <em>artM</em> were upregulated, the smoothness of the cell wall increased, and host autophagy was significantly inhibited (LC3-II transformation decreased, <em>P &lt; 0.01</em>). The <em>nanH</em> gene was highly expressed in drug-resistant strains. Its deletion (<em>ΔnanH</em>) reduced bacterial adhesion by 57 % (<em>P &lt; 0.01</em>), decreased mouse mortality by 70 % (<em>P &lt; 0.005</em>), and inhibited the transcription of COX-2 and TNF-α. The autophagy-targeted chimeric (NanH-AUTAC) designed based on the targeted protein degradation (TPD) strategy achieved a degradation rate of 60 % for NanH-EGFP at 40 μM.</div></div><div><h3>Conclusion</h3><div>NanH is a key regulatory factor in the co-evolution of <em>G. parasuis</em> drug resistance and virulence, and can serve as a potential target for anti-infection treatment. The \"disarming\" strategy based on TPD provides a new direction for dealing with drug-resistant bacterial infections.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110905"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146114385","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":"Development of an inactivated H9N2 subtype avian influenza serological DIVA vaccine using the chimeric A/B NA epitope approach","authors":"Jingfeng Zhang ,&nbsp;Zhiyu Fan ,&nbsp;Qunxing Pan ,&nbsp;Fei Yu ,&nbsp;Huawei Sun ,&nbsp;Minhua Sun ,&nbsp;Jinping Fu ,&nbsp;Jiasheng Song","doi":"10.1016/j.vetmic.2026.110917","DOIUrl":"10.1016/j.vetmic.2026.110917","url":null,"abstract":"<div><div>Vaccination is a critical strategy for controlling H9N2 avian influenza, a subtype with significant implications for poultry health and public safety. Current vaccines hinder serological differentiation between naturally infected and vaccinated animals, complicating disease surveillance and eradication efforts. Here, we developed a novel H9-subtype differentiating-infected-from-vaccinated-animals (DIVA) vaccine using reverse genetics. The recombinant virus, Re-H9-DIVA-J2, was engineered by replacing the neuraminidase (NA) gene of a clinically isolated H9 strain (A/chicken/Guangdong/J2/2016) with the NA ectodomain from a B/Yamagata-lineage influenza virus (B/Massachusetts/2/2012), while retaining six internal genes from the H1N1 PR8 strain. The chimeric virus exhibited low pathogenicity in chicken embryos, high growth titers (HA≥8 log₂), and stable genetic inheritance of the B-type NA marker over 10 passages. Three batches of inactivated vaccines were tested in specific-pathogen-free (SPF) chickens, demonstrating robust immunogenicity with hemagglutination inhibition (HI) antibody titers peaking at 10 log₂ by 21 days post-vaccination. Challenge experiments confirmed full clinical protection and reduced viral shedding (above 90 % protection). Critically, sera from Re-H9-DIVA-J2-vaccinated chickens showed no cross-reactivity with A-type N2 protein in immunofluorescence (IFA) and ELISA assays, distinguishing them from sera of wild-type-infected or conventional H9N2-vaccinated animals. This study presents a safe, immunogenic H9 marker vaccine compatible with DIVA diagnostics, offering a promising tool for H9N2 control and eradication.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110917"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137893","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":"Faecalibacterium prausnitzii derived postbiotic attenuates PEDV-induced mitochondrial apoptosis through blocking viral entry","authors":"Lingcong Deng ,&nbsp;Rui Luo ,&nbsp;Shihan Yang ,&nbsp;Letian Li ,&nbsp;Nan Li ,&nbsp;Yu Dong ,&nbsp;Jiayi Hao ,&nbsp;Ju Li ,&nbsp;Anqi Deng ,&nbsp;Xueyan Ai ,&nbsp;Maopeng Wang ,&nbsp;Chang Li","doi":"10.1016/j.vetmic.2026.110880","DOIUrl":"10.1016/j.vetmic.2026.110880","url":null,"abstract":"<div><div>Porcine epidemic diarrhea virus (PEDV) damaged to the intestinal epithelial cells of suckling piglets, resulting in elevated mortality rates and substantial economic losses. This study aimed to evaluate the effect of <em>F. prausnitzii</em> on PEDV invasion and mitochondrial function in cells. Our study demonstrated that <em>F. prausnitzii</em> exhibited strongly