Veterinary microbiology最新文献_第7页

Phosphorylation of T425 and methylation of R426 synergistically regulate IBDV VP1 function and viral replication T425磷酸化和R426甲基化协同调节IBDV VP1功能和病毒复制。

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-05 DOI: 10.1016/j.vetmic.2026.110871

Huiping Liang , Xiangxiang Gao , Yan Xiao , Rongzhao Sun , Biao Chen , Qinghua Zeng , Zheng Chen , Xiangdong Wu , Huansheng Wu

Post-translational modifications (PTMs) are essential regulators of viral protein function and replication efficiency. Infectious bursal disease virus (IBDV) polymerase VP1 has been reported to undergo multiple PTMs; however, the interplay among different modifications remains poorly understood. In this study, we identified a novel phosphorylation site at threonine 425 (T425) adjacent to the previously characterized arginine 426 (R426) methylation site of VP1. Mass spectrometry and phospho-specific antibodies confirmed phosphorylation at T425 during IBDV replication. Functional assays demonstrated that phosphorylation at T425 enhances VP1 polymerase activity and promotes viral replication, whereas mutation of this site markedly impaired viral growth. Inhibition experiments further indicated that inhibitor IX significantly inhibit T425 phosphorylation. Importantly, we revealed a synergistic relationship between T425 phosphorylation and PRMT5-mediated R426 methylation, as loss of either modification attenuated the other. Recombinant IBDV harboring the T425A/R426A double mutation exhibited significantly reduced replication capacity compared to single mutants. Together, our findings uncover a previously unrecognized crosstalk between adjacent phosphorylation and methylation sites in VP1, providing new insights into the fine-tuned regulation of IBDV replication and offering potential targets for antiviral strategies and vaccine development.

翻译后修饰（PTMs）是病毒蛋白功能和复制效率的重要调节因子。据报道，传染性法氏囊病病毒（IBDV）聚合酶VP1可发生多次ptm；然而，不同修饰之间的相互作用仍然知之甚少。在这项研究中，我们在苏氨酸425 （T425）上发现了一个新的磷酸化位点，与先前表征的VP1的精氨酸426 （R426）甲基化位点相邻。质谱分析和磷酸化特异性抗体证实了IBDV复制过程中T425位点的磷酸化。功能分析表明，T425位点的磷酸化增强了VP1聚合酶的活性，促进了病毒的复制，而该位点的突变明显损害了病毒的生长。抑制实验进一步表明，抑制剂IX显著抑制T425磷酸化。重要的是，我们揭示了T425磷酸化和prmt5介导的R426甲基化之间的协同关系，因为失去任何一种修饰都会减弱另一种修饰。与单突变体相比，携带T425A/R426A双突变的重组IBDV的复制能力显著降低。总之，我们的研究结果揭示了VP1中相邻磷酸化和甲基化位点之间先前未被识别的串扰，为IBDV复制的微调调控提供了新的见解，并为抗病毒策略和疫苗开发提供了潜在的靶点。

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引用次数: 0

Transcriptomic analysis reveals the host factor VCAM-1 affecting porcine delta coronavirus infection 转录组学分析显示宿主因子VCAM-1影响猪冠状病毒感染

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-03 DOI: 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.

猪三角冠状病毒（PDCoV）是一种新兴的猪冠状病毒，主要在仔猪中引起急性水样腹泻。然而，PDCoV感染的机制尚不清楚，这阻碍了新的有效药物和疫苗的开发。本研究采用基于RNA测序（RNA-seq）的转录组分析方法筛选与PDCoV感染相关的宿主因子。从差异基因中选择粘附分子血管细胞粘附分子1 （vascular cell Adhesion molecule 1, VCAM-1）。通过定量RT-PCR进一步验证VCAM-1的表达。在仔猪激射实验中也得到了验证。在主要感染的肠道中，检测到VCAM-1在核酸和蛋白水平上显著上调。这表明VCAM-1在PDCoV感染中起作用。这些结果有助于我们了解PDCoV感染对宿主细胞的影响，为进一步筛选药物靶点提供研究基础。

引用次数: 0

APOBEC3F restricts PRRSV replication through its CD2 domain and interaction with host antiviral proteins APOBEC3F通过其CD2结构域和与宿主抗病毒蛋白的相互作用来限制PRRSV的复制。

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-02 DOI: 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。

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引用次数: 0

Evaluation of residual virulence and protective efficacy for Brucella melitensis vaccine strain M5-90 in mice and guinea pigs M5-90布氏菌疫苗在小鼠和豚鼠体内的残留毒力和保护效果评价。

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-02 DOI: 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.

