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Identification of the methionine transporter MetQ in Streptococcus suis and its contribution to virulence and biofilm formation. 猪链球菌中蛋氨酸转运蛋白MetQ的鉴定及其在毒力和生物膜形成中的作用。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-05-08 DOI: 10.1186/s13567-025-01522-y
Camila Bosch, Carla García, Luis Saralegui, Lucille van Beek, Marien I de Jonge, Clara Marín, Jesús Arenas
{"title":"Identification of the methionine transporter MetQ in Streptococcus suis and its contribution to virulence and biofilm formation.","authors":"Camila Bosch, Carla García, Luis Saralegui, Lucille van Beek, Marien I de Jonge, Clara Marín, Jesús Arenas","doi":"10.1186/s13567-025-01522-y","DOIUrl":"https://doi.org/10.1186/s13567-025-01522-y","url":null,"abstract":"<p><p>Streptococcus suis is a Gram-positive bacterium responsible for various infections in both pigs and humans. This study investigates the role of methionine acquisition in the growth and virulence of S. suis. The putative methionine transport system is organised as an operon comprising the metQ gene and genes encoding a transposase and an ATPase, forming a typical tripartite ABC transporter. This operon is conserved across multiple streptococcal species, including both animal and human pathogens. We examined whether MetQ functions as a methionine-binding protein and its role in bacterial infection. Using Western blotting and flow cytometry with a specific antiserum, we demonstrated that MetQ is produced in vitro by the S. suis reference strain P1/7 under methionine-limited conditions and is located on the bacterial cell surface. Growth assays in chemically defined media revealed that a metQ deletion mutant (P1/7∆metQ) exhibited impaired growth under methionine-restricted conditions but grew normally in a nutrient-rich medium, suggesting that MetQ primarily transports methionine. Isothermal Titration Calorimetry demonstrated that MetQ binds L-methionine with a dissociation constant (K<sub>D</sub>) of 7.1 µM. In a murine infection model, the metQ mutant showed reduced dissemination to internal organs compared to the wild type. Furthermore, the mutant showed decreased intracellular survival in murine macrophages and increased sensitivity to oxidative stress, while exhibited enhanced biofilm formation compared to the wild type. Our findings indicate that MetQ is essential for methionine uptake under methionine-restricted conditions, which is critical for bacterial nutrition, immune evasion, and pathogenicity during infection.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"99"},"PeriodicalIF":3.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12063423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ingestion of Artemisia argyit essential oil combats Salmonella pullorum infections by altering gut microbiota composition in chicks. 摄入银艾精油可通过改变雏鸡肠道菌群组成来对抗白痢沙门氏菌感染。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-05-06 DOI: 10.1186/s13567-025-01527-7
Linlin Ding, Kaige Qi, Yutong Zhou, Qingjie Li, Minda Liu, Na Hu, Jianfeng Wang, Jiazhang Qiu, Xuming Deng, Lei Xu
{"title":"Ingestion of Artemisia argyit essential oil combats Salmonella pullorum infections by altering gut microbiota composition in chicks.","authors":"Linlin Ding, Kaige Qi, Yutong Zhou, Qingjie Li, Minda Liu, Na Hu, Jianfeng Wang, Jiazhang Qiu, Xuming Deng, Lei Xu","doi":"10.1186/s13567-025-01527-7","DOIUrl":"https://doi.org/10.1186/s13567-025-01527-7","url":null,"abstract":"<p><p>Pullorum disease, caused by Salmonella pullorum (S. pullorum), is a highly contagious illness affecting the poultry industry. Emerging evidence suggests that Artemisia argyit essential oil can influence the composition of gut microbes in the host, thereby promoting overall health. However, the specific mechanisms by which Artemisia argyit essential oil modulates gut microbiota to combat S. pullorum infection remains unclear. This study explored the effectiveness of various doses of Artemisia argyit essential oil in preventing S. pullorum infection in chicks. Our findings indicate that consuming this essential oil can mitigate the intestinal mucosal barrier damage and excessive inflammatory response caused by S. pullorum, as well as reverse the weight loss seen in infected chicks. Additionally, chicks that received faecal microbiota transplantation (FMT) from