Veterinary microbiology最新文献

{"title":"An engineered canine-mouse chimeric neutralizing antibody provides therapeutic effects against canine parvovirus infection","authors":"Zhihao Wang ,&nbsp;Pengfei Shi ,&nbsp;Ying Li ,&nbsp;Sheng Wang ,&nbsp;Yuanbao Zhou ,&nbsp;Chengguang Zhang ,&nbsp;Ling Zhao ,&nbsp;Sizhu Suolang ,&nbsp;Jiahui Zou ,&nbsp;Hongbo Zhou","doi":"10.1016/j.vetmic.2025.110572","DOIUrl":"10.1016/j.vetmic.2025.110572","url":null,"abstract":"<div><div>Canine parvovirus (CPV) is a highly contagious and severe infectious disease that can lead to hemorrhagic enteritis and even acute death in dogs. Despite mouse monoclonal antibodies (mAbs) have been employed in clinical treatment, their application in non-murine species is restricted due to immune rejection. In this study, we screened a mouse mAb (5E7) with high neutralizing activity against CPV using hybridoma technology. Subsequently, the variable regions of the heavy (VH) and light (VL) chains of 5E7 were amplified by PCR and fused with the constant regions of canine IgG antibody to produce canine-mouse chimeric antibody (CM-5E7). The chimeric antibody was successfully expressed in HEK293 cells and exhibited high neutralizing activity against multiple CPV subtypes <em>in vitro</em>. Furthermore, CM-5E7 exhibited effective therapeutic potential in dogs subjected to lethal dose CPV-2c challenge <em>in vivo</em>. Overall, CM-5E7 demonstrated high neutralizing activity against CPV and showed significant efficacy in treating CPV-2c infections, positioning it as a promising candidate therapeutic antibody for the treatment of CPV infection.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110572"},"PeriodicalIF":2.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167476","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":"Streptococcus suis AdcA interacts with factor H and inhibits C3b deposition on the bacteria to participate in complement evasion","authors":"Siqi Pang ,&nbsp;Zhulin Qiao ,&nbsp;Jiajia Xu ,&nbsp;Hao Tang ,&nbsp;Qiuhong Zhang ,&nbsp;Weiyao Han ,&nbsp;Lu Peng ,&nbsp;Jiaojiao Yang ,&nbsp;Jiao Zhang ,&nbsp;Qi Huang ,&nbsp;Rui Zhou ,&nbsp;Lu Li","doi":"10.1016/j.vetmic.2025.110561","DOIUrl":"10.1016/j.vetmic.2025.110561","url":null,"abstract":"<div><div><em>Streptococcus suis</em> is an important zoonotic pathogen. It can escape from the host complement attack through various strategies. In this study, the possible complement C3b interacted proteins of <em>S. suis</em> were screened by co-immunoprecipitation (Co-IP) using C3b antibody in human serum. A bacterial Zn²⁺ transporter AdcA detected to be a cell wall protein was identified. The interaction of AdcA with C3b was verified in the same Co-IP setup using AdcA antibody by western-blot, but after far-western blot analysis, AdcA was found to not interact with C3b directly, but interacted directly with factor H (FH), the complement regulatory factor inhibiting the cleavage of C3 and the production of C3b. Thereafter, the interaction sites of AdcA and FH were predicted using molecular docking. Then, an <em>adcA</em> gene deletion mutant Δ<em>adcA</em>, a complementary strain CΔ<em>adcA</em> and point mutant strains containing AdcA-FH interaction sites Δ<em>adcA</em>_{<em>FH(P-G)</em>} (N-terminal) and Δ<em>adcA</em>_{<em>FH(Y-P)</em>} (C-terminus) were constructed. The deposition of C3b on the surface of Δ<em>adcA</em>, Δ<em>adcA</em>_{<em>FH(P-G)</em>} and Δ<em>adcA</em>_{<em>FH(Y-P)</em>} was significantly increased compared to the wild-type (WT) or CΔ<em>adcA</em>. The resistance to opsonophagocytosis and survival rates in serum of Δ<em>adcA</em> and Δ<em>adcA</em>_{<em>FH(P-G)</em>} were significantly reduced compared to WT or CΔ<em>adcA</em>. Additionally, deletion of <em>adcA</em> decreased bacterial loads of <em>S. suis</em> in the blood, brain and lung of mice. Taken together, AdcA inhibited C3b deposition on the surface of <em>S. suis</em> by binding to FH, further inhibiting the C3b-mediated opsonophagocytosis and serum survivability of <em>S. suis</em>. Both the complement evasion and the known Zn²⁺ transport roles of AdcA contributed to pathogenicity of <em>S.suis</em>.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110561"},"PeriodicalIF":2.