Virulence毒力
Virulence(英文缩写 VIRULENCE),ISSN 2150-5594,eISSN 2150-5608,中文译名:毒力 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.428 | Q2 |
| 2022 | 5.200 | Q2 |
| 2023 | 5.500 | Q1 |
| 2024 | 5.400 | Q1 |
| 2025 | 6.800 | Q1 |
Virulence 最新收录文献
-
1. Coordination of quorum sensing with T3SS and T6SS: Bacterial strategies for combating fungal pathogens.
1. 群体感应与T3SS和T6SS的协调：细菌对抗真菌病原体的策略PMID:日期:2026-09-28Bacterial-fungal interactions are essential for ecosystem balance, where secretion systems like the Type III Secretion System (T3SS) and Type VI Secretion System (T6SS) play crucial roles. T6SS acts as a multifunctional weapon by delivering antifungal effectors that disrupt fungal cell integrity and metabolism, while T3SS mediates both mutualistic and antagonistic interactions, with mutualistic roles documented primarily in plant-associated bacteria-fungi systems. Quorum sensing (QS) facilitates these interactions by allowing bacteria to adjust their secretion responses based on fungal signals. This review delves into the antifungal mechanisms of T6SS and T3SS and emphasizes QS as a regulatory framework that influences microbial community dynamics. Understanding these relationships can lead to innovative strategies for combating fungal pathogens, contributing to agricultural sustainability and paving the way for future clinical and environmental research.
-
2. Integrated multi-omics analysis identifies PPAR signaling network associations with metabolic-immune dysregulation and intestinal injury in PDCoV-infected piglets.
PMID:日期:2026-09-27Porcine deltacoronavirus (PDCoV) is an emerging enteric coronavirus that causes severe diarrhea and high mortality in neonatal piglets and has demonstrated the capacity to infect human cells. However, the host response networks that govern disease outcome remain poorly understood. Here, we performed integrated transcriptomic, proteomic, and metabolomic profiling of jejunal tissues from PDCoV-infected piglets, representing the first such analysis in the primary target organ of this pathogen. Multi-omics integration identified a core host-response network characterized by concurrent activation of a potent type I interferon-mediated antiviral response and notable alterations in lipid metabolism. The peroxisome proliferator-activated receptor (PPAR) signaling pathway was among the most significantly enriched pathways, marked by coordinated upregulation of , , and and downregulation of . Metabolomic analysis demonstrated widespread degradation of membrane glycerophospholipids and alterations in the arachidonic acid-prostaglandin inflammatory axis, as evidenced by substrate consumption and accumulation of the pro-inflammatory mediator 20-hydroxy-PGE2. We propose a hypothetical working model in which PDCoV infection is associated with PPAR network modulation, potentially contributing to lipid resource reallocation and the establishment of a pro-inflammatory microenvironment that may exacerbate intestinal injury. Notably, similarities can be observed between these PDCoV-associated alterations and the metabolic-immune dysregulation reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, raising the hypothesis of shared pathogenic features across coronaviruses. Our findings highlight the PPAR pathway and its downstream lipid mediators as potential therapeutic targets warranting further investigation, and suggest that existing PPAR agonists may merit evaluation as candidate drugs for repurposing in future studies.
-
3. Exploiting virulence determinants for precision management of melioidosis: A multi-omics roadmap from pathogenesis to point-of-care : A perspective review.
3. 利用毒力决定因素实现类鼻疽的精准管理：从发病机制到即时检测的多组学路线图：一篇视角综述PMID:日期:2026-09-27Melioidosis, caused by , remains challenging to diagnose promptly, partly due to limited use of virulence factors as diagnostic targets. Most existing biomarkers fail to capture the dynamic expression of bacterial virulence factors during active infection. In vivo‑upregulated virulence determinants, such as Hcp1, POMCR/PPEP, and GroEL, are intrinsically superior diagnostic targets. Hcp1 is a paradigm: it is the most advanced virulence factor translated into a point‑of‑care test, with prospective validation in endemic settings. Mechanistic understanding of virulence regulation transforms empirical antigen hunting into rational target selection. We propose a virulence‑driven pipeline that converted Hcp1 into a point‑of‑care immunochromatography test (sensitivity 88.3%, specificity 86.1-100%) with prospective validation. Finally, multi‑omics data integration with explainable machine learning can prioritize virulence factor combinations for multiplex diagnostics. This framework addresses the need for rapid melioidosis diagnostics and provides a replicable template for other infectious diseases caused by intracellular pathogens.
