{"title":"Exosomes mediate intercellular transmission of Tembusu virus via the NS4A-Rab27a axis.","authors":"Dalin He, Jing Yang, Yitong Cui, Bingrong Wu, Feng Wei, Siming Zhu, Youxiang Diao, Yi Tang","doi":"10.1186/s13567-026-01772-4","DOIUrl":"10.1186/s13567-026-01772-4","url":null,"abstract":"<p><p>Accumulating data support the role of exosomes from virus-infected cells (especially RNA viruses) in the selective encapsulation of viral proteins, genomic material, and even whole virions, thereby mediating intercellular communication events and contributing to viral transmission. Tembusu virus (TMUV), a single-stranded RNA virus, has posed a threat to global public health since its emergence in 2010. However, whether exosomes can mediate TMUV intercellular transmission remains obscure. Here, we show that exosomes derived from TMUV-infected cells (TMUV-exosomes) contained viral genomic RNA and partial viral proteins (C, prM, E, NS1, NS2B, NS4B, and NS5). TMUV-exosomes enter HEK293 cells primarily via a dynamin-dependent, cholesterol-sensitive caveolae-mediated (CavME) endocytosis pathway, thereby suppressing the subsequent expression of key antiviral immune genes to create a proviral microenvironment that supports productive TMUV infection. Remarkably, central to this exosomal hijacking mechanism, the viral NS4A protein and host Rab27a protein form a critical regulatory axis. Specifically, NS4A upregulates Rab27a expression to potentiate the release of exosomes encapsulating viral nucleic acids and proteomic components. Overall, our study provides a mechanistic model for understanding the role of exosomes in TMUV intercellular transmission and identifies the NS4A-Rab27a axis as a critical regulatory node. Disrupting this interaction may represent a potential therapeutic strategy for TMUV infection, warranting further investigation.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13453093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701778","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}
{"title":"Investigating Mycoplasma wenyonii and Candidatus Mycoplasma haematobovis coinfection patterns in cattle from southwestern France reveals strain-specific traits.","authors":"Chloé Saada, Renaud Maillard, Claire Pelletier, Marie-Claude Hygonenq, Hortensia Robert, Christine Citti, Laurent-Xavier Nouvel","doi":"10.1186/s13567-026-01821-y","DOIUrl":"10.1186/s13567-026-01821-y","url":null,"abstract":"<p><p>Hemotropic mycoplasmas (hemoplasmas) infecting cattle were first detected in France in 2019 during a clinical outbreak, but their prevalence both at the species and strain levels remains unknown. This study therefore aimed to determine the prevalence of hemoplasmas and their coinfections, and to assess the within and between herd diversity in five fully sampled dairy herds. Detection was performed using 16S rRNA quantitative polymerase chain reaction (qPCR), as well as three strain-specific rnpB qPCR assays targeting Candidatus Mycoplasma haematobovis (CMh, formerly Ca. M. haemobos), Mycoplasma wenyonii strain Mexico (Mex), and Mycoplasma wenyonii strain Massachusetts (Mass). A total of 1011 cattle were sampled, of which 88.7% (897/1011) tested positive by 16S rRNA qPCR. Detection rates for CMh, Mex, and Mass were 67.7% (684/1011), 65.9% (666/1011), and 19.8% (200/1011), respectively. Concordance between 16S rRNA qPCR and strain-specific rnpB qPCR was 92% (931/1011). Coinfections were detected in 67.8% (565/833) of 16S PCR-positive animals, with the CMh + Mex combination being the most frequent. The Mass strain was predominantly found in association with the two other hemoplasmas. For all four PCR assays, hemoplasma positivity was significantly associated with both herd and animal age in the five fully sampled dairy herds. Further studies are needed to elucidate transmission routes and pathogenicity mechanisms of hemoplasmas.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669702","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}
Qiumei Wang, Guoxin Zheng, Tao Tian, Anli Chen, Guihong Zhang, Heng Wang
{"title":"RNF187 inhibits porcine reproductive and respiratory syndrome virus replication by recruiting the autophagy receptor NDP52 to degrade nsp12.","authors":"Qiumei Wang, Guoxin Zheng, Tao Tian, Anli Chen, Guihong Zhang, Heng Wang","doi":"10.1186/s13567-026-01824-9","DOIUrl":"10.1186/s13567-026-01824-9","url":null,"abstract":"<p><p>Porcine reproductive and respiratory syndrome is one of the most devastating diseases affecting global swine production. Viral nonstructural protein 12 (nsp12) is a key factor in viral replication during viral subgenomic RNA synthesis. We identified the host E3 ubiquitin ligase RING finger protein 187 (RNF187) as a novel anti-porcine reproductive and respiratory syndrome virus (PRRSV) host-restriction factor. RNF187 directly interacts with nsp12, and the overexpression of RNF187 significantly inhibits the expression of the viral nucleocapsid (N) protein and the titer of viruses, whereas the knockdown of RNF187 promotes