the gut microbiota of Artemisia argyit essential oil donors exhibited notable recovery from S. pullorum infections. This suggests that the observed protection may be linked to the modulation of gut microbiota. Furthermore, 16S rRNA sequencing revealed an increased abundance of Lactobacillus reuteri (L. reuteri), which along with the activation of Wnt/β-catenin pathways, played critical roles in the enhanced health of S. pullorum-infected chicks treated with Artemisia argyit essential oil. In summary, these findings highlight that the dietary inclusion of Artemisia argyit essential oil promotes the intestinal enrichment of L. reuteri, offering a promising strategy for the treatment and prevention of pullorum disease in chicks.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"98"},"PeriodicalIF":3.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SIRT2 inhibition enhances mitochondrial apoptosis in Brucella-infected bovine placental trophoblast cells. SIRT2抑制促进布鲁氏菌感染的牛胎盘滋养细胞线粒体凋亡。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-05-02 DOI: 10.1186/s13567-025-01518-8
Mengyu Zhang, Lin Qi, Junmei Li, NingQiu Yuan, Yunyi Zhai, Mingyue Hao, Dong Zhou, Wei Liu, Yaping Jin, Aihua Wang
{"title":"SIRT2 inhibition enhances mitochondrial apoptosis in Brucella-infected bovine placental trophoblast cells.","authors":"Mengyu Zhang, Lin Qi, Junmei Li, NingQiu Yuan, Yunyi Zhai, Mingyue Hao, Dong Zhou, Wei Liu, Yaping Jin, Aihua Wang","doi":"10.1186/s13567-025-01518-8","DOIUrl":"https://doi.org/10.1186/s13567-025-01518-8","url":null,"abstract":"<p><p>Brucella is a successful pathogen that employs a plethora of immune evasion mechanisms. This contributes to pathogenesis and persistence and limits the efficacy of available treatments. An increasing understanding of host‒pathogen interactions suggests that integrating host-directed strategies with existing anti-Brucella treatments could lead to more effective bacterial clearance and a reduction in drug-resistant strains. SIRT2 is a nicotinamide adenine dinucleotide (NAD<sup>+</sup>)-dependent deacetylase found in mammals. It can deacetylate various transcription factors and regulatory proteins, playing crucial roles in host‒pathogen interactions and pathogen infection-induced apoptosis. In this study, we investigated the role of SIRT2 in Brucella-induced cell apoptosis using bovine placental trophoblast cells. Our results indicate that B. abortus A19 infection upregulates SIRT2 protein expression and significantly induces mitochondrial apoptosis in these cells. Furthermore, inhibition of SIRT2 exacerbates B. abortus A19-induced mitochondrial apoptosis and markedly inhibits intracellular bacterial survival. These results prove the role of SIRT2 in Brucella pathogenesis and the mechanism of action.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"97"},"PeriodicalIF":3.7,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Astragaloside IV mitigates influenza-induced inflammatory responses by suppressing the Wnt/β-catenin signalling pathway in alveolar macrophages. 黄芪甲苷通过抑制肺泡巨噬细胞中Wnt/β-catenin信号通路减轻流感诱导的炎症反应。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-30 DOI: 10.1186/s13567-025-01529-5
Jianli Tang, Yu Gao, Yuchen Fu, Zhaoqing Han, Ping Xu, Xin Li, Shuaiyong Wang, Xin Wang
{"title":"Astragaloside IV mitigates influenza-induced inflammatory responses by suppressing the Wnt/β-catenin signalling pathway in alveolar macrophages.","authors":"Jianli Tang, Yu Gao, Yuchen Fu, Zhaoqing Han, Ping Xu, Xin Li, Shuaiyong Wang, Xin Wang","doi":"10.1186/s13567-025-01529-5","DOIUrl":"https://doi.org/10.1186/s13567-025-01529-5","url":null,"abstract":"<p><p>Respiratory viruses, including the influenza virus (IAV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), pose significant health threats. As tissue-resident macrophages, alveolar macrophages (AM) are crucial for defending against respiratory viral infection by producing cytokines, engulfing virus-infected cells, and promoting wound healing. However, excessive inflammatory responses can lead to tissue injury. Growing evidence indicates that astragaloside IV (AST IV) regulates innate immune responses. Specifically, AST IV balances the inflammatory response to mitigate tissue damage and promote tissue repair. However, whether AST IV directly targets AM to alleviate lung damage induced by