Veterinary microbiology最新文献

{"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}

{"title":"Canine adenovirus type 1 induces PANoptosis in canine splenocytes via AIM2 inflammasome activation","authors":"Yajun Li ,&nbsp;Yuqing Zhao ,&nbsp;Weihai Wang ,&nbsp;Baojie Qi ,&nbsp;Yiting Lv ,&nbsp;Shujie Wang ,&nbsp;Chunsheng Wang","doi":"10.1016/j.vetmic.2026.110965","DOIUrl":"10.1016/j.vetmic.2026.110965","url":null,"abstract":"<div><div>Canine adenovirus type 1 (CAV-1) is a primary causative agent of infectious hepatitis in canines, posing a significant health threat. Nevertheless, the mechanism by which CAV-1 infection induces a deleterious inflammatory response remains incompletely understood. In this study, two-month-old Beagles were inoculated with a defined dose of CAV-1, and samples were collected from seven organs. Analysis revealed that the expression of AIM2 in primary target organs, the liver and kidney, was not significantly altered. In contrast, AIM2 expression was markedly upregulated in immune organs—specifically the spleen, tonsils, and lymph nodes—where the expression level of the key pyroptotic core protein also increased significantly. Further investigation demonstrated that CAV-1 induced PANoptosis of T cells and B cells in the spleen of infected Beagles. Subsequent <em>in vitro</em> studies using canine splenocytes corroborated these findings and identified that the interaction between CAV-1 double-stranded DNA (dsDNA) and AIM2 initiates PANoptosis. In conclusion, CAV-1 triggers PANoptosis in canine splenocytes by activating the AIM2 inflammasome pathway. Our study reveals the death pathway of canine splenocytes caused by CAV-1 for the first time. These findings provide a foundation for elucidating the mechanism of CAV-1 induced inflammatory response of canine splenocytes.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110965"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373302","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":"TGEV infection activates pro‑inflammatory signaling via the YY1/HSP40/NF‑κB pathway in intestinal epithelial cells and organoids","authors":"Shuai Gao ,&nbsp;Zhe Chao ,&nbsp;Zongxi Cao ,&nbsp;Feng Wang ,&nbsp;Ruiping Sun ,&nbsp;Guangliang Liu","doi":"10.1016/j.vetmic.2026.110985","DOIUrl":"10.1016/j.vetmic.2026.110985","url":null,"abstract":"<div><div>Transmissible gastroenteritis virus (TGEV) is a porcine enteropathogenic coronavirus that causes severe intestinal inflammation and diarrhea in pigs, leading to substantial economic losses to the swine industry worldwide. Inflammation is a major cause of death in pigs infected with TGEV. However, the role of host-mediated inflammatory responses in TGEV pathogenesis remains poorly understood. Here, we report for the first time that the heat shock protein HSP40 (DNAJB6) is highly expressed in the jejunum and ileum of Wuzhishan pigs during TGEV infection, and that its transcription is activated by the transcription factor <em>YY1</em>. Gain- and loss-of-function experiments revealed that HSP40 enhances both the inflammatory response and TGEV replication by modulating NF-κB signaling. Mechanistically, HSP40 facilitates the recruitment of β-TRCP, an E3 ubiquitin ligase of IκB, promoting its interaction with IκB and subsequent proteasomal degradation. Under basal conditions, IκB binds to and sequesters p65 (RelA) in the cytoplasm, preventing its nuclear translocation and transcriptional activity. During TGEV infection, HSP40-mediated degradation of IκB releases p65, enabling its nuclear translocation and the transcriptional activation of multiple inflammatory genes. Furthermore, β-TRCP was found to be essential for HSP40-mediated production of inflammatory cytokines. Collectively, these findings uncover a pivotal role for HSP40 in regulating inflammation and viral replication during TGEV infection, and suggest that targeting HSP40 may represent a promising therapeutic approach against TGEV.