Virulence最新文献_第9页

Preliminary assessment of the therapeutic potential of staphylococcal enterotoxin-like W via biological activity and TCR binding sites analysis. 通过生物活性和TCR结合位点分析初步评估葡萄球菌肠毒素样W的治疗潜力。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-31 DOI: 10.1080/21505594.2025.2550622

Yuhua Yang, Xiaoyue Wei, Fanliang Meng, Yanan Gong, Yahui Guo, Lijin Long, Jiaming Fan, Yakun Zhao, Wanting Wang, Di Xiao, Lei Wang, Maojun Zhang, Dongliang Hu, Jianzhong Zhang, Xiaomei Yan

{"title":"Preliminary assessment of the therapeutic potential of staphylococcal enterotoxin-like W via biological activity and TCR binding sites analysis.","authors":"Yuhua Yang, Xiaoyue Wei, Fanliang Meng, Yanan Gong, Yahui Guo, Lijin Long, Jiaming Fan, Yakun Zhao, Wanting Wang, Di Xiao, Lei Wang, Maojun Zhang, Dongliang Hu, Jianzhong Zhang, Xiaomei Yan","doi":"10.1080/21505594.2025.2550622","DOIUrl":"10.1080/21505594.2025.2550622","url":null,"abstract":"Staphylococcal enterotoxin-like W (SElW) is a novel, widely prevalent enterotoxin-like protein that functions as a classical staphylococcal superantigen (SAg) and has been shown to exacerbate infections caused by the S. aureus epidemic clone CC398. However, the genetic distribution and amino acid polymorphisms, biological and antitumor activity, and T cell receptor (TCR) binding sites of SElW in S. aureus strains prevalent in China have not been investigated. The carrier rate and distribution of selw were determined by PCR, the stability and antitumor activity of recombinant SElW (rSElW) protein were evaluated. The superantigen activity of the five mutants (Y18A, N19A, W55A, C88A, and C98A) was compared to that of wild-type SElW (WT-rSElW) to assess the role of these sites in mediating TCR binding. The selw gene was detected in all (986/986, 100%) dominant clonal lineages of S. aureus and most strains (69.1%, 56/81) had a full-length selw open reading frame with a sequence identity of 90.5%. rSElW was heat-stable but not resistant to pepsin and trypsin digestion. Additionally, rSElW significantly inhibited the proliferation of MCF-7 and AGS, but not A549 in vitro. The rSElW mutants C88A and C98A markedly reduced T cell proliferation and IL-2, IFN-γ and TNF-α secretion compared to WT-rSElW. rSElW is a highly prevalent SAg that binds to the TCR via C98 and C88, which may serve as novel therapeutic targets for S. aureus infections and its application in anti-tumor activity needs to be further evaluated in vivo.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2550622"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144971144","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

Ubiquitin degradation of the Ribonuclease H2 subunit B Rnh2B regulates the virulence of Cryptococcus neoformans. 核糖核酸酶H2亚基B Rnh2B的泛素降解调节新生隐球菌的毒力。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-31 DOI: 10.1080/21505594.2025.2554303