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167329","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":"Aetiology and environmental factors of the Watery Mouth Disease associated with neonatal diarrhoea in lambs","authors":"Álvaro Cañete-Reyes ,&nbsp;Jorge Gutiérrez González ,&nbsp;Lauren V. Alteio ,&nbsp;David Rodríguez-Lázaro ,&nbsp;Marta Hernández","doi":"10.1016/j.vetmic.2025.110542","DOIUrl":"10.1016/j.vetmic.2025.110542","url":null,"abstract":"<div><div>Watery Mouth Disease is the main disease in neonatal lambs, causing great economic losses. Despite this, the cause of the condition remains poorly understood. Therefore, we have analysed the main bacteria found in sick animals, their intestinal and temporal distribution, as well as the main sources of contamination. Twelve different farms were sampled, from which 331 samples were taken in total. From these samples, 184 environments were analyzed using <em>16S rRNA</em> amplicon sequencing, 164 isolates were identified by whole genome sequencing and 35 bacterial counts were performed. The dominant bacterial groups at the rectal level were <em>Escherichia-Shigella</em> (36 %) and <em>Clostridium</em> (29 %), with a homogeneous distribution along the digestive tract and a maximum abundance ranging between 12 and 24 hours of lamb life. Within <em>Escherichia-Shigella</em>: <em>Escherichia coli</em> and <em>Escherichia fergusonii</em> and within <em>Clostridium</em>: <em>Clostridium perfringens</em>, <em>Clostridium cadaveris</em>, <em>Clostridium tertium and Clostridium paraputricum</em> were identified as the main isolates present in sick animals<strong>.</strong> The high presence of <em>Clostridium</em> strains, especially potentially pathogenic species like <em>C. perfringens</em> in sick animals, point out <em>Clostridium</em> as a new important protagonist of watery mouth disease and the need of their inclusion in future studies. In particular, bedding was established as the main microbial contaminating factor, reaching the highest increase 48 hours after removal and cleaning of the lambing area (i.e. 8.03 ×10⁸, 1.88 ×10⁶, 3.88 ×10⁶, 4.85 ×10⁷ and 4.00 ×10⁵ CFU/g for mesophilic aerobes, coliforms, <em>E. coli</em>, mesophilic anaerobes and sporulates, respectively). These results highlight the need to increase cleanliness in bedding to reduce the presence of these bacteria.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110542"},"PeriodicalIF":2.4,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167295","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":"M341I substitution of penicillin binding protein 2X contributes to the emergence of high-level penicillin resistant Streptococcus suis in China","authors":"Aijuan Li ,&nbsp;Jiaqi Zhao ,&nbsp;Peiyu Liu ,&nbsp;Xiaomin Wang ,&nbsp;Liping Wang ,&nbsp;Jinhu Huang","doi":"10.1016/j.vetmic.2025.110569","DOIUrl":"10.1016/j.vetmic.2025.110569","url":null,"abstract":"<div><div><em>Streptococcus suis</em> is a major zoonotic pathogen, with penicillins being the first-line treatment for <em>S. suis</em> infections. However, increasing reports of penicillin-non-susceptible (PNS) <em>S. suis</em> have raised concerns, yet the underlying resistance mechanisms remain poorly understood. In this study, we analyzed 107 PNS <em>S. suis</em> isolates to investigate the genetic and phenotypic basis of penicillin resistance. Antimicrobial susceptibility testing revealed that PNS <em>S. suis</em> isolates exhibited higher resistant rates to a number of antimicrobials, including tetracyclines, macrolides and lincosamides. Indeed, high-level penicillin-resistant (HLPR) isolates exhibited even higher resistant rates to these antimicrobials. Serotyping and multilocus sequence typing (MLST) revealed the presence of diverse genetic backgrounds, indicating a potential for widespread transmission. A detailed amino acid analysis of penicillin-binding proteins (PBPs) identified specific substitutions in PBP2x—M341I, I373V, and M401I—associated with HLPR. Recombinant expression of PBP2x proteins containing these substitutions allowed further investigation of their binding affinity to β-lactam antibiotics. Acylation efficiency assays revealed that the M341I substitution significantly reduced the binding affinity of PBP2x for penicillins but not for cephalosporins. These findings provide new insights into the molecular mechanisms underlying HLPR in <em>S. suis</em> and underscore the importance of PBP2x substitutions in driving penicillin resistance.