viral replication. Mechanistic studies showed that RNF187 mediates the degradation of nsp12 in a dose-dependent manner. This degradation process can be blocked by the autophagy inhibitor, 3-methyladenine (3-MA). These results indicate that RNF187 degrades nsp12 via the autophagy pathway rather than the proteasome pathway. Mechanistically, RNF187 acts as a scaffold protein to recruit the autophagic cargo receptor NDP52 and promotes the K63-linked polyubiquitination at lysine 130 (K130) of nsp12, thereby targeting nsp12 for autophagy-lysosomal degradation. This study revealed a novel host defense mechanism mediated by the RNF187-NDP52 axis, which restricts PRRSV infection by targeting nsp12, thereby providing a potential target for the development of antiviral strategies.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13428412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148654323","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}
{"title":"Viperin suppresses goose astrovirus type 2 replication through inhibition of viral RdRP activity.","authors":"Haoran Xu, Jinhang Gao, Junjie Yang, Wenwen Cheng, Yan Cheng, Yingjun Lv","doi":"10.1186/s13567-026-01817-8","DOIUrl":"10.1186/s13567-026-01817-8","url":null,"abstract":"<p><p>Goose astrovirus 2 (GAstV-2) infection induces visceral gout in goslings, resulting in high mortality rates in birds aged 3-15 days. Despite extensive research since the virus was first identified in 2018, the innate immune defense mechanisms of the host against GAstV-2 remain incompletely characterized, impeding the development of effective vaccines and therapeutics. Here, we demonstrated that GAstV-2 infection upregulated Viperin expression both in vitro and in vivo, suggesting a potential role for Viperin as a host restriction factor. Further studies revealed that the P2 domain of viral ORF2 contributed to stimulate Viperin. Overexpression and knockdown experiments confirmed that Viperin exerts antiviral activity against GAstV-2. However, Viperin did not affect attachment or internalization. Mechanistic studies revealed that Viperin inhibits GAstV-2 by attenuating viral RNA-dependent RNA polymerase (RdRp) activity in a manner dependent on its S-adenosylmethionine (SAM) domain. The SAM domain was found to promote the production of 3'-deoxy-3',4'-didehydro-cytidine-5'-triphosphate (ddhCTP), which correlated with reduced RdRp activity and suppression of viral replication. Furthermore, intramuscular administration of ddhCTP reduced mortality and viral loads, and ameliorated GAstV-2-induced pathological injury in the kidney, spleen, and liver of goslings. Collectively, these findings identify Viperin as a key host restriction factor against GAstV-2 and highlight its potential as a target for antiviral strategies.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13422359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148631788","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}
Lu Peng, Qiuhong Zhang, Qingyi Zhou, Weiyao Han, Delan Yang, Zhen Luo, Zhichang Liu, Rui Zhou, Yunfeng Song, Paul R Langford, Lu Li
{"title":"WH01-3A: a DIVA-compliant, ApxIA, ApxIIA, and ApxIIIA expressing Actinobacillus pleuropneumoniae live attenuated vaccine strain that protects mice and pigs against homologous and heterologous serovars.","authors":"Lu Peng, Qiuhong Zhang, Qingyi Zhou, Weiyao Han, Delan Yang, Zhen Luo, Zhichang Liu, Rui Zhou, Yunfeng Song, Paul R Langford, Lu Li","doi":"10.1186/s13567-026-01819-6","DOIUrl":"10.1186/s13567-026-01819-6","url":null,"abstract":"<p><p>Actinobacillus pleuropneumoniae is the causative agent of porcine pleuropneumonia, a major economic burden to the worldwide swine industry. Many available vaccines protect against one or a few of the 19 serovars known. Live attenuated vaccines can potentially protect against many different serovars. In this study, the highly virulent parental A. pleuropneumoniae serovar 1 strain WH01 was used to construct WH01-3A, expressing nontoxic (nonacylated) versions of the three major toxin antigens ApxIA, ApxIIA, and ApxIIIA. In addition, the vivo-induced toxin ApxIVA was deleted, enabling use in a differentiation of vaccinated from infected animals (DIVA) strategy. Compared with WH01, the virulence of WH01-3A in mice was significantly reduced, and, when used as a live attenuated vaccine, WH01-3A protected 87.5%, 75%, and 87.5% animals against A. pleuropneumoniae challenge with serovars 1, 5, and 15, respectively. Pigs immunized with up to 5 × 10<sup>8</sup> CFU WH01-3A had normal body temperatures and behaviors, and normal lung and tonsil pathology. WH01-3A immunization of pigs at 1 × 10<sup>8</sup> CFU resulted in 66.7% and 100% protection after challenge with A. pleuropneumoniae serovars 1 and 15, respectively. WH01-3A immunization induced antibodies against ApxI, ApxII, ApxIII, and whole-cell proteins of serovars 1 and 15. Compared to the unvaccinated group, the average lung lesion scores were reduced by 42.6% and 67.8% after challenge with serovars 1 and 15, respectively. We conclude that WH01-3A is a safe and effective live attenuated vaccine, providing effective immunological protection against A. pleuropneumoniae serovars 1 and 15.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13422351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148631883","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}