布鲁氏菌病是由布鲁氏菌引起的一种全球重要的人畜共患病，可导致严重的生殖并发症，包括动物和人类的流产和不孕。疫苗接种仍然是控制布鲁氏菌病传播的基石战略。在20世纪70年代至80年代，中国通过对毒力强的M28菌株进行减毒，研制出了梅利氏布鲁氏菌疫苗株M5‑90。本研究在小鼠和豚鼠模型中系统评价了M5‑90的安全性和保护作用。结果表明，皮下接种10⁸CFU后15周内，小鼠体内的M5‑90被完全清除，恢复时间（RT50）为9.27 ± 1.26周，为50% %。细菌复制不依赖于剂量。在10⁶CFU的攻毒剂量下，M5‑90感染小鼠的细菌负荷比M28毒力组减少了1-3 log10

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引用次数: 0

Corrigendum to “ASFV activates STAT3 to induce proviral M2 macrophage polarization” [Vet. Microbiol. 311 (2025) 110733] “ASFV激活STAT3诱导病毒前M2巨噬细胞极化”的勘误。微生物学。311 (2025)110733 [j]

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-01 DOI: 10.1016/j.vetmic.2025.110833

Yanru Chen , Haowei Chen , Weijia Zhang , Penghao Lv , Zhichao Wang , Hanlin Liao , Kaiyue Wei , Qigai He , Min Cui

引用次数: 0

The disruption of two putative peptidases affects the extracellular proteolytic and metabolic activity of Mycoplasma bovis 两种假定的肽酶的破坏影响了牛支原体的细胞外蛋白水解和代谢活性。

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-01 DOI: 10.1016/j.vetmic.2025.110856

Shijie Geng , Dilhani Ekanayake , Anna Kanci Condello , David P. De Souza , Sheik Nadeem Elahee Doomun , Chintha K. Premachandre , Jordi Hondrogiannis , Glenn F. Browning , Sara M. Klose , Kelly A. Tivendale , Nadeeka K. Wawegama

Although proteolytic activity has been shown to be critical for virulence in mycoplasmas, the role of this activity in the pathogenesis of infections with Mycoplasma bovis is yet to be fully elucidated. Two putative peptidase genes (MBOVPG45_0176 and MBOVPG45_0685) of M. bovis were previously shown to be required for the survival of the organism in association with host cells. To investigate the metabolic functions of the two genes, proteolytic screening of M. bovis cell-associated and secreted proteins, together with metabolomic profiling by gas chromatography-mass spectrometry (GC-MS), were used in this study to compare mutants in which the genes were disrupted by a transposon with their parent strain. Cloning and expression of the two genes were also attempted to study their enzymatic activity. Zymography using different peptidase substrates detected secreted proteins of M. bovis with proteolytic activity against gelatin and collagen. Although peptidase activity was reduced in the mutant in which the MBOVPG45_0176 gene was disrupted, the expressed glutathione S-transferase-tagged recombinant product of this gene had no detectable proteolytic activity, possibly due to the absence of propeptide cleavage required for peptidase maturation. Comparative metabolomic profiling revealed that mutants with either of these genes disrupted had significantly lower abundances of amino acids, nucleoside metabolites, and glycolytic intermediates. These results suggest the two putative peptidase genes have a role in metabolic and extracellular proteolytic activity of M. bovis, although further investigation is needed to determine the targets of the proteolytic activity of their products and their precise role in host-mycoplasma interactions.

虽然蛋白水解活性已被证明对支原体的毒力至关重要，但这种活性在牛支原体感染的发病机制中的作用尚未完全阐明。两个假定的肽酶基因（MBOVPG45_0176和MBOVPG45_0685）先前被证明是与宿主细胞相关的生物体存活所必需的。为了研究这两个基因的代谢功能，本研究使用了牛分枝杆菌细胞相关蛋白和分泌蛋白的蛋白水解筛选，以及气相色谱-质谱（GC-MS）的代谢组学分析，将基因被转座子破坏的突变体与其亲本菌株进行了比较。并对这两个基因的克隆和表达进行了研究。利用不同的肽酶底物酶谱法检测牛分枝杆菌分泌的蛋白对明胶和胶原蛋白具有水解活性。虽然在MBOVPG45_0176基因被破坏的突变体中，肽酶活性降低，但表达的谷胱甘肽s -转移酶标记的重组产物没有检测到蛋白水解活性，可能是由于缺乏肽酶成熟所需的前肽裂解。比较代谢组学分析显示，这些基因中任何一个被破坏的突变体氨基酸、核苷代谢物和糖酵解中间体的丰度显著降低。这些结果表明，这两个假定的肽酶基因在牛支原体的代谢和细胞外蛋白水解活性中起作用，尽管需要进一步的研究来确定它们产物的蛋白水解活性的目标和它们在宿主-支原体相互作用中的确切作用。