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110569"},"PeriodicalIF":2.4,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124104","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":"Differential systemic antibody responses to Mycoplasma synoviae MSPA variants after vaccination and/ or field challenge","authors":"Oluwadamilola S. Omotainse ,&nbsp;Amir H. Noormohammadi ,&nbsp;Nathan Jeffery ,&nbsp;Nadeeka K. Wawegama ,&nbsp;Somayeh Kordafshari ,&nbsp;Denise O’Rourke ,&nbsp;Andrew W. Stent","doi":"10.1016/j.vetmic.2025.110570","DOIUrl":"10.1016/j.vetmic.2025.110570","url":null,"abstract":"<div><div><em>Mycoplasma synoviae</em> has a major immunodominant surface protein VlhA (variable lipoprotein and haemagglutinin) which undergoes post-translational cleavage to form two separate proteins, MSPA and MSPB. Both these proteins are targets of the host immune response undergo high frequency antigenic variation and are thought to contribute to the pathogenesis of <em>M. synoviae</em> infection. In order to assess variation of MSPA in response to vaccination and/ or field challenge host systemic humoral responses after inoculation with <em>M. synoviae</em> strain 86079/7NS (7NS), vaccine strain MS-H and/or field strain 94011/v-18d (v-18d) were evaluated against eight variable regions of MSPA derived from <em>M. synoviae</em> type strain WVU-1853. At 21 days post-infection, chickens inoculated with 7NS had significantly higher antibody levels against MSPA B3 and B4 compared to those inoculated with the vaccine strain MS-H. Also, at 21 days post-challenge, chickens which had been inoculated with the MS-H vaccine strain prior to challenge had significantly lower antibody responses against MSPA C2 compared to those which had not been. This suggests that variants of MSPA are differentially expressed after vaccination and/ or challenge and antibodies against these variants may be strain dependent. The results of this study have implications for the differentiation of serological responses after <em>M. synoviae</em> vaccination and field challenge.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110570"},"PeriodicalIF":2.4,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124106","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":"Naringenin inhibits PRV replication by regulating the TLR4/NF-κB pathway mediated inflammatory response","authors":"Juanjuan Xu,&nbsp;Zhiying Wang,&nbsp;Zhiyuan Ren,&nbsp;Zhaokun Wan,&nbsp;Yanfeng Zhang,&nbsp;Ruifei Li,&nbsp;Yan Zhu","doi":"10.1016/j.vetmic.2025.110563","DOIUrl":"10.1016/j.vetmic.2025.110563","url":null,"abstract":"<div><div>Pseudorabies is an acute and highly contagious disease caused by the pseudorabies virus (PRV). PRV has a wide range of host susceptibilities and has caused significant economic losses to the global swine industry. Currently, no specific drugs for the treatment or prevention of PRV are known. Therefore, safe and effective anti-PRV drugs are urgently needed. We extensively screened monomeric compounds and ultimately found that the flavonoid compound naringenin exhibited potent anti-PRV activity. The experimental results revealed that naringenin inhibited PRV proliferation in PK-15 cells in a dose-dependent manner. The effects of naringenin on the TLR4/NF-κB pathway were detected at the gene and protein levels. The results demonstrated that PRV infection triggered activation of the NF-κB signaling pathway, whereas naringenin exerted anti-inflammatory effects through multiple mechanisms. Specifically, naringenin suppressed the expression of TLR4 and P65 proteins, thereby inhibiting NF-κB pathway activation. This intervention subsequently attenuated the expression levels of pro-inflammatory mediators (IL-18, IL-1β, TNF-α, and IL-6) and reduced nuclear translocation of the P65 protein. All the mice in the PRV infection group died during the experimental period, whereas the survival rate of the mice in the medium-dose naringenin group (100 mg/kg) reached 57.14 %. Naringenin at high, medium, and low doses significantly inhibited the replication of PRV in the brain, lungs, and kidneys of the mice and alleviated the pathological changes induced by PRV infection. These data suggest that naringenin has potent anti-PRV activity, which provides a novel strategy for the prevention and control of PRV.