-
4. Comparative pathogenicity study of monkeypox virus Clade Ib and Clade IIb in a rabbit model.
4. 猴痘病毒Ib分支和IIb分支在兔模型中的比较致病性研究PMID:日期:2026-09-23Mpox has emerged as a significant public health concern, spreading across continents with the emergence of new variants. Clade IIb, from the recent global outbreak, and the newly identified Clade Ib have shown changes in transmission dynamics and possibly in severity. We developed a New Zealand White rabbit model of Mpox by using a combination of intradermal and intravenous routes of administration. Following infection, the rabbits developed erythematous papular lesions on the skin, which progressed to crust and scab formation by the second week, ultimately leading to healing and seroconversion. Infection with the Clade Ib and IIb.A.2.1 lineages revealed that both Monkeypox virus (MPXV) variants caused skin and testicular lesions, as well as viral excretion from the nasal cavity, skin, and testicular tissue. However, there were no significant differences in disease severity between the two variants. These findings suggest that this rabbit model could be useful for evaluating countermeasures against MPXV.
-
5. {"_":"Interaction of polystyrene nanoplastics and modulates gastric cancer cellular functions and metastasis.","i":["Helicobacter pylori"]}
5. 聚苯乙烯纳米塑料与幽门螺杆菌的相互作用调节胃癌细胞功能和转移PMID:日期:2026-09-21Polystyrene nanoplastics (PS-NPs) accumulate in human digestive tissues. They pose health risks as a new pollutant. Chronic infection is the primary risk factor for gastric cancer (GC). This study tested whether PS-NPs and internalize GC cells and their separate or combined exposure on cell proliferation, apoptosis, autophagy, and metastasis. PS-NPs were co-cultured with . A liver metastasis model was established by exposing the GC cell line HGC-27 to PS-NPs alone or to PS-NPs + , which were then injected into nude mice. Scanning electron microscopy (SEM) demonstrated PS-NPs' adhesion to surface. A 100 μg/mL PS-NPs, for 24 h, inhibited bacterial growth and raised reactive oxygen species (ROS) levels inside bacteria. When HGC-27 cells were co-exposed to PS-NPs + , they internalized both agents. This co-exposure elicited a synergistic cytotoxic response, reduced cell viability and proliferation, increased apoptosis, reduced mitochondrial membrane potential, and enhanced autophagosome formation. Exposure to both agents in vivo differed from that observed in vitro. PS-NPs alone promoted liver and lung metastasis and aggravated hepatic lesions, whereas co-exposure showed mixed, context-dependent effects. These findings indicate that PS-NPs associate with in invading gastric cancer cells, thereby modulating multiple carcinogenesis processes. Integrating and models when assessing the potential long-term health risks of PS-NPs in the gastrointestinal environment is inevitable.
-
6. {"_":" and related gut microbiome species modulate biofilm formation through the production of bioactive small molecules.","i":["Enterocloster citroniae","Vibrio cholerae"]}
PMID:日期:2026-09-16Cholera is a diarrheal disease that affects millions of people globally. Although the causative agent, , has been extensively studied in isolation, investigation of its interactions with the gut microbiota started relatively recently. We and others previously showed that microbiota-derived metabolites significantly influence behavior. By investigating how an organic extract of human feces affects gene expression, we showed that gut metabolites strongly suppress swimming motility, a trait important for host colonization. Interestingly, extracts of pure cultures of a gut commensal, , recapitulated this inhibition. Here, we present a comprehensive examination of the effect of small molecules produced by and related species on behavior. We show that small molecules inhibit motility by various strains, and that several phylogenetically related species produce this activity, although the magnitude of the effect varies between strains. Using biofilm formation assays in static and flow conditions, we show that strongly induces biofilm formation in response to metabolites. Transcriptome and reporter analyses showed that several genes involved in the synthesis of an extracellular polysaccharide are induced by metabolites. Finally, we show that interactions with host cells are also modulated by this commensal. These findings advance our understanding of microbiome-pathogen interactions and how commensal bacteria influence virulence through the production of small molecules. In the future, this knowledge may be used to design novel microbiome-based therapeutic approaches to combat cholera and other infections.
-
7. {"_":" culture supernatant impairs alveolar macrophage function and promotes persistence.","i":["Prevotella intermedia","Mycobacterium avium"]}
7. 培养上清液损害肺泡巨噬细胞功能并促进持续存在PMID:日期:2026-09-15Microbiome analyses using 16S ribosomal RNA gene sequencing have revealed a higher prevalence of species in patients with nontuberculous mycobacterial pulmonary disease (NTM-PD) than in those with non-NTM-PD bronchiectasis. culture supernatant (.) has been reported to exacerbate pneumonia, but its effect on infection remains unclear. Thus, we manipulated bone marrow cells to differentiate into alveolar macrophage-like cells (AMLCs), infected them with in the presence of . sup. or control medium, and analyzed their phagocytic and bactericidal activities. Intracellular bacteria were quantified, and antimicrobial gene expression was assessed using real-time reverse transcription PCR and bulk RNA sequencing. In vivo, female C57BL/6J mice (7-8 weeks old) were oropharyngeally inoculated with with or without . sup. . sup. impaired intracellular killing of in AMLCs. RNA sequencing revealed downregulation of autophagy, type I interferon, and anti-mycobacterial genes in the . sup.-treated group. Furthermore, flow cytometry analysis revealed that . sup. increases levels of microtubule-associated protein 1 light chain 3 and may inhibit lysosome maturation. In mice, . sup. increased the pulmonary load and suppressed type I and II interferon expression in the lungs. In this experimental mouse model of NTM-PD, . sup. increased pulmonary burden, while in mouse derived AMLCs sup. was associated with impaired autophagy‑related and interferon responses and reduced antimicrobial gene expression, supporting a potential role for in NTM-PD progression.