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110985"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147378709","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":"Proteomic profiling identifies nucleolin as a U3-interacting protein that inhibits avian leukosis virus replication","authors":"Ziqi An ,&nbsp;Qinghua Huang ,&nbsp;Yawen Liu ,&nbsp;Peipei Wang ,&nbsp;Ning Cui ,&nbsp;Chuantian Xu ,&nbsp;Shuai Su","doi":"10.1016/j.vetmic.2026.110957","DOIUrl":"10.1016/j.vetmic.2026.110957","url":null,"abstract":"<div><div>The long terminal repeat (LTR) of the avian retroviruses has been extensively characterized as a model of a strong transcription regulatory unit. U3 gene of LTR contains many cis-acting elements and trans-acting factors that bind to a variety of host transcription factors to form a complex network regulating high levels of transcription of viral and host genes. However, the host proteins that bind to the U3 gene and their complex mechanisms are largely unknown. In the present study, coupling surface-plasmon resonance and mass spectrometry were performed to identify proteins binding to the U3 gene of avian leukosis virus (ALV). A total of 181 U3-binding proteins with score &gt; 20 were identified. Six of the proteins with score &gt; 120 were successfully knockdown using siRNA transfection and the transcription of ALV gp85 mRNA was significantly increased when the nucleolin (NCL) was down regulated. The effect of NCL interference was optimized by combining siRNAs and we found that down regulation of NCL significantly increased the transcription activity of LTR, the enhancer ability of U3, and furthermore enhanced the expression of viral protein. On the contrary, over expression of NCL significantly decreased the transcription activity of LTR, the enhancer ability of U3, and the expression level of viral protein. These data demonstrate that NCL is critical for inhibition ALV replication and laid a molecular basis for development of efficient strategies against retroviruses from a new perspective.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110957"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372444","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 PERK-eIF2α branch activates the NLRP3 inflammasome through the NF-κB signaling pathway to suppress NDV replication","authors":"Jiaxin Ding ,&nbsp;Jiaxuan Feng ,&nbsp;Chunhong Guo ,&nbsp;Zhuang Ding ,&nbsp;Jing Qian ,&nbsp;Jindou Li","doi":"10.1016/j.vetmic.2026.110968","DOIUrl":"10.1016/j.vetmic.2026.110968","url":null,"abstract":"<div><div>Viral replication in host cells commonly induces endoplasmic reticulum (ER) stress, thereby initiating the unfolded protein response (UPR) to regulate viral infection. However, the precise connection between virus-induced ER stress and the replication and pathogenesis of Newcastle disease virus (NDV) remains unclear. Here, we observed that NDV infection led to alterations in the structure of the endoplasmic reticulum in DF-1 cells and activated endoplasmic reticulum stress. Subsequent studies revealed that all three branches of the UPR were activated, including protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6). Treatment of DF-1 cells with endoplasmic reticulum stress inducers or inhibitors strongly inhibited or promoted viral replication. Specifically, activation of the PERK-eIF2α pathway hindered the proliferation of NDV. Furthermore, NDV infection activated the NF-κB pathway through the PERK-eIF2α axis, leading to the formation of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes and the production of pro-inflammatory cytokines. Collectively, these data reveal how the UPR regulates the inflammatory response to inhibit NDV replication, which might guide the rational design of anti-NDV strategies.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110968"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372581","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":"Ursodeoxycholic acid against TGEV infection via the JAK-STAT1 signaling pathway","authors":"Zhiwei Sun ,&nbsp;Aobo Liu ,&nbsp;Yi Zhong ,&nbsp;Ziyan Song,&nbsp;Guisong Liao,&nbsp;Yi Li,&nbsp;Yanwen Song,&nbsp;Qingyang Li,&nbsp;Xingcui Zhang ,&nbsp;Zhenhui Song","doi":"10.1016/j.vetmic.2026.110973","DOIUrl":"10.1016/j.vetmic.2026.110973","url":null,"abstract":"<div><div>Transmissible gastroenteritis virus (TGEV) causes transmissible gastroenteritis (TGE), leading to severe diarrhea, vomiting, and dehydration in pigs. Mortality rates among newborn