Seung-Chai Kim, Hwan-Ju Kim, Sang Chul Kang, Ji-Hyun Ryu, Byungkwan Oh, Sang-Ik Oh, Bumseok Kim, Won-Il Kim
{"title":"Immunopathogenesis and pathological features of NADC34-like PRRSV infection in pregnant sows during late gestation.","authors":"Seung-Chai Kim, Hwan-Ju Kim, Sang Chul Kang, Ji-Hyun Ryu, Byungkwan Oh, Sang-Ik Oh, Bumseok Kim, Won-Il Kim","doi":"10.1186/s13567-026-01792-0","DOIUrl":"10.1186/s13567-026-01792-0","url":null,"abstract":"<p><p>The recently emerged NADC34-like PRRSV-2 strain (Lineage 1A) has been increasingly linked to severe reproductive failures in sow herds, yet its immunopathogenic mechanisms remain poorly understood, especially in pregnant sow models. In this study, we compared the pathogenic and immunological characteristics of a NADC34-like isolate (JBNU-22-N01) with a prevalent NADC30-like strain (PJ73, Lineage 1C) in pregnant sows during late gestation. JBNU-22-N01 infection resulted in earlier peak viremia, more severe maternal pathology, and greater fetal growth restriction compared with PJ73, despite comparable overall fetal viral loads. Notably, JBNU-22-N01-infected fetuses were overrepresented in high viral burden clusters, suggesting enhanced transplacental viral transmission. Transcriptomic and cytokine profiling at the maternal-fetal interface revealed strain-specific downregulation of epithelial junction genes (e.g., CLDN1, CDH1) and immune effector genes in JBNU-22-N01 infection, accompanied by elevated local IFN-α but attenuated immune activation. In contrast, PJ73 elicited more robust antiviral transcriptional responses. Additionally, JBNU-22-N01 infection induced a higher serum kynurenine/tryptophan ratio, indicative of systemic activation of the immunosuppressive kynurenine pathway, which may have contributed to local immune dampening at the maternal-fetal interface. Cytokine analyses across maternal and fetal compartments demonstrated compartmentalized regulation, with maternal cytokine expression shaped by viral strain and fetal cytokine responses more strongly correlated with absolute viral burden. Together, these findings suggest that NADC34-like PRRSV impairs maternal barrier and immune defenses via local and systemic modulation, facilitating fetal infection and compromise. This study expands our understanding of immunopathogenic mechanisms driving PRRSV-induced reproductive failure during late gestation and provides insights for future vaccine development strategies.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13401299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148585407","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}
{"title":"Integration of ATAC-seq and RNA-seq analysis identifies host genes related with PRRSV infection.","authors":"Houchun Liu, Zhong Xu, Hongbo Chen, Xianwen Peng, Liangyu Shi, Cheng Wang, Ao Zhou, Shuqi Mei, Junjing Wu","doi":"10.1186/s13567-026-01804-z","DOIUrl":"10.1186/s13567-026-01804-z","url":null,"abstract":"<p><p>The porcine reproductive and respiratory syndrome virus (PRRSV) is a highly contagious pathogen. Viral infections often enhance their replication by modulating the structure and expression of host genes. However, it remains unclear whether PRRSV employs a similar mechanism to achieve self-replication. To address this question, the current study combined assay for transposase accessible chromatin sequencing (ATAC-seq) and ribonucleic acid (RNA) sequencing (RNA-seq) to identify accessible chromatin regions and key host genes associated with PRRSV infection. By comparing the PRRSV-infected group with the control group, we initially detected 8664 differentially accessible chromatin regions and 4037 differentially expressed genes. Motif analysis of these differential chromatin regions revealed several potential cis-regulatory elements containing binding sites for transcription factors. Further integration of ATAC-seq and RNA-seq results identified 1352 overlapping genes between the PRRSV-infected and control groups. A significant positive correlation between differential gene expression and chromatin accessibility signals suggests that chromatin remodeling may drive transcriptional changes during infection. Protein-protein interaction (PPI) network analysis highlighted candidate genes potentially associated with PRRSV infection in hosts, such as IL1B, CCL20, CXCL10, CSF3, etc. Given their potential association with the infection mechanism, these genes could serve as candidate targets for the future development of prophylactic vaccines and therapeutic strategies. Additionally, several signaling pathways that may regulate immune and inflammatory responses were significantly enriched in our ATAC-seq and RNA-seq analyses. These findings provide valuable insights into the molecular mechanisms underlying PRRSV infection and pave the way for developing more effective preventive and treatment measures.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13397763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148580262","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}