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引用次数: 0

ASFV activates STAT3 to induce proviral M2 macrophage polarization ASFV激活STAT3诱导原病毒M2巨噬细胞极化

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2026-01-01 DOI: 10.1016/j.vetmic.2025.110832

Yanru Chen , Haowei Chen , Weijia Zhang , Penghao Lv , Zhichao Wang , Hanlin Liao , Kaiyue Wei , Qigai He , Min Cui

African swine fever (ASF) is an acute and highly infectious disease caused by African swine fever virus (ASFV) that has dealt a massive blow to the development of the pig industry in China. Macrophages, the primary target cells of ASFV, exhibit high plasticity, however, their phenotypic changes during infection remain poorly understood. In this study, we observed a significant increase in M2 monocytes within the peripheral blood cells of ASFV-infected pigs. In vitro experiments demonstrated that ASFV drives macrophage polarization toward the M2 phenotype through early phosphorylation of STAT3. STAT3 inhibition with STATTIC not only blocked M2 polarization but also suppressed ASFV replication. While M2 macrophages do not impede viral attachment or internalization, they displayed reduced killing capacity compared to M1 macrophages. Furthermore, in a mixed lymphocyte reaction (MLR) system, CD4⁺ T cells cocultured with ASFV-infected M2-polarized macrophages presented suppressed early activation, marked by downregulated CD25 expression, ultimately impairing adaptive immunity. These findings reveal a critical immune evasion strategy employed by ASFV and provide key insights into ASF pathogenesis and viral persistence.

非洲猪瘟（African swine fever， ASF）是由非洲猪瘟病毒（African swine fever virus， ASFV）引起的一种急性高传染性疾病，对中国养猪业的发展造成了巨大的打击。巨噬细胞是ASFV的主要靶细胞，具有高度的可塑性，但其在感染过程中的表型变化尚不清楚。在本研究中，我们观察到感染asfv的猪外周血中M2单核细胞显著增加。体外实验表明，ASFV通过STAT3的早期磷酸化驱动巨噬细胞向M2表型极化。STAT3抑制剂不仅能阻断M2极化，还能抑制ASFV的复制。虽然M2巨噬细胞不阻碍病毒附着或内化，但与M1巨噬细胞相比，它们的杀伤能力有所降低。此外，在混合淋巴细胞反应（MLR）系统中，CD4+ T细胞与asfv感染的m2极化巨噬细胞共培养的早期活化受到抑制，以CD25表达下调为标志，最终损害适应性免疫。这些发现揭示了ASFV采用的关键免疫逃避策略，并为ASF发病机制和病毒持久性提供了关键见解。

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引用次数: 0

Beyond macrophages: FIPV tropism includes T and B lymphocytes 除巨噬细胞外：趋向性FIPV包括T和B淋巴细胞。

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2025-12-31 DOI: 10.1016/j.vetmic.2025.110864

Aadhavan Balakumar , Patrawin Wanakumjorn , Kazuto Kimura , Ehren McLarty , Katherine Farrell , Terza Brostoff , Jully Pires , Tamar Cohen-Davidyan , Jennifer M. Cassano , Brian Murphy , Krystle Reagan , Amir Kol

If untreated, feline infectious peritonitis (FIP) is a fatal disease that is caused by feline infectious peritonitis virus (FIPV), a virulent biotype of feline coronavirus (FCoV) that disseminates broadly and triggers severe systemic inflammation. While the prevailing model holds that FIPV selectively infects monocytes/macrophages, the full range of susceptible cell types and the mechanisms of immune cell invasion remain poorly defined. Here, we applied single-cell RNA sequencing, multiplex immunofluorescence, and in situ hybridization to mesenteric lymph node aspirates and formalin fixed and paraffin embedded lymph node tissues from cats with naturally occurring effusive FIP. We identified FIPV RNA and nucleocapsid protein in T and B lymphocytes and myeloid cells, and subgenomic viral RNA in T cells, demonstrating cell entry and viral genomic replication across multiple immune compartments. Rare FIPV RNA–positive lymphocytes persisted after antiviral treatment cessation and resolution of clinical signs. These findings revise current models of FIPV pathogenesis and reveal new insights into coronavirus-driven immune dysregulation, viral persistence, and relapse. Our study highlights the utility of FIP as a naturally occurring animal model for exploring adaptive immune cell infection in coronavirus diseases, providing a translational platform for understanding virus–host interactions that drive chronic or relapsing immunopathology.