respiratory viral infection remains unclear. Our results demonstrate that AST IV treatment significantly reduces morbidity and mortality in mice during IAV infection. AST IV markedly decreases proinflammatory cytokine levels, mitigates lung injury and promotes lung recovery through enhancing the repair capacity mediated by alveolar type II cells. Mechanistically, AST IV suppresses the Wnt/β-catenin signalling pathway, which is critical for driving inflammatory responses in AM while maintaining mitochondrial fitness. Thus, our findings suggest that AST IV effectively targets AM to alleviate inflammation and lung damage caused by respiratory viral infections, highlighting its potential as a therapeutic agent for managing viral pneumonia.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"95"},"PeriodicalIF":3.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Neospora caninum hijacks host PFKFB3-driven glycolysis to facilitate intracellular propagation of parasites. 犬新孢子虫劫持宿主pfkfb3驱动的糖酵解以促进寄生虫的细胞内繁殖。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-30 DOI: 10.1186/s13567-025-01524-w
De-Liang Tao, Jin-Ming Chen, Jiang-Ping Wu, Shan-Shan Zhao, Bu-Fan Qi, Xin Yang, Ying-Ying Fan, Jun-Ke Song, Guang-Hui Zhao
{"title":"Neospora caninum hijacks host PFKFB3-driven glycolysis to facilitate intracellular propagation of parasites.","authors":"De-Liang Tao, Jin-Ming Chen, Jiang-Ping Wu, Shan-Shan Zhao, Bu-Fan Qi, Xin Yang, Ying-Ying Fan, Jun-Ke Song, Guang-Hui Zhao","doi":"10.1186/s13567-025-01524-w","DOIUrl":"https://doi.org/10.1186/s13567-025-01524-w","url":null,"abstract":"<p><p>Infection with Neospora caninum leads to reproductive failure in ruminants, such as cattle and goats; however, no effective vaccines or treatments are currently available to control this infection. Carefully regulating the glycolysis of host cells is essential for the intracellular survival of pathogens. Nonetheless, the impact of N. caninum infection on host cell glycolysis and the effects and mechanisms of host cell glycolysis on the intracellular survival of this parasite remains unclear. In this study, the analysis of metabolomics and transcriptomics revealed that N. caninum infection increases the expression of glycolysis-related enzymes and lactate production in caprine endometrial epithelial cells (EECs). The study's findings demonstrate that the inhibition of host cell glycolysis using 2-DG or sodium oxamate (an LDH-A inhibitor) inhibits host cell glycolysis and the intracellular propagation of N. caninum tachyzoites. Moreover, the addition of lactate further promotes the replication of N. caninum tachyzoites both in vivo and in vitro. Further investigation found that N. caninum infection induces host cell glycolysis via up-regulating 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) expression, while knockdown of PFKFB3 with small-interfering RNA or 3-PO significantly inhibits host cell glycolysis and the propagation of N. caninum tachyzoites both in vivo and in vitro. Additionally, a mechanistic study showed that N. caninum infection activates the JNK signalling pathway and inhibits the ubiquitination degradation of HIF-1α. Chromatin immunoprecipitation and dual-luciferase reporter assays revealed that N. caninum infection induces the expression of HIF-1α, which binds to the promoter region of pfkfb3. Our findings indicate that cellular glycolysis may serve as a potential therapeutic target for neosporosis, offering a novel insight for further investigating the intracellular survival mechanisms of N. caninum.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"94"},"PeriodicalIF":3.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MARCH8 promotes the proteasomal degradation of foot-and-mouth disease virus VP1, VP2, and VP3 to negatively regulate viral replication. MARCH8促进口蹄疫病毒VP1、VP2和VP3的蛋白酶体降解,负向调节病毒复制。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-30 DOI: 10.1186/s13567-025-01521-z
Mengge Yin, Xiangmin Li, Min Zhang, Qiongqiong Zhao, Haoyuan Wang, Huiyan Zhang, Zengjun Lu, Ping Qian