Meng-Ru Guo, Jun-Ming Chen, Qiu-Hong Liao, Ji-Chong Shi, Tong-Bao Liu

{"title":"Ubiquitin degradation of the Ribonuclease H2 subunit B Rnh2B regulates the virulence of Cryptococcus neoformans.","authors":"Meng-Ru Guo, Jun-Ming Chen, Qiu-Hong Liao, Ji-Chong Shi, Tong-Bao Liu","doi":"10.1080/21505594.2025.2554303","DOIUrl":"10.1080/21505594.2025.2554303","url":null,"abstract":"The ubiquitin-proteasome system (UPS) regulates protein degradation in eukaryotes by polyubiquitinating substrate proteins, with F-box proteins serving as key components for substrate recognition. Research has shown that the absence of Cdc4, an F-box protein in C. neoformans, decreases virulence, yet the mechanisms by which Cdc4 affects these processes remain unclear. Using an iTRAQ-based proteomic strategy, we recognized Ribonuclease H2 subunit B (Rnh2B) as a target substrate for Cdc4. Protein-protein interaction assays have confirmed the interaction between Cdc4 and Rnh2B, indicating that Cdc4 regulates Rnh2B stability through ubiquitination. Functional analyses revealed that both the knockout and overexpression of RNH2B impair growth at 37°C, with the latter also affecting cellular membrane integrity and growth under osmotic stress conditions. Pathogenicity assays revealed that the deletion of RNH2B results in reduced virulence, whereas its overexpression leads to a complete loss of pathogenicity. Longitudinal tracking of fungal infection progression illustrated that mice lungs infected with rnh2BΔ mutants maintained a low yet stable fungal burden, in contrast to a significant reduction in fungal load observed in conjunction with RNH2B overexpression, ultimately leading to complete clearance. Analysis of host immune responses indicated a correlation between diminished virulence in the RNH2BOE strain and robust host immune activation. Notably, both the RNH2BOE strain and the cdc4Δ mutant induced analogous adaptive immune responses, facilitating the clearance of C. neoformans infection. Collectively, our findings propose a model wherein Cdc4 mediates the ubiquitination and degradation of Rnh2B, thereby exerting regulatory control over the pathogenicity of C. neoformans.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2554303"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144971335","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

Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways. 非洲猪瘟病毒的免疫逃避策略：抗原呈递途径的调节。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-15 DOI: 10.1080/21505594.2025.2541711

Penghao Lv, Zhichao Wang, Haowei Chen, Yanru Chen, Hanlin Liao, Kaiyue Wei, Shuying Lv, Min Cui

{"title":"Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways.","authors":"Penghao Lv, Zhichao Wang, Haowei Chen, Yanru Chen, Hanlin Liao, Kaiyue Wei, Shuying Lv, Min Cui","doi":"10.1080/21505594.2025.2541711","DOIUrl":"10.1080/21505594.2025.2541711","url":null,"abstract":"African swine fever virus (ASFV), a highly lethal pathogen, poses a catastrophic threat to global pork production. While some commercial vaccines exist, their availability remains regional limitations. This review investigates the mechanistic interplay between ASFV and antigen-presenting cells (APCs), with a particular focus on viral evasion strategies that disrupt antigen presentation pathways. Although current understanding of ASFV immunology has largely focused on monocyte/macrophage infection, we provide a systematic analysis of ASFV-mediated immunosuppression across various APCs, including dendritic cells (DCs), B lymphocytes, and γδ T cells, and compare these mechanisms with those employed by other viral pathogens. Key objectives include: (1) synthesizing ASFV-induced dysregulation of antigen presentation, (2) identifying critical gaps in APC-virus interactions, and (3) guiding vaccine development priorities. By highlighting understudied DC-ASFV interplay and potential molecular targets, this work provides a strategic framework for next-generation vaccine design based on host-pathogen conflict at the antigen presentation interface.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2541711"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859683","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

Combination of isobavachalcone and amphotericin B has antifungal effect against Cryptococcus neoformans and protects host tissue damage by inhibiting ferroptosis. 异巴伐恰尔酮联合两性霉素B对新型隐球菌具有抗真菌作用，并通过抑制铁下垂保护宿主组织损伤。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-19 DOI: 10.1080/21505594.2025.2543981

