Virulence[JOURNAL]
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200 papers
-derived extracellular vesicles promote herpes simplex virus infection in oral epithelia.
Kim TL, Oh SY, Lee KY … +7 more , Lee HJ, Kwon TG, Kim JW, Shin CG, Jang S, Hong SH, Choi SY
Virulence · 2026 Dec · PMID 41379645 · Full text
The oral cavity contains the second most diverse bacterial community after the intestines, with bacteria and viruses coexist. is a major pathogenic bacterium in the oral cavity, commonly associated with dental caries. W...
The oral cavity contains the second most diverse bacterial community after the intestines, with bacteria and viruses coexist. is a major pathogenic bacterium in the oral cavity, commonly associated with dental caries. We investigated the effects of derived extracellular vesicles (Sm EVs) on herpes simplex virus 1 (HSV-1) infection, which is prevalent in the oral cavity. We performed our experiments in human oral keratinocyte (HOK) cells and mucosal tissue-derived organoids, and analyzed human whole saliva ( = 50) for associations between and HSV-1 envelope glycoprotein D (gD) mRNA levels by qPCR. Sm EVs significantly enhanced HSV-1 production in mucosal organoids. Indeed, mRNA and/or protein levels of type I (IFN-α and IFN-β), type II (IFN-γ), and type III (IFN-λ, IFN-λ, and IFN-λ) interferons were significantly lower in Sm EV-treated mucosal organoids compared with the vehicle control under mock-infection. When HSV-1 was introduced after Sm EV pretreatment, these IFN levels showed a general trend of statistically significant reduction compared with those in the vehicle control. Moreover, Sm EVs suppressed IFN mRNA and protein levels by upregulating the EGFR - ERK pathway in mucosal cells, creating an environment that enhances HSV-1 production. Interestingly, a positive correlation was noted between and HSV-1 detected in human whole saliva samples. These results suggest that can negatively modulate the host innate antiviral responses by secreting EVs, thereby enhancing viral production. This study might provide a new perspective for controlling viral infections in humans.
Correction.
Virulence · 2026 Dec · PMID 41379098 · Full text
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Roles and mechanisms of and -encoded proteins in adhesion to and invasion of intestinal cells and neonatal rats.
Zhao C, Li P, Zhu D … +5 more , Xiao Z, Jiao J, Li Y, Du X, Wang S
Virulence · 2025 Dec · PMID 41378975 · Full text
() is a foodborne pathogen whose initial process involves intestinal cell adhesion mediated by numerous virulence factors encoded in various genes. The key metabolic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPD...
() is a foodborne pathogen whose initial process involves intestinal cell adhesion mediated by numerous virulence factors encoded in various genes. The key metabolic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH, also known as GapA), is encoded by in the glycolysis pathway and acts as an adhesin in some bacteria. In , there is also a key enzyme in the gluconeogenesis pathway, Gap, with type I GAPDH and erythrose-4-phosphate dehydrogenase activities and encoded by . This study aimed to investigate the virulence properties of GapA and Gap of in adhesion to and invasion of HCT-8 and HIEC-6 cells and damage to the colon and brain of neonatal rats, by gene silencing. In addition, the role of both recombinant proteins in intestinal cell adhesion and invasion was investigated, and their role in inducting inflammatory cytokine expression was assessed by ELISA and Western blot. Silencing or decreased the viability and swimming motility of bacterial cells and reduced bacterial adhesion to and invasion of both types of intestinal cells. Both recombinant proteins contributed to adhesion in both cells, enhanced protein phosphorylation of NF-κB, and induced inflammatory cytokine expression. Finally, silenced expression of GapA and Gap also weakened bacterial damage to the brain and colon of neonatal rats. In conclusion, we demonstrated for the first time the virulence properties of GapA and Gap in adhesion to and invasion of intestinal cells and neonatal rats and induction of inflammatory responses.
7653 R regulates the endophytic bacterial communities and disease resistance pathways to promote clubroot resistance in .
Li C, Zhang Z, Rao F … +8 more , Xu Z, Cheng J, Xie J, Lin Y, Hsiang T, Fu Y, Jiang D, Chen T
Virulence · 2025 Dec · PMID 41378974 · Full text
Clubroot is a global soilborne disease caused by that severely affects cruciferous crops. Currently, there are no effective control measures to completely eliminate pathogens in the field. Pot experiments have shown tha...