如果不及时治疗，猫传染性腹膜炎（FIP）是一种由猫传染性腹膜炎病毒（FIPV）引起的致命疾病，FIPV是一种毒力强的猫冠状病毒（FCoV），可广泛传播并引发严重的全身炎症。虽然流行的模型认为FIPV选择性地感染单核/巨噬细胞，但各种易感细胞类型和免疫细胞入侵机制仍然不明确。在这里，我们将单细胞RNA测序、多重免疫荧光和原位杂交应用于自然发生的渗出性FIP猫的肠系膜淋巴结抽吸物和福尔马林固定和石蜡包埋的淋巴结组织。我们在T淋巴细胞、B淋巴细胞和髓细胞中鉴定了FIPV RNA和核衣壳蛋白，在T细胞中鉴定了亚基因组病毒RNA，证明了细胞进入和病毒基因组复制跨越多个免疫区室。罕见的FIPV rna阳性淋巴细胞在抗病毒治疗停止和临床症状消退后仍然存在。这些发现修订了目前关于FIPV发病机制的模型，并揭示了冠状病毒驱动的免疫失调、病毒持续存在和复发的新见解。我们的研究强调了FIP作为一种自然发生的动物模型的效用，用于探索冠状病毒疾病中的适应性免疫细胞感染，为理解驱动慢性或复发性免疫病理的病毒-宿主相互作用提供了一个翻译平台。

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引用次数: 0

NSP9 is a key virulence determinant in highly pathogenic PRRSV-mediated thymic injury via synergistic activation of apoptotic and metabolic pathways 在高致病性prrsv介导的胸腺损伤中，NSP9是一个关键的毒力决定因素，通过凋亡和代谢途径的协同激活。

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2025-12-31 DOI: 10.1016/j.vetmic.2025.110868

Fanliang Meng , Chenchen Cui , Xinyi Huang , Qianru Zhang , Longshuai Yao , Xuehui Cai , Tongqing An , Gang Wang

Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) induces severe thymic atrophy, contributing to immunosuppression in infected piglets. This study investigated the roles of viral nonstructural proteins NSP9 and NSP10 in thymic pathogenesis using chimeric viruses (HC9 and HC10) generated by replacing NSP9/NSP10 of the HP-PRRSV HuN4 strain with those from the classical CH-1a strain. In vitro replication was significantly affected by these swaps, with NSP9 showing a more pronounced effect. In vivo replication kinetics, pathogenicity, and thymus damage were analyzed in piglets inoculated with the HuN4 strain or the chimeric strains. The study found that NSP9 and NSP10 are closely associated with PRRSV replication efficiency and pathogenicity, with NSP9 having a greater impact on thymus atrophy and both NSP9 and NSP10 playing a key role in inducing thymocytes apoptosis. Transcriptomic analysis revealed that HuN4 infection significantly upregulated genes associated with apoptosis, inflammatory responses, and metabolic pathways (e.g., NF-κB, PI3K-Akt, and p53 signaling), while HC9 showed attenuated effects. Flow cytometry confirmed HuN4-induced depletion of CD4⁺CD8⁺ thymocytes and dysregulated surface marker expression (CD4). TUNEL assays and apoptosis-related gene profiling further implicated NSP9 in activating both intrinsic and extrinsic apoptotic pathways. Notably, metabolic pathway enrichment suggested crosstalk between apoptosis and energy sensing (e.g., AMPK-mTOR). These findings highlight NSP9 as a critical virulence factor driving thymic atrophy through synergistic immune hyperactivation, apoptotic cascades, and metabolic reprogramming, providing novel insights for PRRSV vaccine design and immunomodulatory strategies.