Weidong Qian, Na Liu, Jiaxing Lu, Qiming Liu, Si Chen, Ting Wang

{"title":"Combination of isobavachalcone and amphotericin B has antifungal effect against Cryptococcus neoformans and protects host tissue damage by inhibiting ferroptosis.","authors":"Weidong Qian, Na Liu, Jiaxing Lu, Qiming Liu, Si Chen, Ting Wang","doi":"10.1080/21505594.2025.2543981","DOIUrl":"10.1080/21505594.2025.2543981","url":null,"abstract":"Despite recent advancements in antifungal therapy, the antifungal armamentarium remains limited compared to antibiotics available for bacterial infections. Developing novel and effective therapeutic strategies is imperative but challenging. One promising approach involves synergizing existing antifungals with complementary agents to enhance efficacy and reduce the required dosages. This study investigates the synergistic effect of isobavachalcone (IBC) and amphotericin B (AmB) against Cryptococcus neoformans in vitro and in vivo, focusing on ferroptosis modulation. Ferroptosis-related markers, including glutathione (GSH), malondialdehyde (MDA), ferrous ions, and reactive oxygen species (ROS), were analyzed in Caenorhabditis elegans model infected with C. neoformans. IBC (4 μg/mL) significantly lowered AmB's MIC from 1 μg/mL to 0.25 μg/mL, indicating a fourfold enhancement in potency. The IBC-AmB combination caused structural damage to C. neoformans, compromising membrane permeability and cell wall integrity. The combination elevated host GSH levels while reducing ferrous ions, MDA, and ROS in the infected C. elegans model. Mechanistically, the treatment upregulated antioxidant/stress response genes (SKN-1, GST-4, GST-5, GPX-1, DAF-16, CNC-11) and antimicrobial peptides (NLP-29). Conversely, the pro-inflammatory pathway gene PMK-1 was downregulated. The IBC-AmB combination not only reduces the MIC of AmB by fourfold but also enhances antifungal efficacy through a multifaceted mechanism that directly targets the fungal pathogen and modulates the host response. This dual action has the potential to reduce the adverse effects of AmB and improve therapeutic outcomes in the treatment of cryptococcal infections.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2543981"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12366827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883856","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

Moderate altitude exposure impacts extensive host-microbiota multi-kingdom connectivity with serum metabolome and fasting blood glucose. 中等海拔暴露会影响宿主-微生物群与血清代谢组和空腹血糖的广泛联系。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-07-13 DOI: 10.1080/21505594.2025.2530660

Xiaoran Huang, Xiaoyan Gao, Yanqun Fan, Dingchen Wang, Xuanfu Chen, Xin Qi, Zhibo Yang, Yu-E Wang, Jinxiu Meng, Guoxiang Zou, Zhipeng Liu, Xin Li

{"title":"Moderate altitude exposure impacts extensive host-microbiota multi-kingdom connectivity with serum metabolome and fasting blood glucose.","authors":"Xiaoran Huang, Xiaoyan Gao, Yanqun Fan, Dingchen Wang, Xuanfu Chen, Xin Qi, Zhibo Yang, Yu-E Wang, Jinxiu Meng, Guoxiang Zou, Zhipeng Liu, Xin Li","doi":"10.1080/21505594.2025.2530660","DOIUrl":"10.1080/21505594.2025.2530660","url":null,"abstract":"The contributions and interactions of multi-kingdom microbiota (i.e. bacteriome, mycobiome, archaeome, and phageome) with serum metabolome and host phenome in healthy individuals under moderate altitude exposure remain unclear. We applied shotgun metagenomic sequencing in feces and targeted metabolomics technology in serum to explore how human gut multi-kingdom microorganisms influence the serum metabolome and phenome in healthy Chinese individuals following moderate altitude exposure. The results indicated that individuals with moderate altitude exposure exhibited more substantial alterations in gut bacteriome and phageome compared to those in mycobiome and archaeome. Both intra-kingdom and inter-kingdom correlations at baseline were denser than those following moderate altitude exposure. Bacteriophages-host interaction analysis revealed symbiosis between bacteriophages and Bacteroidetes, Proteobacteria, and short-chain fatty acids (SCFAs) producers. Furthermore, bacteriophage Shirahamavirus PTm1 (odds ratio (OR) = 3.82; 95% confidence interval (CI): 1.20-12.16), archaeon Crenarchaeota (OR = 3.70; 95% CI: 1.35-10.14) and bacterium Bacteroidetes (OR = 3.69; 95% CI: 1.34-10.15) showed a positive association with lowered fasting blood glucose (FBG) benefits, while bacteriophage Candidatus Nitrosopelagicus brevis (OR = 0.30; 95% CI: 0.10-0.89) and butyric acid (OR = 0.07; 95% CI: 0.01-0.37) exhibited a negative association with lowered FBG benefits. These findings suggest that targeting gut multi-kingdom microorganisms could serve as an alternative therapeutic approach to mitigate dysglycemia and its associated metabolic disorders.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2530660"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144592397","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

MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway. mab_0676c诱导的IL-10生成增强通过MTOR/RUBCN途径抑制自噬通量。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-07-10 DOI: 10.1080/21505594.2025.2529493

Dong Ho Kim, Kyungho Woo, Ho-Sung Park, Hye-Soo Park, Hwa-Jung Kim, Chul Hee Choi

{"title":"MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway.","authors":"Dong Ho Kim, Kyungho Woo, Ho-Sung Park, Hye-Soo Park, Hwa-Jung Kim, Chul Hee Choi","doi":"10.1080/21505594.2025.2529493","DOIUrl":"10.1080/21505594.2025.2529493","url":null,"abstract":"Mycobacterium abscessus subsp. abscessus (M.abs) is a nontuberculous mycobacterium that can infect human lung macrophages, which poses a public health concern. Understanding its mechanism is crucial for developing strategies to combat M.abs infections. M.abs survives within host cells by inhibiting autophagy, a defense mechanism used against intracellular pathogens; therefore, we investigated the mechanism underlying autophagy inhibition and human lung macrophage infection by M.abs. This study focuses on the M.abs UC22 strain, which exhibits stronger inhibition of autophagic flux compared to the M.abs ATCC 19,977 strain. Central to this study is MAB_0676c, a protein secreted by M.abs UC22, and its effects on autophagic flux and the innate immune response, particularly its role in enhancing IL-10 production, a known autophagy regulator. Experiments showed that MAB_0676c expression stabilizes autophagy-related proteins while reducing LC3-LAMP2 co-localization in macrophages, thereby inhibiting autophagy and promoting bacterial growth. Furthermore, blocking IL-10 reduced both autophagy-related protein levels and the intracellular growth of MAB_0676c-expressing bacteria. Therefore, M.abs UC22 mediates intracellular survival by inhibiting autophagy through IL-10 production. Our study reveals bacterial immune-evasion tactics and identifies a potential therapeutic target for treating infectious diseases caused by nontuberculous mycobacteria.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2529493"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12258243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144609742","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

Contribution of a LysM domain-containing protein regulated by VicRK to Streptococcus sanguinis virulence. 由VicRK调控的LysM结构域蛋白对血链球菌毒力的贡献。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-07-18 DOI: 10.1080/21505594.2025.2532036

Eduardo M Franco, Lívia A Alves, Isabela Camargo, Geovanny C Salvatierra, Maíra Terra Garcia, Tsute Chen, Juliana C Junqueira, Débora C Bastos, Renata O Mattos-Graner