{"title":"MARCH8 promotes the proteasomal degradation of foot-and-mouth disease virus VP1, VP2, and VP3 to negatively regulate viral replication.","authors":"Mengge Yin, Xiangmin Li, Min Zhang, Qiongqiong Zhao, Haoyuan Wang, Huiyan Zhang, Zengjun Lu, Ping Qian","doi":"10.1186/s13567-025-01521-z","DOIUrl":"https://doi.org/10.1186/s13567-025-01521-z","url":null,"abstract":"<p><p>The host cell membrane-associated RING-CH8 protein (MARCH8) functions as an antiviral host factor by targeting viral envelope glycoproteins. Foot-and-mouth disease virus (FMDV) is a non-enveloped, positive-sense, single-stranded RNA virus. The potential impact of MARCH8 on FMDV replication remains uncertain. Here, we found that the overexpression of MARCH8 significantly inhibited FMDV replication in a dose-dependent manner. Conversely, the knockdown of MARCH8 facilitated FMDV replication. Specifically, MARCH8 interacted with VP1, VP2, and VP3, mediating their degradation in a proteasome-dependent manner. MARCH8 catalyzed the K33-linked polyubiquitination of VP1, VP2, and VP3. Moreover, the Lys210 residue of VP1, the Lys63 residue of VP2, and the Lys118 residue of VP3 were identified as critical target sites for MARCH8-mediated degradation. Overall, we conclude that MARCH8 is an intrinsic antiviral factor against FMDV.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"96"},"PeriodicalIF":3.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12044826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lumpy skin disease virus suppresses the antiviral response of bovine peripheral blood mononuclear cells that support viral dissemination. 肿块性皮肤病病毒抑制支持病毒传播的牛外周血单个核细胞的抗病毒反应。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-26 DOI: 10.1186/s13567-025-01516-w
Manoj Kumar, Ohad Frid, Asaf Sol, Alexander Rouvinski, Sharon Karniely
{"title":"Lumpy skin disease virus suppresses the antiviral response of bovine peripheral blood mononuclear cells that support viral dissemination.","authors":"Manoj Kumar, Ohad Frid, Asaf Sol, Alexander Rouvinski, Sharon Karniely","doi":"10.1186/s13567-025-01516-w","DOIUrl":"https://doi.org/10.1186/s13567-025-01516-w","url":null,"abstract":"<p><p>Lumpy skin disease virus (LSDV) causes a severe emerging and transboundary disease in cattle. Infection with LSDV leads to the development of widespread dermal nodules. In addition to the skin, LSDV resides in multiple internal organs and can be isolated from the blood of infected cattle. We have characterised the tropism, replication, and dissemination of both a field isolate of LSDV and an attenuated vaccine strain in vitro. To study virus infection and dissemination in living cells, we generated recombinant viruses that express a green fluorescent protein (GFP) under a synthetic viral promoter. The recombinant LSDVs expressing GFP displayed replication kinetics similar to their parental strains in a bovine kidney cell line. These LSDV-GFP strains also replicated effectively in a bovine macrophage cell line and primary bovine foreskin cells, showing no apparent differences between the field isolate and the vaccine strain. Bovine peripheral blood mononuclear cells (PBMCs) infected with either LSDV-GFP strain displayed specific viral-driven GFP fluorescence and significant viral gene expression. However, these infected PBMCs did not support substantial viral DNA replication or the release of infectious progeny. Further analysis of the anti-viral response revealed that heat-treated LSDV, but not infectious viruses, induced the expression of interferon-stimulated genes (ISGs) in PBMCs. Thus, although LSDV did not replicate productively in PBMCs, it evaded the anti-viral response of these cells. Finally, we demonstrated that despite the lack of productive replication, infected PBMCs effectively transmitted LSDV to recipient permissive cells in co-culture, leading to the formation of infection foci. This suggests a potential role for PBMCs in the dissemination of LSDV.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"93"},"PeriodicalIF":3.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cytolethal distending toxin from Glaesserella parasuis induces ferroptosis in porcine alveolar macrophages and mice. 副猪小绿杆菌细胞致死膨胀毒素诱导猪肺泡巨噬细胞和小鼠铁下垂。
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-25 DOI: 10.1186/s13567-025-01520-0
Shiyu Xu, Li Lei, Zhen Yang, Yu Wang, Senyan Du, Qin Zhao, Xiaobo Huang, Sanjie Cao, Rui Wu, Yiping Wang, Qigui Yan, Yiping Wen