adhesion to PEDV virions, thereby preventing their entry into cells and enhancing cell viability. Notably, <em>F. prausnitzii</em> inhibited PEDV-induced apoptosis in Vero-E6 cells, as indicated by decreased activation of PARP, caspase-3/9, and the Bax/Bcl-2 ratio, while preserving mitochondrial structure and membrane potential. Moreover, the adhesion-mediated inhibition of the PEDV-induced mitochondrial apoptotic pathway was correlated with reduced reactive oxygen species (ROS) production and cytochrome c translocation. These results suggested that <em>F. prausnitzii</em> as postbiotic may serve as a preventive measures against different subtype PEDV infection by targeting mitochondrial apoptotic pathways, and broadened the horizons for the antiviral effects of postbiotic.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110880"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079300","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":"Salt inactivation kinetics of six porcine viruses in a 3D collagen model, simulating natural sausage casings","authors":"Tinka Jelsma ,&nbsp;Joris J. Wijnker ,&nbsp;Eline Verheij ,&nbsp;Wim H.M. van der Poel ,&nbsp;Henk J. Wisselink","doi":"10.1016/j.vetmic.2026.110902","DOIUrl":"10.1016/j.vetmic.2026.110902","url":null,"abstract":"<div><div>Natural sausage casings are derived from intestines of regularly slaughtered pigs, bovines and small ruminants. Although casings are derived only from healthy animals after mandatory veterinary inspection, some slaughtered animals may originate from areas where contagious animal viral diseases are endemic. A validated 3D collagen model was used to establish inactivation kinetics of bovine viral diarrhoea virus (BVDV), porcine epidemic diarrhoea virus (PEDV), porcine reproductive and respiratory syndrome virus (PRRSV), pseudorabies virus (PrV), swine vesicular disease virus (SVDV) and transmissible gastroenteritis virus (TGEV) following treatment with saturated sodium chloride (NaCl) brine in line with the common production process of natural casings and alternatively a phosphate supplemented sodium chloride (P-salt). Decimal reduction values (<span>D</span>-values), representing time needed to reduce the initial viral load by 1 log₁₀ (or 90 %), were determined at 4°C, 12°C and 20°C. For PRRSV and PrV, NaCl treatment at 12°C and 20°C was effective in lowering <span>D</span>-values significantly, while opposite results were found for BVDV, PEDV, SVDV and TGEV. Compared to the non-treatment, P-salt significantly decreased <span>D</span>-values for each virus at all temperatures, except for PrV and SVDV at 4°C. Despite clear thermal inactivation, no consistent correlation was found between salt inactivation and virus characteristics, like enveloped versus non-enveloped, DNA versus RNA viruses, and virion sizes. However, for individual viruses, the presented <span>D</span>-values can be used for future quantitative microbial risk assessment (QMRA) and to support emergency protocols and precautionary measures for sourcing of natural casings in cases of an acute outbreak of viral disease in endemic areas.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110902"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079312","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":"A two-component system regulating suilysin production in ST1 serotype 2 Streptococcus suis","authors":"Michelle Wiebe,&nbsp;Angelo Antiguas,&nbsp;Sashi Kant,&nbsp;Michael Beck,&nbsp;Raksha Tiwari,&nbsp;Philip R. Hardwidge,&nbsp;Luchang Zhu","doi":"10.1016/j.vetmic.2026.110878","DOIUrl":"10.1016/j.vetmic.2026.110878","url":null,"abstract":"<div><div><em>Streptococcus suis</em> is a major zoonotic bacterial pathogen that poses significant challenges to both the swine industry and human health. Suilysin, a secreted cytotoxin produced by <em>S. suis</em>, is a critical virulence factor that facilitates bacterial invasion, dissemination, and disruption of the blood-brain barrier. However, the regulation of suilysin production remains incompletely understood. This study demonstrates that the Ihk/Irr two-component system regulates suilysin