Pub Date : 2026-01-03DOI: 10.1016/j.vetmic.2026.110873
Jiale Wei , Zehui Li , Shiwen Li , Yunfei Xing , Feifei Wang , Xiaohui Jin , Zhanyong Wei
Porcine deltacoronavirus (PDCoV) is an emerging porcine coronavirus that causes acute watery diarrhea mainly in piglets. However, the mechanism of PDCoV infection is unclear, which hinders the development of new effective drugs and vaccines. In this study, host factors that involved in PDCoV infection were screened using RNA sequencing (RNA-seq) based transcriptome analysis. Adhesion molecule, vascular cell adhesion molecule 1 (VCAM-1), was selected from the differential genes. The expression of VCAM-1 was further verified by quantitative RT-PCR. It has also been validated in piglet challenge experiments. In the intestine mainly infected, VCAM-1 was detected to be significantly upregulated at the nucleic acid and protein levels. This indicates that VCAM-1 plays a role in the infection of PDCoV. These results help us to understand of the effects of PDCoV infection on host cells, providing a research basis for further screening of drug targets.
{"title":"Transcriptomic analysis reveals the host factor VCAM-1 affecting porcine delta coronavirus infection","authors":"Jiale Wei , Zehui Li , Shiwen Li , Yunfei Xing , Feifei Wang , Xiaohui Jin , Zhanyong Wei","doi":"10.1016/j.vetmic.2026.110873","DOIUrl":"10.1016/j.vetmic.2026.110873","url":null,"abstract":"<div><div>Porcine deltacoronavirus (PDCoV) is an emerging porcine coronavirus that causes acute watery diarrhea mainly in piglets. However, the mechanism of PDCoV infection is unclear, which hinders the development of new effective drugs and vaccines. In this study, host factors that involved in PDCoV infection were screened using RNA sequencing (RNA-seq) based transcriptome analysis. Adhesion molecule, vascular cell adhesion molecule 1 (VCAM-1), was selected from the differential genes. The expression of VCAM-1 was further verified by quantitative RT-PCR. It has also been validated in piglet challenge experiments. In the intestine mainly infected, VCAM-1 was detected to be significantly upregulated at the nucleic acid and protein levels. This indicates that VCAM-1 plays a role in the infection of PDCoV. These results help us to understand of the effects of PDCoV infection on host cells, providing a research basis for further screening of drug targets.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"313 ","pages":"Article 110873"},"PeriodicalIF":2.7,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939819","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}
Pub Date : 2026-01-02DOI: 10.1016/j.vetmic.2026.110872
Pengcheng Wang, Xuan Hu, Lang Tian, Xiaoyu Lu, Qian Xiong, Kangli Liang, Qiaomu Deng, Guilan Wen, Anchun Cheng
Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen that causes substantial economic losses to the global swine industry. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 F (APOBEC3F), a key constituent of cytoplasmic processing bodies (P-bodies) and a member of the deaminase protein family, possesses intrinsic antiviral activity. This study systematically investigates the effects of APOBEC3F and its functional domains on PRRSV replication. This study systematically investigated the effects of APOBEC3F and its functional domains on PRRSV replication. We found that overexpression of APOBEC3F and its C-terminal deaminase domain (CD2) markedly suppressed PRRSV replication (including transcription, protein expression, and viral titers) in susceptible porcine cells. Conversely, APOBEC3F knockdown enhanced viral replication. Notably, several PRRSV proteins—NSP1α, NSP1β, NSP5, NSP7, GP4, GP5, and N—were found to downregulate endogenous APOBEC3F mRNA expression in host cells. Moreover, IP-MS analysis identified several potential candidate interactors, including DEAD-box helicases (such as DDX6 and MOV10) and other host factors, suggesting that APOBEC3F may associate with P-body components to exert its antiviral function. These results offer new insights into the molecular mechanisms of APOBEC3F-mediated antiviral defense against PRRSV and underscore its potential as a therapeutic target.
猪繁殖与呼吸综合征病毒（PRRSV）是给全球养猪业造成重大经济损失的主要病原体。载脂蛋白B mrna编辑酶催化多肽样3 F （APOBEC3F）是细胞质加工体（P-bodies）的关键成分，也是脱胺酶蛋白家族的成员，具有内在的抗病毒活性。本研究系统地探讨了APOBEC3F及其功能域对PRRSV复制的影响。本研究系统地探讨了APOBEC3F及其功能域对PRRSV复制的影响。我们发现APOBEC3F及其c端脱氨酶结构域（CD2）的过表达显著抑制PRRSV在易感猪细胞中的复制（包括转录、蛋白表达和病毒滴度）。相反，敲低APOBEC3F可增强病毒复制。值得注意的是，几种PRRSV蛋白（nsp1 α、NSP1β、NSP5、NSP7、GP4、GP5和n）在宿主细胞中下调内源性APOBEC3F mRNA的表达。此外，IP-MS分析发现了几种潜在的候选相互作用物，包括DEAD-box解旋酶（如DDX6和MOV10）和其他宿主因子，表明APOBEC3F可能与p体成分结合发挥其抗病毒功能。这些结果为apobec3f介导的PRRSV抗病毒防御的分子机制提供了新的见解，并强调了其作为治疗靶点的潜力。