{"title":"Contribution of a LysM domain-containing protein regulated by VicRK to Streptococcus sanguinis virulence.","authors":"Eduardo M Franco, Lívia A Alves, Isabela Camargo, Geovanny C Salvatierra, Maíra Terra Garcia, Tsute Chen, Juliana C Junqueira, Débora C Bastos, Renata O Mattos-Graner","doi":"10.1080/21505594.2025.2532036","DOIUrl":"10.1080/21505594.2025.2532036","url":null,"abstract":"Streptococcus sanguinis is a commensal member of the oral microbiome involved in opportunistic cardiovascular infections. In the present study, we investigated the contribution of ssa_0094, a gene strongly regulated by the two-component system VicRK, to functions associated with biofilm formation, immune evasion, and cardiovascular virulence. In silico analysis showed that ssa_0094 encodes a protein with a LysM domain, which is highly conserved among S. sanguinis. Although not an ubiquitous gene, several commensal streptococcal species of the oronasopharynx and zoonotic strains of Streptococcus suis harbor ssa_0094 homologues. A ssa_0094 isogenic mutant (SK0094) showed defects in initiating biofilms on saliva-coated surfaces, reduced hydrophobicity, and lower production of amyloid-like components when compared to the parent strain (SK36) or to the complemented mutant (SK0094+), although it showed mild changes in DNA release and production of H2O2. Deletion of ssa_0094 also impaired S. sanguinis binding to multiple human glycoproteins of plasma and/or extracellular matrix (ECM) (plasminogen, fibronectin, fibrinogen, fibrin, type I collagen, and elastin) and promoted clear increases in C3b deposition and in induction of NEtosis by neutrophils of peripheral blood. Moreover, SK0094 showed impaired invasiveness into HCAEC cells and reduced ex vivo persistence in human blood, but no clear change in virulence in a Galleria mellonella infection model. These findings indicate that ssa_0094 is highly conserved within S. sanguinis strains and required for biofilm initiation as well as for multiple functions of immune evasion and cardiovascular virulence in S. sanguinis in a host-specific fashion.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2532036"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144609743","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

Fumarate and nitrate reduction regulator (FNR) modulates hypermucoviscosity and virulence in hypervirulent Klebsiella pneumoniae through anaerobic adaptation. 富马酸和硝酸盐还原调节剂（FNR）通过厌氧适应调节高致病性肺炎克雷伯菌的高黏性和毒力。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-07-28 DOI: 10.1080/21505594.2025.2536186

Yidan Xu, Ruolan Guo, Ruomei Wang, Zhe Su, Yulu Wu, Chengbin Xie, Pinjia Wang

{"title":"Fumarate and nitrate reduction regulator (FNR) modulates hypermucoviscosity and virulence in hypervirulent Klebsiella pneumoniae through anaerobic adaptation.","authors":"Yidan Xu, Ruolan Guo, Ruomei Wang, Zhe Su, Yulu Wu, Chengbin Xie, Pinjia Wang","doi":"10.1080/21505594.2025.2536186","DOIUrl":"10.1080/21505594.2025.2536186","url":null,"abstract":"Hypervirulent Klebsiella pneumoniae (hvKP), a pathogen responsible for severe invasive infections, exhibits a hypermucoviscosity (HMV) phenotype that is closely associated with its virulence. While fumarate and nitrate reduction regulator (FNR), a global transcription regulator, is critical for bacterial adaptation to hypoxic conditions, its role in hvKP pathogenicity remains unexplored. This study demonstrates that FNR modulates the HMV phenotype and virulence of the hvKP strain NTUH-K2044 under anaerobic conditions. Through targeted deletion and complementation of the fnr gene, combined with phenotypic, molecular, cellular, and animal infection assays, we show that FNR positively regulates the HMV phenotype. Notably, this regulation is independent of several genes previously implicated in HMV formation, including rmpA, rmpA2, wzy-K1 (magA), rmpC, and rmpD. In the absence of fnr, the HMV phenotype was abolished, while the transcript levels of these genes increased significantly, suggesting a compensatory or indirect regulatory mechanism that warrants further investigation. Functionally, FNR-mediated HMV enhanced bacterial resistance to phagocytosis and serum killing while suppressing host colonization features such as fimbriae formation, biofilm production, and epithelial cell adhesion. In animal infection models, FNR also contributed positively to hvKP virulence. These findings highlight the role of FNR in regulating the HMV phenotype and virulence in hvKP, facilitating host adaptation and immune evasion. Targeting FNR may thus represent a promising strategy for the development of novel therapeutics.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2536186"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733549","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

MaMsb2, a signaling mucin, is involved in conidiation, stress tolerances, and virulence in the entomopathogenic fungus Metarhizium acridum. MaMsb2是一种信号粘蛋白，参与了昆虫病原真菌Metarhizium acridum的分生、胁迫耐受性和毒力。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-02 DOI: 10.1080/21505594.2025.2541708