{"title":"Cytolethal distending toxin from Glaesserella parasuis induces ferroptosis in porcine alveolar macrophages and mice.","authors":"Shiyu Xu, Li Lei, Zhen Yang, Yu Wang, Senyan Du, Qin Zhao, Xiaobo Huang, Sanjie Cao, Rui Wu, Yiping Wang, Qigui Yan, Yiping Wen","doi":"10.1186/s13567-025-01520-0","DOIUrl":"https://doi.org/10.1186/s13567-025-01520-0","url":null,"abstract":"<p><p>Glaesserella parasuis cytolethal distending toxin (GpCDT) is a bacterial genotoxin whose main action is to activate DNA damage responses, induce cell cycle arrest, and induce the apoptosis of host cells. In our previous studies, we reported that cells incubated with GpCDT exhibited changes in the expression of ferroptosis-related proteins; thus, we hypothesized that, in addition to apoptosis, GpCDT may also cause ferroptosis, a novel mode of cell death. Here, we observed that treatment of 3D4/21 cells with GpCDT resulted in cytoplasmic iron overload, depletion of GSH (reduced glutathione), and overproduction of reactive oxygen species (ROS) and malondialdehyde (MDA), indicating that GpCDT disrupted iron metabolism and redox homeostasis in these cells. These phenomena were counteracted by the specific ferroptosis inhibitor ferrostatin-1 and the iron chelator deferoxamine mesylate. In vitro infection with the Glaesserella parasuis field isolate strain SC1401 (CDT positive) induced changes in the expression of ferroptosis biomarkers and proteins. Infection of C57BL/6 mice yielded similar results. Our results suggest that ferroptosis may play a substantial role in GpCDT-induced cellular injury.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"92"},"PeriodicalIF":3.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Seroprevalence of West Nile, Usutu and tick-borne encephalitis viruses in equids from south-western France in 2023. 2023年法国西南部马科动物中西尼罗河病毒、乌苏图病毒和蜱传脑炎病毒的血清流行率
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-24 DOI: 10.1186/s13567-025-01508-w
Noémie Chevalier, Camille V Migné, Teheipuaura Mariteragi-Helle, Marine Dumarest, Margaux De Mas, Manon Chevrier, Emilie Queré, Christel Marcillaud-Pitel, Coralie Lupo, Clément Bigeard, Thierry Touzet, Agnès Leblond, Benoît Durand, Marianne Depecker, Gaëlle Gonzalez
{"title":"Seroprevalence of West Nile, Usutu and tick-borne encephalitis viruses in equids from south-western France in 2023.","authors":"Noémie Chevalier, Camille V Migné, Teheipuaura Mariteragi-Helle, Marine Dumarest, Margaux De Mas, Manon Chevrier, Emilie Queré, Christel Marcillaud-Pitel, Coralie Lupo, Clément Bigeard, Thierry Touzet, Agnès Leblond, Benoît Durand, Marianne Depecker, Gaëlle Gonzalez","doi":"10.1186/s13567-025-01508-w","DOIUrl":"https://doi.org/10.1186/s13567-025-01508-w","url":null,"abstract":"<p><p>The circulation of West Nile virus (WNV), Usutu virus (USUV), and tick-borne encephalitis virus (TBEV) was investigated in south-western France during the first six months of 2023, following the emergence of WNV in equids in Gironde, a département in south-western France, in 2022. Blood samples were collected from 494 horses located in the Gironde département and divided into three zones: the Confluence zone, the Intermediate zone and the Arcachon Basin. Samples were tested for WNV-, USUV- and TBEV-specific antibodies. An overall seroprevalence of 14% (95% CI [11-18%]) for orthoflavivirus antibodies was detected in Gironde. The highest seroprevalence rates for WNV and USUV were observed in the Confluence Zone (9%, 95% CI [6-13%] and 5%, 95% CI [3-8%], respectively), where the type of housing (animals kept in pasture only) and proximity to a special bird protection area were identified as risk factors for WNV seropositivity. This study presents the first seroprevalence investigation of WNV, USUV and TBEV infections in equids located on the Atlantic coast of France and demonstrates intense circulation of WNV in this region, as well as evidence of equine USUV-specific infection.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"56 1","pages":"91"},"PeriodicalIF":3.7,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Isolation, characterization, and application of the novel polyvalent bacteriophage vB_EcoM_XAM237 against pathogenic Escherichia coli. 抗致病性大肠杆菌的新型多价噬菌体vB_EcoM_XAM237的分离、鉴定及应用
IF 3.7 1区 农林科学
Veterinary Research Pub Date : 2025-04-24 DOI: 10.1186/s13567-025-01514-y
Jiyun Chai, Hongfei Sun, Stefan Schwarz, Yuxuan Huang, Shuangyu Xie, Qiu Xu, Longhua Lin, Caiping Ma, Jie Hou, Yao Zhu, Wanjiang Zhang
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