piglets are particularly alarming, causing significant economic losses to the livestock industry. In the absence of effective antiviral drugs, developing novel antiviral agents is crucial. Ursodeoxycholic acid (UDCA), as a hydrophilic endogenous bile acid, plays a key role in regulating bile acid metabolism and treating hepatobiliary diseases. Studies indicate that UDCA exhibits specific antiviral effects against the novel coronavirus. Through validation using Western Blot, qPCR, and IFA techniques, we found that UDCA significantly downregulated TGEV N gene copy number, protein levels, viral load, and nuclear translocation in IPEC-J2 cells. Negative staining electron microscopy revealed that UDCA disrupted the structural integrity of TGEV viral particles. In vivo experiments confirmed that UDCA effectively alleviated TGEV infection symptoms and improved piglet survival rates. Data indicate that UDCA exhibits potent antiviral activity against the TGEV Miller strain. Transcriptomic analysis and validation elucidated its mechanism of action: UDCA significantly activates the TLR3-IRF3 signaling axis, induces IFN-λ3 secretion, activates the JAK-STAT1 pathway, and upregulates transcription of downstream interferon-stimulated genes (ISGs). These synergistic effects collectively establish a defense barrier against TGEV invasion and exert antiviral efficacy.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110973"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147387729","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":"Overcoming gastrointestinal mucosal barriers: Mechanistic innovations and technical advances in mucosal targeting strategies for animal oral vaccines","authors":"Meijun Yu ,&nbsp;Yue Li ,&nbsp;Zhaojun Wang ,&nbsp;Ping Han ,&nbsp;Yanping Jiang ,&nbsp;Wen Cui ,&nbsp;Yijing Li ,&nbsp;Lijie Tang ,&nbsp;Shuo Jia ,&nbsp;Hongzhe Zhao ,&nbsp;Yingying Ma ,&nbsp;Jiaxuan Li ,&nbsp;Xiaona Wang","doi":"10.1016/j.vetmic.2026.110983","DOIUrl":"10.1016/j.vetmic.2026.110983","url":null,"abstract":"<div><div>Infectious diseases caused by pathogenic microorganisms (such as <em>Escherichia coli</em>, <em>Avian influenza virus</em> (AIV), <em>Rotavirus</em>, etc.) that primarily invade through mucosal surfaces like the digestive tract and respiratory tract not only severely restrict the development of the livestock and poultry breeding industry, resulting in huge economic losses, but also threaten public health security due to the risk of cross-species transmission. Oral vaccines, by simulating natural infection routes to activate the mucosal immune system, have advantages such as ease of administration, wide applicability, and avoidance of injection stress, thus becoming an important means to prevent and control mucosal infectious diseases. However, due to the acidic environment of the gastrointestinal tract, degradation by digestive enzymes, and obstruction by mucosal barriers, the stability and immunogenicity of antigens are significantly reduced, which greatly limits the application of oral vaccines. Mucosal targeting strategy is the core technology to break through the above bottlenecks. Through antigen protection and sustained release, precise targeting of immune cells, and carrier adjuvant effect, it can efficiently activate synergistic responses between mucosal immunity (such as secretory immunoglobulin A (SIgA) production) and systemic immunity. This article systematically reviews the technological advances in mucosal targeting strategies for oral vaccines, including the dynamic process of vaccines <em>in vivo</em>, the biological barriers to be overcome, and specific targeting techniques for immune cells such as M cells and dendritic cells. Meanwhile, drawing on cutting-edge applications of drug targeting technology and artificial intelligence in antigen design, it provides theoretical references and research ideas for the construction of safe and efficient mucosal-targeted oral vaccines for animals.