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110563"},"PeriodicalIF":2.4,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138033","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 effector protein Hcp1 of avian pathogenic Escherichia coli causes mitochondrial dysfunction by interacting with PHB2","authors":"Xiyang Wei ,&nbsp;Zhao Qi ,&nbsp;Xiaoru Wang ,&nbsp;Jingwen Zhang ,&nbsp;Bingyu Zhao ,&nbsp;Yaqing Tian ,&nbsp;Chenchen Sheng ,&nbsp;Mei Xue ,&nbsp;Zhenyu Wang ,&nbsp;Ying Shao ,&nbsp;Jiumeng Sun ,&nbsp;Jian Tu ,&nbsp;Xiangjun Song","doi":"10.1016/j.vetmic.2025.110564","DOIUrl":"10.1016/j.vetmic.2025.110564","url":null,"abstract":"<div><div>The pathogenic mechanisms of virulence factors in avian pathogenic <em>Escherichia coli</em> (<strong>APEC</strong>) targeting eukaryotic cells have gained extensive attention. Hemolysin co-regulatory protein (<strong>Hcp</strong>), a key element for the secretion of the type VI secretion system (<strong>T6SS</strong>), functions as an effector protein mediating attacks on host cells. Mitochondria in eukaryotic cells are increasingly considered key participants in host-pathogen interactions. While Hcp in APEC has been extensively studied, the potential for Hcp1, one of the core proteins in the <em>hcp</em> family, to modulate mitochondrial function during infection remains unexplored. In this study, we discovered that the deletion of <em>hcp1</em> influences bacterial biological characteristics and is critical for bacterial virulence. Previous studies have shown that bacterial virulence factors can interfere with mitochondrial function. Therefore, we further investigated the impact of Hcp1 on cellular mitochondria. After incubating Hcp1 with HD-11 cells, we observed a significant decrease in the mitochondrial membrane potential, an increase in the mitochondrial Ca^2 + concentration, elevated levels of reactive oxygen species, and a reduction in ATP levels, suggesting that Hcp1 induces mitochondrial dysfunction in HD-11 cells. To evaluate the molecular mechanisms underlying mitochondrial dysfunction, we employed LC-MS/MS to identify mitochondria-associated proteins potentially interacting with Hcp1, and PHB2 was identified as a candidate. Protein and molecular docking results demonstrated strong binding activity between Hcp1 and PHB2, and co-immunoprecipitation confirmed their interaction. In summary, T6SS effector protein Hcp1 influences the pathogenicity of APEC, potentially by interacting with PHB2 to induce HD-11 cells’ mitochondrial dysfunction.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110564"},"PeriodicalIF":2.4,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144123995","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":"FoxO4 reduces the damage and mechanism of PEDV-infected IPEC-J2 cells through the NF-κB/MLCK pathway","authors":"Yiming Wei ,&nbsp;Shihui Zhao ,&nbsp;Han Zhao ,&nbsp;Di Bao ,&nbsp;Jiuyuan Liu ,&nbsp;Hongze Shao ,&nbsp;Shuang Zhang ,&nbsp;Shushuai Yi ,&nbsp;Kai Wang ,&nbsp;Guixue Hu","doi":"10.1016/j.vetmic.2025.110568","DOIUrl":"10.1016/j.vetmic.2025.110568","url":null,"abstract":"<div><div>Porcine epidemic diarrhea (PED) incurs substantial economic losses to the pig industry. During viral infection of cells, the activity of NF-κB is upregulated. As an endogenous inhibitor, FoxO4 plays a crucial role in antagonizing NF-κB activity, inhibiting the NF-κB-mediated MLCK signaling pathway, altering the expression of cellular tight junctions (TJs) and pro-inflammatory cytokines, and protecting intestinal epithelial cells from damage. However, there are limited reports on this inhibitory and protective effect in PEDV-infected IPEC-J2 cells. Therefore, this experiment employed methods such as homologous recombination, qRT-PCR, Western blotting, co-immunoprecipitation, laser confocal microscopy, and cell transmembrane resistance assays to investigate the effect of FoxO4 on indicators related to cell damage through the NF-κB/MLCK pathway in infected cells. The results demonstrated the successful construction of FoxO4 and NF-κB factor p65 expression vectors, confirming the interaction between the two in IPEC-J2 cells. FoxO4 effectively antagonizes the expression of NF-κB/MLCK pathway factors in infected cells, and through this action, it reduces the permeability of infected cells, maintains the integrity of the cell membrane, upregulates the expression of TJ proteins, antagonizes the expression of pro-inflamma-tory factors, and exerts effects in promoting cell apoptosis and antagonizing viral replication.This study further elucidates the molecular mechanisms underlying cell damage caused by PEDV and offers new potential targets for protecting intestinal epithelial barrier function.