Hongfen Dai, Zhiqiong Wen, Yuxian Xia, Kai Jin

{"title":"MaMsb2, a signaling mucin, is involved in conidiation, stress tolerances, and virulence in the entomopathogenic fungus Metarhizium acridum.","authors":"Hongfen Dai, Zhiqiong Wen, Yuxian Xia, Kai Jin","doi":"10.1080/21505594.2025.2541708","DOIUrl":"10.1080/21505594.2025.2541708","url":null,"abstract":"Entomopathogenic fungi are pivotal microbial resources for crop protection in agriculture, offering a natural and environmentally friendly alternative to chemical pesticides. The signalling mucin gene Msb2 contributes to the modulation of fungal development and virulence, yet its functions have remained unexplored in entomopathogenic fungi. In this study, we aimed to characterize the functions of Msb2 in the model entomopathogenic fungus Metarhizium acridum using gene knockout and complementation strategies. The absence of MaMsb2 led to a delay in conidial germination and an increase in conidial yield due to a shift in the conidiation pattern. Additionally, the MaMsb2-disruption bring about the significantly reduced tolerances to various adversities in M. acridum. Moreover, inactivation of MaMsb2 resulted in the decreased virulence of M. acridum owing to the decrease in conidial hydrophobicity and adhesion, the impairment of appressorium formation, and the reduction of M. acridum growth in the locust haemolymph. To elucidate the molecular mechanisms by which MaMsb2 exerts its influence, we conducted an RNA-seq analysis during appressorium formation. As a result, 880 differentially expressed genes (DEGs) regulated by MaMsb2 were identified. Our data indicated that MaMsb2 governs the appressorium formation of M. acridum by mediating the expression of genes associated with conidia adhesion, appressorium formation, and host cuticle penetration. These findings not only shed light on the multifaceted role of MaMsb2 in the biology of entomopathogenic fungi but also lay the groundwork for future research aimed at unravelling the intricate mechanisms by which MaMsb2 regulates conidiation and pathogenesis.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2541708"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769136","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

Antibody-dependent enhancement of ORFV uptake into host cells. 抗体依赖性增强ORFV进入宿主细胞的摄取。

IF 5.4 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-02-15 DOI: 10.1080/21505594.2025.2466503

Xidian Tang, Chenyibo Zhang, Qingru Geng, Dekun Chen, Wentao Ma

{"title":"Antibody-dependent enhancement of ORFV uptake into host cells.","authors":"Xidian Tang, Chenyibo Zhang, Qingru Geng, Dekun Chen, Wentao Ma","doi":"10.1080/21505594.2025.2466503","DOIUrl":"10.1080/21505594.2025.2466503","url":null,"abstract":"Orf virus (ORFV) has been demonstrated to infect both goat non-immune cells, specifically goat epithelial cells, and goat blood immune cells. Our previous studies have indicated that ORFV gains entry into goat epithelial cells via clathrin-mediated endocytosis and macropinocytosis pathways. However, the pathway by which ORFV enters goat blood immune cells has not yet been elucidated. Our findings revealed a differential viral internalization pathway in ORFV-infects goat immune cells contrasting the internalization pathways in goat epithelial cells, potentially involving an antibody-related mechanism. Therefore, our hypothesis posits that ORFV gains entry into goat immune cells via the antibody-dependent enhancement (ADE) pathway. Our experimental findings confirm the presence of the ADE effect in ORFV-infected goat immune cells, mediated by Fc receptors (FcRs) as demonstrated in antibody-blocking experiments. Furthermore, the ADE effect was also observed in goat epithelial cells. Nevertheless, the ADE effect observed in goat epithelial cells was not found to be dependent on the interaction between the virus-antibody complex and Fc receptors, as demonstrated by antibody-blocking experiments. Instead, it is suggested that an alternative mechanism involving the complement factor and complement receptors (CRs) may be responsible. Overall, this research offers insights into the unique ADE pathway of ORFV infection in different cell types, offering a novel perspective on the infection and pathogenic mechanisms of ORFV.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2466503"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426363","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}

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