-
8. Rethinking the immune recognition of cell walls in human fungal pathogens: Mechanisms, controversies and translational significance.
8. 重新审视人类真菌病原体细胞壁的免疫识别：机制、争议及转化意义PMID:日期:2026-09-14Fungal cell wall polysaccharides - such as β-glucans, chitin, and mannans - are key immunogenic structures recognized by Toll-like receptors and C-type lectin receptors on innate immune cells, initiating phagocytosis, cytokine production, and antigen presentation, and shaping downstream adaptive immunity. CD4 T cells differentiate into Th1, Th2, Th17, and Treg subsets to maintain immune balance, whereas B cells contribute to fungal clearance and memory through species-specific antibodies. The boundary between protective and pathogenic immunity varies with fungal species, infection stage, and host immune status, collectively influencing PRR signaling and lymphocyte effector outcomes. This review summarizes recognition mechanisms, signaling pathways, and immunoregulatory roles of immune cells in response to fungal cell wall polysaccharides, highlighting the dual roles of innate and adaptive immunity in antifungal defense and immunopathology, and discussing current controversies, knowledge gaps, and prospects for immunomodulatory and vaccine-based antifungal strategies.
-
9. {"_":"Endogenous RNA virus-derived elements exhibit functional divergence in modulating development and virus susceptibility in .","i":["Bombyx mori"]}
9. {"_":"内源性RNA病毒衍生元件在调控家蚕发育和病毒易感性方面表现出功能分化。","i":["家蚕"]}PMID:日期:2026-09-14Non-retroviral endogenous viral elements (nrEVEs) are increasingly recognized as potential regulators of host biology, but their functional roles in Lepidoptera remain largely unexplored. Here, we identified seven nrEVEs derived from four RNA virus families in . All seven nrEVEs were transcriptionally active and exhibited distinct developmental and tissue-specific expression patterns. Their small-RNA profiling revealed that these elements could generate small interfering RNA (siRNA)-like RNAs, primary PIWI-interacting RNA (piRNA)-like RNAs, or ping-pong-associated piRNAs. Functional analyses of the derived BmToEVE and the -derived BmChuEVE3 revealed markedly divergent physiological roles. Depletion of either nrEVE delayed larval development and reduced body weight, while differentially affecting reproductive and cocoon traits. Yeast two-hybrid screening and transcriptomic analyses further implicated both nrEVEs with cuticle-associated and reproductive processes. Importantly, BmChuEVE3 knockdown broadly suppressed metabolic and immune responses, accompanied by increased (BmNPV) and (BmCPV). By contrast, BmToEVE silencing markedly reduced BmNPV accumulation and enhanced host defense-related transcriptional responses. Its effect on BmCPV was comparatively modest and emerged only at the later infection stage. Overall, our findings reveal functional diversification of silkworm nrEVEs and highlight the contribution of virus-derived sequences to developmental regulation and antiviral physiology in a lepidopteran host.
-
10. {"_":"Phenotypic heterogeneity and genetic mechanisms of phage resistance in hypervirulent carbapenem-resistant .","i":["Klebsiella pneumoniae"]}
10. {"_":"高毒力碳青霉烯耐药肺炎克雷伯菌的噬菌体抗性表型异质性及遗传机制。","i":["肺炎克雷伯菌"]}PMID:日期:2026-09-13Phage resistance represents a major obstacle to the clinical application of phage therapy for multidrug-resistant bacterial pathogens. A comprehensive understanding of the phenotypic heterogeneity and molecular mechanisms underlying phage resistance is critical for deciphering bacterium-phage interactions and optimizing therapeutic strategies. In this study, we identified four distinct resistance phenotypes in K2-serotype hypervirulent carbapenem-resistant (CR-hvKP) under the selective pressure of phage Kpph1. These resistant strains exhibited either complete or partial resistance, variable fitness costs, and diverse genetic mutations, suggesting multifaceted resistance strategies, including receptor masking, growth inhibition, and community-level resistance. Among these, mutations were identified as the predominant resistance mechanism, arising from base insertions and integrations of mobile genetic elements, which serve as an efficient pre-adaptive strategy enabling CR-hvKP to evade phage infection. To circumvent this resistance, we isolated a secondary phage, K2V3, which specifically targets -mutant strains. The rationally designed phage cocktail comprising Kpph1 and K2V3 effectively suppressed all resistant variants and prevented the emergence of further resistance. Collectively, these findings deepen the understanding of phage-bacteria interaction dynamics and provide a crucial theoretical foundation for optimizing clinical phage therapy against multidrug-resistant pathogens.