高致病性猪繁殖与呼吸综合征病毒（HP-PRRSV）引起仔猪严重胸腺萎缩，导致仔猪免疫抑制。本研究利用HC9和HC10嵌合病毒将HP-PRRSV HuN4株的NSP9/NSP10替换为经典CH-1a株的NSP9/NSP10，研究了病毒非结构蛋白NSP9和NSP10在胸腺发病中的作用。这些交换显著影响了体外复制，其中NSP9表现出更明显的影响。研究了HuN4株和嵌合株接种仔猪的体内复制动力学、致病性和胸腺损伤情况。研究发现，NSP9和NSP10与PRRSV的复制效率和致病性密切相关，其中NSP9对胸腺萎缩的影响更大，NSP9和NSP10在诱导胸腺细胞凋亡中都起着关键作用。转录组学分析显示，HuN4感染显著上调了与凋亡、炎症反应和代谢途径相关的基因（如NF-κB、PI3K-Akt和p53信号传导），而HC9的作用减弱。流式细胞术证实了hun4诱导的CD4+CD8+胸腺细胞耗竭和表面标记物表达失调（CD4）。TUNEL实验和凋亡相关基因谱进一步表明，NSP9在激活内源性和外源性凋亡通路中都有作用。值得注意的是，代谢途径的富集表明细胞凋亡和能量感应（如AMPK-mTOR）之间存在串扰。这些发现强调了NSP9是通过协同免疫超激活、凋亡级联和代谢重编程驱动胸腺萎缩的关键毒力因子，为PRRSV疫苗设计和免疫调节策略提供了新的见解。

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引用次数: 0

ANXA2 stabilizes mTOR at the plasma membrane to facilitate autophagic flux for CSFV release ANXA2稳定质膜上的mTOR，促进CSFV释放的自噬通量

IF 2.7 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology

Pub Date : 2025-12-31 DOI: 10.1016/j.vetmic.2025.110863

Tao Wang , Liangcai Da , Junfang Zhao , Hong Yuan , Ying Sun , Liang Zhang , Kun Li , Jing Zhang , Pu Sun , Zhixun Zhao , Qiang Zhang , Yuanji Zhang , Yebing Liu , Xingwen Bai , Zengjun Lu

Classical swine fever virus (CSFV), a member of the Flaviviridae family, remains a major pathogen responsible for substantial economic losses in the global swine industry. Autophagy plays a critical role in the life cycle and virulence of CSFV, however, the mechanisms through which the virus regulates autophagy are still not fully understood. In this study, we identified ANXA2, a calcium-dependent phospholipid-binding protein, within autophagy-derived vesicles that facilitate CSFV transmission. We demonstrated that ANXA2 modulates CSFV release in a manner dependent on autophagy. Moreover, multiple lines of evidence, including Western blot, LC3 puncta formation, tandem fluorescence assay, and electron microscopy, consistently showed that ANXA2 promotes CSFV-induced autophagy. Mechanistically, ANXA2 overexpression reduced mTOR phosphorylation, while its knockout increased phosphorylation. Comprehensive binding assays revealed that both ANXA2 and the CSFV envelope protein E2 interact with mTOR with high affinity. Domain mapping further indicated that ANXA2 and E2 bind to distinct regions of mTOR, suggesting a synergistic mechanism for autophagy activation. Confocal microscopy showed that ANXA2 facilitates mTOR accumulation at the plasma membrane during infection. Importantly, relocalizing ANXA2 to mitochondria attenuated CSFV-induced autophagy. Collectively, these results indicate that ANXA2 modulates CSFV-triggered autophagy by controlling mTOR subcellular localization, thereby influencing viral production. This study unveils a novel strategy by which CSFV co-opts the ANXA2–mTOR axis to manipulate autophagic processes, highlighting potential targets for future antiviral interventions.

经典猪瘟病毒（CSFV）是黄病毒科的一员，仍然是造成全球养猪业重大经济损失的主要病原体。自噬在猪瘟病毒的生命周期和毒力中起着至关重要的作用，然而，病毒调控自噬的机制尚不完全清楚。在这项研究中，我们在自噬衍生的囊泡中发现了ANXA2，一种钙依赖性磷脂结合蛋白，可促进猪瘟病毒的传播。我们证明了ANXA2以依赖于自噬的方式调节猪瘟病毒的释放。此外，包括Western blot、LC3斑点形成、串联荧光实验和电镜在内的多种证据一致表明，ANXA2促进了csfv诱导的自噬。机制上，ANXA2过表达降低了mTOR的磷酸化，而敲除则增加了磷酸化。综合结合实验显示，ANXA2和CSFV包膜蛋白E2都与mTOR有高亲和力的相互作用。结构域定位进一步表明，ANXA2和E2结合到mTOR的不同区域，提示自噬激活的协同机制。共聚焦显微镜显示，在感染过程中，ANXA2促进了mTOR在质膜上的积累。重要的是，将ANXA2重新定位到线粒体可以减弱猪瘟病毒诱导的自噬。综上所述，这些结果表明ANXA2通过控制mTOR亚细胞定位来调节猪瘟引发的自噬，从而影响病毒的产生。这项研究揭示了CSFV利用ANXA2-mTOR轴操纵自噬过程的一种新策略，突出了未来抗病毒干预的潜在靶点。

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引用次数: 0