{"title":"In vitro and in vivo studies of GAPLINC identify it as a critical host factor involved in the regulation of influenza A virus infection.","authors":"Lulu Wang, Haiyan Xu, Jiajie Li, Qianxi Zhang, Guanghui Chui, Shihong Yan, Song Wang, Shile Huang, Ji-Long Chen","doi":"10.1186/s13567-026-01783-1","DOIUrl":"10.1186/s13567-026-01783-1","url":null,"abstract":"<p><p>Although previous studies have suggested a role for GAPLINC in regulating influenza A virus (IAV) infection, the functional involvement of GAPLINC in IAV infection in vitro and in vivo remains largely unknown. Here, we found that expression of lncRNA GAPLINC is significantly downregulated by infections with several strains of IAV, including PR8, WSN, H3N2, and H9N2. Interestingly, infections with several other viruses, such as pseudorabies virus (PRV), Sendai virus (SeV), and Herpes simplex virus (HSV), also result in a significant reduction in GAPLINC expression. During IAV infection, activation of NF-κB and the downstream IL-6/STAT3 signaling pathway contribute, at least in part, to the downregulation of GAPLINC expression. Knockdown of GAPLINC in host cells impairs the viral replication, whereas overexpression of GAPLINC increases the viral titers. Both heterozygous GAPLINC knockout (KO) mice (GAPLINC<sup>+/-</sup>) and homozygous GAPLINC KO mice (GAPLINC<sup>⁻/⁻</sup>) were further employed to determine its function in vivo. GAPLINC knockout renders mice more resistant to IAV infection than wild-type counterparts, as evidenced by lower viral load and lung injury, slower body weight loss, and improved survival. We confirmed that GAPLINC obviously suppresses the IRF3 activation in IAV-infected cells. Moreover, we noticed that inhibition of ATG7-involved autophagy weakens the pro-viral activity of GAPLINC. Together, the results support the conclusion that GAPLINC plays a critical role in enhancing the pathogenesis of IAV, at least by targeting the IRF3 and ATG7-mediated autophagy pathway.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13377811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148472950","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}
Meizhen Li, Mengli Qiao, Keshun Bao, Yuanhang Zhang, Panchi Zhang, Jing Chen, Qi Luan, Kun Li, Li Wang, Bin Zhou
{"title":"Whole-genome characterization and pathogenicity of novel human-porcine reassortant rotavirus strains G9P[7] and G1P[7] in China.","authors":"Meizhen Li, Mengli Qiao, Keshun Bao, Yuanhang Zhang, Panchi Zhang, Jing Chen, Qi Luan, Kun Li, Li Wang, Bin Zhou","doi":"10.1186/s13567-026-01775-1","DOIUrl":"10.1186/s13567-026-01775-1","url":null,"abstract":"<p><p>The prevalence of porcine rotavirus A (PoRVA) in China has increased significantly, threatening the swine industry. Pigs serve as \"mixing vessels\" for rotaviruses, facilitating reassortment between human and animal strains, leading to the emergence of zoonotic variants. In this study, two PoRVA strains, XXW2023 (G9P[7]) and HD2023 (G1P[7]), were isolated from diarrheic piglets in Guangdong Province, China. Genomic analysis revealed that both strains were human-porcine reassortants, with VP1, VP3, and NSP1 genes closely related to human rotaviruses. Intragenic recombination was identified in the VP4 and VP6 genes. Pathogenicity was evaluated in 7-day-old mice and 1-day-old piglets. Both strains caused persistent diarrhea in mice and severe watery diarrhea, intestinal lesions, and death within 48 h in piglets. Systemic infection was confirmed, with viral replication detected in the lungs. Infectious virus titers, VP6 antigen, and NSP4 were detected in lung tissues, providing evidence of active replication in the respiratory tract. The strains exhibited distinct tissue tropism, with XXW2023 being enterotropic and HD2023 showing pulmonary tropism. Viral RNA and antigen levels in the lungs of HD2023-infected piglets exceeded those in their intestines, and the infectious virus titer in their lungs was significantly higher than that in the lungs of XXW2023-infected piglets. These findings demonstrate that reassortant rotavirus strains infect the respiratory tract, extending the conventional view of rotavirus as a strictly enteric pathogen. The emergence of these highly pathogenic, phenotypically divergent human-porcine reassortants underscores their zoonotic risk, highlighting the need for enhanced surveillance and reconsideration of vaccine coverage.</p>","PeriodicalId":23658,"journal":{"name":"Veterinary Research","volume":"57 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13371254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148456629","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}