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110983"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147387743","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":"Engineering bright and genetically stable fluorescent Streptococcus suis strains for functional in vitro and in vivo applications","authors":"Luis Saralegui ,&nbsp;Carla García ,&nbsp;Paula Jurado ,&nbsp;Camila Bosch ,&nbsp;Marga van Setten ,&nbsp;Vloet Wessel ,&nbsp;Rocío Bermúdez ,&nbsp;Clara Marín ,&nbsp;Jesús Arenas","doi":"10.1016/j.vetmic.2026.110964","DOIUrl":"10.1016/j.vetmic.2026.110964","url":null,"abstract":"<div><div><em>Streptococcus suis</em> is a major cause of streptococcal infections in pigs and an emerging zoonotic pathogen, resulting in substantial economic losses in the swine production industry. The limited efficacy of current vaccine strategies and the rise in antimicrobial resistance have intensified efforts to investigate the biology and pathogenesis of the microorganism as a basis for developing alternative control strategies. In this work, we engineered a genetically stable <em>S. suis</em> strain producing a superfolder green fluorescent protein that may serve to study this pathogen in a variety of in vitro and in vivo assays. Multiple <em>S. suis</em> strains from different genetic backgrounds were successfully transformed, exhibiting strong and stable fluorescence without compromising bacterial growth. Fluorescence intensity remained consistent over 15 serial passages in culture without the need for antibiotic selection, supporting its suitability for long-term experiments. The fluorescent strains were nicely distinguishable by fluorescence microscopy and enabled the detailed study of various biological aspects, including biofilm formation, interactions with eukaryotic cells, and differential growth. In murine infection models, the engineered strains caused streptococcal disease, unlike unencapsulated mutant derivatives, and were detected in internal organs via fluorescence microscopy. Altogether, this work provides a valuable tool for advancing research into <em>S. suis</em>.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110964"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373310","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":"YTHDF2 promotes m6A-modified HSPA2 translation to restrict Newcastle Disease Virus","authors":"Zixuan Wang ,&nbsp;Bohan Yin ,&nbsp;Yuechi Hou ,&nbsp;Yongqiang Zhao ,&nbsp;Libin Chen ,&nbsp;Tao Ren ,&nbsp;Weifeng Yuan","doi":"10.1016/j.vetmic.2026.110960","DOIUrl":"10.1016/j.vetmic.2026.110960","url":null,"abstract":"<div><div>Newcastle disease virus (NDV), a highly contagious avian pathogen, causes devastating economic losses in poultry worldwide, yet the role of epitranscriptomic regulators in its pathogenesis remains poorly defined. Here we demonstrate that the m6A reader protein YTHDF2 functions as a potent antiviral effector against NDV. Through integrated functional genomics and multi-omics approaches, we establish that YTHDF2 deficiency significantly enhances NDV replication, while its overexpression suppresses viral propagation. Temporal transcriptomics and machine learning algorithms converged on HSPA2, ATF3, and IRF9 as high-confidence YTHDF2-regulated targets during infection, with HSPA2 emerging as the principal mechanistic mediator. Mechanistically, YTHDF2 directly binds m6A-modified sites within the HSPA2 coding sequence to augment its translational efficiency, as validated by RNA immunoprecipitation, isothermal titration calorimetry, and m6A-modified reporter assays. HSPA2 overexpression reduced NDV nucleoprotein levels by 68–74%, establishing its direct antiviral function. Crucially, this YTHDF2-HSPA2 axis operates independently of classical innate immune pathways, as transcriptomics revealed intact induction of antiviral genes in YTHDF2-knockout cells. Our findings unveil a previously unrecognized epitranscriptome-governed antiviral strategy wherein YTHDF2 amplifies host defense through selective translational enhancement of m6A-modified effector transcripts. This paradigm extends beyond canonical RNA decay functions of YTHDF2 and identifies the HSPA2 chaperone as a novel restriction factor against paramyxoviruses, offering new avenues for targeted antiviral interventions.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"316 ","pages":"Article 110960"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372707","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}