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110568"},"PeriodicalIF":2.4,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144090189","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":"Co-circulation of lineage 1 and lineage 3 porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2) in Taiwan during 2018–2024","authors":"Kun-Lin Kuo ,&nbsp;Wei-Hao Lin ,&nbsp;Ming-Tang Chiou ,&nbsp;Jianqiang Zhang ,&nbsp;Chao-Nan Lin","doi":"10.1016/j.vetmic.2025.110567","DOIUrl":"10.1016/j.vetmic.2025.110567","url":null,"abstract":"<div><div>Porcine reproductive and respiratory syndrome virus (PRRSV) remains a major concern in swine production. This study investigates the molecular epidemiology of lineage 1 and lineage 3 PRRSV-2 in Taiwan between 2018 and 2024. A total of 43,977 samples were collected across 15 counties in Taiwan, and 13,611 tested positive for PRRSV by real-time PCR. Among of them, 501 complete ORF5 sequences were determined and analyzed. The identified PRRSV-2 sequences belonged to either lineage 1 (specifically sublineage L1A which could be divided into at least Clade A, Clade B, and Clade C; 117/501, 23.4 %) or lineage 3 (384/501, 76.6 %). Surprisingly, among the 117 lineage 1 PRRSV-2 sequences, 103 (88.0 %) were from sow-related specimens whereas only 14 (12.0 %) from nursery pigs. Phylogeographic data revealed multiple bidirectional transmissions between central and southern Taiwan, followed by spread to the northern and eastern regions. This imply that the lineage 1 PRRSV-2 caused high mortality and abortion rates in sows and has spread to the entire Taiwan island. The present study provides the first description of the current epidemic state and spread of foreign lineage 1 PRRSV-2 strains in Taiwan during 2018–2024.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110567"},"PeriodicalIF":2.4,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124105","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 G219A hemagglutinin substitution increases pathogenicity and viral replication of Eurasian avian-like H1N1 swine influenza viruses","authors":"Cong He ,&nbsp;Xiaokun Hu ,&nbsp;Junmei Huang ,&nbsp;Congjun Jia ,&nbsp;Mengling Zhang ,&nbsp;Weilin Xu ,&nbsp;Meidi Li ,&nbsp;Mengkai Cai","doi":"10.1016/j.vetmic.2025.110565","DOIUrl":"10.1016/j.vetmic.2025.110565","url":null,"abstract":"<div><div>The Eurasian avian-like swine (EA) H1N1 virus has been widely prevalent in the Chinese swine population and has caused infections in human. However, knowledge regarding its pathogenic mechanisms remains limited. In this study, we analyzed the pathogenic determinants of two G4 genotype EA H1N1 viruses (A/Swine/Guangdong/SS12/2017 and A/Swine/Jiangxi/1110/2017) with differing pathogenicity by constructing a series of reassortant and mutant viruses. The HA-G219A mutation was found to be determinant of pathogenicity in mice. Subsequent analyses revealed that this mutation enhances viral replication in human cells, improves thermal stability, reduces HA activation pH, and alters receptor-binding properties. Furthermore, HA-G219A mutation may be an adaptive mutation that facilitates influenza virus adaptation to swine, with its prevalence increasing in the swine population. This mutation may support cross-species transmission of EA H1N1 swine influenza viruses or genetic exchange with other virus subtypes/genotypes, potentially contributing to the emergence of pandemic viruses. These findings improve our understanding of EA H1N1 pathogenicity and highlight the critical need for ongoing surveillance of influenza viruses in pigs.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"306 ","pages":"Article 110565"},"PeriodicalIF":2.4,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115836","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}