expression in highly virulent ST1 serotype 2 <em>S. suis</em> strains. Deletion of the <em>ihk</em> and <em>irr</em> genes resulted in significant reductions in suilysin transcript levels and protein abundance. Furthermore, loss of the Ihk/Irr system decreased bacterial cytotoxicity to a level comparable to that observed in a suilysin deletion mutant. Genome-wide transcriptomic analysis revealed that, in addition to suilysin, this two-component system regulates a broad array of genes, including those encoding transcriptional regulators, ABC transporters, and putative virulence factors such as the surface antigen Sao and the cell wall endopeptidase PepO. Overall, this work identifies new regulatory targets of the Ihk/Irr system in <em>S. suis</em>, providing deeper insight into how this pathogen coordinates the expression of its virulence factors.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110878"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145941330","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":"Genomic characterization of Salmonella enterica serotype Saintpaul isolates from horses","authors":"Tirth Uprety ,&nbsp;Carrie L. Shaffer ,&nbsp;Alan Loynachan ,&nbsp;Jennifer Janes ,&nbsp;Lynne Cassone ,&nbsp;Laura Kennedy ,&nbsp;Uneeda Bryant ,&nbsp;Rebecca Ruby ,&nbsp;Melissa Swan ,&nbsp;Beatrice T. Sponseller ,&nbsp;Emma Adam ,&nbsp;Brian Lubbers ,&nbsp;Erdal Erol","doi":"10.1016/j.vetmic.2026.110923","DOIUrl":"10.1016/j.vetmic.2026.110923","url":null,"abstract":"<div><div>Salmonellosis is a highly contagious, zoonotic disease affecting both animal and human health. Early characterization of emerging <em>Salmonella</em> serotypes and associated antimicrobial resistance patterns are essential for outbreak controls in animals and humans. Between 2018 and 2025, 245 <em>Salmonella enterica</em> subsp. <em>enterica</em> were isolated from both ante-mortem and post-mortem equine cases. The predominant <em>Salmonella</em> serotypes were Typhimurium (83), Newport (28), 1,4,[5],12:i:- (26), Saintpaul (25), Hartford (15), and Mbandaka (12). <em>S.</em> Saintpaul, previously rare in horses, was detected in 21 cases in 2025, all originating from Central Kentucky, and was associated with enterocolitis, bronchopneumonia, omphalitis, and septicemia, primarily in young foals. Sixteen <em>S.</em> Saintpaul isolates were subjected to whole genome sequencing and exhibited a White-Kauffmann-Le Minor scheme antigenic profile of 1,4,[5],12:e,h:1,2, consistent with previously reported <em>S.</em> Saintpaul strains. Multi-locus sequence typing assigned all isolates to sequence type ST50. Core genome MLST revealed low genetic diversity among the isolates, suggesting closely related strain cluster. Antimicrobial susceptibility testing revealed widespread multi-drug resistance, particularly to aminoglycosides, beta-lactams, tetracyclines and sulfonamides. Genotypic analysis confirmed the presence of antimicrobial resistance genes, including <em>bla</em>_CTX-M-32 (not previously reported in <em>Salmonella</em> from horses), <em>bla</em>_CMY-2, <em>sul1</em>, <em>dfrA34</em>, and <em>rmtE1</em>, aligning with phenotypic findings. <em>S.</em> Saintpaul isolates harbored multiple plasmids, primarily of the IncI-gamma/K1 and, to a lesser extent, ColRNAI family. IncI-gamma/K1 plasmids were consistently associated with the MOB_P relaxase and MPF_I mating pair formation system. The emergence of multi-drug-resistant <em>S.</em> Saintpaul in horses underscores the importance of continued surveillance and antimicrobial resistance monitoring to mitigate animal and zoonotic risks.