{"title":"APOBEC3F restricts PRRSV replication through its CD2 domain and interaction with host antiviral proteins","authors":"Pengcheng Wang, Xuan Hu, Lang Tian, Xiaoyu Lu, Qian Xiong, Kangli Liang, Qiaomu Deng, Guilan Wen, Anchun Cheng","doi":"10.1016/j.vetmic.2026.110872","DOIUrl":"10.1016/j.vetmic.2026.110872","url":null,"abstract":"<div><div>Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen that causes substantial economic losses to the global swine industry. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 F (APOBEC3F), a key constituent of cytoplasmic processing bodies (P-bodies) and a member of the deaminase protein family, possesses intrinsic antiviral activity. This study systematically investigates the effects of APOBEC3F and its functional domains on PRRSV replication. This study systematically investigated the effects of APOBEC3F and its functional domains on PRRSV replication. We found that overexpression of APOBEC3F and its C-terminal deaminase domain (CD2) markedly suppressed PRRSV replication (including transcription, protein expression, and viral titers) in susceptible porcine cells. Conversely, APOBEC3F knockdown enhanced viral replication. Notably, several PRRSV proteins—NSP1α, NSP1β, NSP5, NSP7, GP4, GP5, and N—were found to downregulate endogenous APOBEC3F mRNA expression in host cells. Moreover, IP-MS analysis identified several potential candidate interactors, including DEAD-box helicases (such as DDX6 and MOV10) and other host factors, suggesting that APOBEC3F may associate with P-body components to exert its antiviral function. These results offer new insights into the molecular mechanisms of APOBEC3F-mediated antiviral defense against PRRSV and underscore its potential as a therapeutic target.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"313 ","pages":"Article 110872"},"PeriodicalIF":2.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913111","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}
Pub Date : 2026-01-02DOI: 10.1016/j.vetmic.2026.110870
Chenchen Lu , Chenglan Zhang , Yanan Li , Zujian Qiao , Xijun Wang , Weiye Chen , Xiaoyi Chen , Qian Jiang , Da Xu , Zhigao Bu , Sen Hu
Brucellosis, a globally significant zoonosis caused by Brucella species, leads to severe reproductive complications including abortion and infertility in animals and humans. Vaccination remains a cornerstone strategy for the control of brucellosis transmission. The Brucella melitensis vaccine strain M5‑90 was developed in China during the 1970s–1980s by attenuation from virulent M28 strain. This study systematically evaluated the safety and protective efficacy of M5‑90 in mouse and guinea pigs models. Results indicated that M5‑90 was completely cleared from mice within 15 weeks after subcutaneous inoculation of 10⁸ CFU, exhibiting a 50 % recovery time (RT50) of 9.27 ± 1.26 weeks. Bacterial replication was not dose-dependent. The bacterial burden in M5‑90-infected mice reduced by 1–3 log10 compared with the virulent M28 group at a challenge dose of 10⁶ CFU (P < 0.05). Immunization with 10⁵ CFU conferred significant protection against virulent B. melitensis M28 and B. abortus 544 challenges at 45 and 150 days post-vaccination, respectively (P < 0.05 or P < 0.01). In guinea pigs, the splenic bacterial load of M5‑90 was markedly lower than that in the M28 group (2440 ± 240 vs. 223,000 ± 3800 CFU/g; P < 0.001). A dose of 3 × 10⁸ CFU of M5‑90 provided complete (100 %) and strong (90 %) protection against M28 and 544 challenges, respectively. In summary, Brucella melitensis vaccine strain M5‑90 demonstrates favorable safety and protective efficacy in mice and guinea pigs, supporting its potential as a promising vaccine for brucellosis control.
{"title":"Evaluation of residual virulence and protective efficacy for Brucella melitensis vaccine strain M5-90 in mice and guinea pigs","authors":"Chenchen Lu , Chenglan Zhang , Yanan Li , Zujian Qiao , Xijun Wang , Weiye Chen , Xiaoyi Chen , Qian Jiang , Da Xu , Zhigao Bu , Sen Hu","doi":"10.1016/j.vetmic.2026.110870","DOIUrl":"10.1016/j.vetmic.2026.110870","url":null,"abstract":"<div><div>Brucellosis, a globally significant zoonosis caused by <em>Brucella</em> species, leads to severe reproductive complications including abortion and infertility in animals and humans. Vaccination remains a cornerstone strategy for the control of brucellosis transmission. The <em>Brucella melitensis</em> vaccine strain M5‑90 was developed in China during the 1970s–1980s by attenuation from virulent M28 strain. This study systematically evaluated the safety and protective efficacy of M5‑90 in mouse and guinea pigs models. Results indicated that M5‑90 was completely cleared from mice within 15 weeks after subcutaneous inoculation of 10⁸ CFU, exhibiting a 50 % recovery time (RT50) of 9.27 ± 1.26 weeks. Bacterial replication was not dose-dependent. The bacterial burden in M5‑90-infected mice reduced by 1–3 log10 compared with the virulent M28 group at a challenge dose of 10⁶ CFU (<em>P</em> < 0.05). Immunization with 10⁵ CFU conferred significant protection against virulent <em>B. melitensis</em> M28 and <em>B. abortus</em> 544 challenges at 45 and 150 days post-vaccination, respectively (<em>P</em> < 0.05 or <em>P</em> < 0.01). In guinea pigs, the splenic bacterial load of M5‑90 was markedly lower than that in the M28 group (2440 ± 240 vs. 223,000 ± 3800 CFU/g; <em>P</em> < 0.001). A dose of 3 × 10⁸ CFU of M5‑90 provided complete (100 %) and strong (90 %) protection against M28 and 544 challenges, respectively. In summary, <em>Brucella melitensis</em> vaccine strain M5‑90 demonstrates favorable safety and protective efficacy in mice and guinea pigs, supporting its potential as a promising vaccine for brucellosis control.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"313 ","pages":"Article 110870"},"PeriodicalIF":2.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145918515","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}
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