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110923"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137826","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":"Maedi infection modulates oncogenic and inflammatory signaling in ovine pulmonary adenomatosis through TLR4/NF-κB and JAK2/STAT3 pathways: A Trojan horse mechanism","authors":"İsmail Bolat ,&nbsp;Enver Beytut ,&nbsp;Yavuz Selim Sağlam ,&nbsp;Emin Karakurt ,&nbsp;Nüvit Coşkun ,&nbsp;Selim Çomakli ,&nbsp;Berrah Gözegi̇r ,&nbsp;Tuba Karaarslan ,&nbsp;Merve Bolat ,&nbsp;Betül Orhan","doi":"10.1016/j.vetmic.2026.110906","DOIUrl":"10.1016/j.vetmic.2026.110906","url":null,"abstract":"<div><div>Ovine pulmonary adenomatosis (OPA) is a contagious pulmonary tumor of sheep caused by Jaagsiekte sheep retrovirus, whereas Maedi is a chronic lentiviral infection characterized by persistent pulmonary inflammation. Although both diseases affect the lung, their interaction during natural co-infection remains poorly understood. This study investigated how chronic Maedi infection may influence inflammatory, oncogenic, and apoptotic signaling pathways in OPA-affected lung tissue. Lung samples from naturally infected sheep were classified by PCR and histopathological examination into Maedi (n = 6), OPA (n = 6), and Maedi+OPA co-infection (n = 6) groups. Key inflammatory, oncogenic, and apoptotic markers were evaluated at the protein and transcript levels. Maedi and mixed infection groups showed increased activation of the TLR4/NF-κB pathway and elevated pro-inflammatory cytokine expression compared with OPA alone. These changes were associated with significant alterations in apoptotic markers, including increased Bax and Caspase-3 expression and decreased Bcl-2 levels (p &lt; 0.05). In contrast, OPA samples exhibited higher activity of JAK2/STAT3 and PI3K/AKT/mTOR signaling pathways, which appeared reduced under Maedi-associated conditions. Overall, these findings suggest that chronic Maedi infection may modulate the pulmonary microenvironment by influencing inflammatory, apoptotic, and oncogenic signaling pathways in OPA. This immunomodulatory interaction may be relevant for understanding host–virus dynamics in naturally occurring virus-induced lung tumors.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110906"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079299","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":"Distinct mechanisms of ER stress-mediated autophagy induction by high- and low-virulence pseudorabies virus strains","authors":"Yueqing Lv ,&nbsp;Xiangmei Huang ,&nbsp;Zhipei Lu ,&nbsp;Xiaoying Feng ,&nbsp;Kang Ouyang ,&nbsp;Ying Chen ,&nbsp;Zuzhang Wei ,&nbsp;Weijian Huang ,&nbsp;Yifeng Qin","doi":"10.1016/j.vetmic.2026.110914","DOIUrl":"10.1016/j.vetmic.2026.110914","url":null,"abstract":"<div><div>Pseudorabies virus (PRV) is one of the most significant pathogens threatening the swine industry, and its infection has caused substantial economic losses to pig farming worldwide. This study utilized two PRV strains isolated by our laboratory: the GXLB-2015 strain, a natural recombinant between a PRV variant strain and the Bartha-K61 vaccine strain, which exhibits stronger virulence, and the GXGG-2016 strain, a classical genotype II PRV strain with a natural 69-amino acid deletion in its TK gene, which demonstrates weak virulence and is non-pathogenic in mice. Focusing on endoplasmic reticulum stress (ERS) and cellular autophagy, this research explored the molecular mechanisms underlying the significant difference in virulence between these two PRV strains. The results revealed that infection with both strains induced noticeable ERS and autophagy, both of which inhibited viral replication. Further investigation showed that upon ERS induction, the GXLB-2015 strain mediated autophagy by activating both the PERK-eIF2α-ATF4-CHOP and IRE1-XBP1 pathways; inhibiting these pathways suppressed viral replication. In contrast, the GXGG-2016 strain infection mediated autophagy primarily through activating only the IRE1-XBP1 pathway, and inhibiting this pathway had no significant impact on viral replication. These findings indicate that while PRV infection can induce cellular autophagy by activating ERS, the specific unfolded protein response (UPR) pathways involved differ significantly between strains of varying virulence. This study provides a foundation for understanding the pathogenesis of different PRV strains and developing novel antiviral drugs.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"314 ","pages":"Article 110914"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079310","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}