Clubroot is a global soilborne disease caused by that severely affects cruciferous crops. Currently, there are no effective control measures to completely eliminate pathogens in the field. Pot experiments have shown that treatment with 7653 R can relieve clubroot symptoms. However, whether 7653 R can be used in the field to control clubroot disease is unclear, and the mechanism of its resistance remains largely unknown. We conducted two seasons of field trials with and found that 7653 R treatment significantly reduced clubroot disease severity, and that the agronomic traits at the seedling, flowering, and harvesting stages were significantly improved compared to the control group. The average yield per hectare, thousand grain weight, and oil content increased by 83.1%, 10.4%, and 3.7%, respectively. 7653 R also enhanced the resistance and yield of the cruciferous plant var. to clubroot. We characterized the composition and structure of the endophytic microbiota using bacterial 16S sequencing, and showed that treatment with 7653 R shaped the structure of endophytic bacterial communities. The relative abundances of Actinobacteria and Bacteroidetes, which are resistant to oxidative stress, were enriched in the co-inoculation with 7653 R and on . Transcriptome data indicated that genes related to plant immunity, nitrogen uptake and metabolism were significantly up-regulated by co-inoculation with 7653 R and . Our findings provide a theoretical basis for the widespread application of 7653 R in clubroot biocontrol.
Tanshinone I as a novel therapeutic agent targeting von Willebrand factor-binding protein to mitigate pathogenicity.
Zhou S, Zou H, Xu Y … +7 more , Guo D, Su Z, Wang L, Wang B, Zhao Y, Leng X, Wang Y
Virulence · 2025 Dec · PMID 41378973 · Full text
() is a prevalent pathogen responsible for a wide range of diseases in humans, contributing to both hospital-acquired and community-acquired infections. The von Willebrand factor-binding protein (vWbp) is pivotal for pa...
() is a prevalent pathogen responsible for a wide range of diseases in humans, contributing to both hospital-acquired and community-acquired infections. The von Willebrand factor-binding protein (vWbp) is pivotal for pathogenicity because it induces blood coagulation, thereby facilitating bacterial survival and dissemination within the host. Notably, the absence of vWbp does not hinder growth, indicating that vWbp is an attractive target for combating infections while mitigating the risk of antibiotic resistance. Our findings revealed that tanshinone I significantly inhibited vWbp-induced coagulation without affecting the proliferation of . Hemolysis assays confirmed the biocompatibility of tanshinone I, while Western blot analysis, fluorescence quenching, and thermal shift assays (TSAs) demonstrated that tanshinone I does not alter vWbp expression but directly binds to the protein. Molecular docking studies elucidated the interaction mechanism, identifying ARG-479 and GLN-484 as critical residues for tanshinone I binding. Furthermore, studies demonstrated that tanshinone I reduces lung tissue damage in mice infected with , thereby increasing survival rates. Additionally, tanshinone I was tested in greater wax moth larvae and showed similar protective effects. In conclusion, tanshinone I effectively inhibits vWbp, reducing the virulence of . This study underscores the potential of tanshinone I as a therapeutic agent against infections, offering a novel strategy to combat bacterial infections while decreasing the critical issue of antibiotic resistance.
Amyloid fibrils of the Als5p-derived peptide NH-SNGIVIVATTRTV-COOH influence the biofilm formation of by shape-edging microcolony morphology.
Gruber D, Walter JC, Bolotnikov G … +19 more , Miegel B, Bierla E, Bellmann A, Einsiedler CS, Eiblmayr AT, Maser M, Obert D, Sun ELMQ, Schnaubelt J, Söylemezgiller S, Widy BA, Spellerberg B, Stenger S, Rodríguez-Alfonso A, Preising N, Ständker L, Firacative C, Kissmann AK, Rosenau F
Virulence · 2025 Dec · PMID 41371612 · Full text
species are major contributors to nosocomial infections, with biofilm formation being a critical virulence factor that enables persistence in clinical settings and resistance to antifungal therapies. Central to biofilm d...
species are major contributors to nosocomial infections, with biofilm formation being a critical virulence factor that enables persistence in clinical settings and resistance to antifungal therapies. Central to biofilm development is the adhesion of fungal cells, a process mediated by surface proteins such as Als5p in . The amyloid-forming peptide sequence within Als5p (SNGIVIVATTRTV) has been implicated in mediating adhesion and biofilm formation; however, its role in shaping the biofilm architecture has not been fully elucidated. In this study, we demonstrated that the addition of Als5pFP promoted biomass accumulation in biofilms under laboratory conditions, including complex media and at temperatures compatible with clinical biofilm assays. Using advanced image analysis of microscopy images, we show that the Als5p peptide induces a distinct morphological effect on biofilms: a shape-edging of microcolony structures, characterized by the concentration of fungal cells into denser aggregates and the reduction of cells in intermediate spaces. These observations suggest a potential role of amyloid-like fibrils formed by the Als5p peptide in influencing the spatial organization of biofilms. This discovery presents a novel aspect on how these fibrils affect the biofilm architecture extending beyond previous studies, which primarily focused on biomass accumulation. Our findings contribute to the understanding of the architectural development of biofilms and provide a foundation for future research aimed at targeting the amyloid structures within fungal biofilms. Furthermore, the results may support the design of biofilm-targeting antifungal agents and development of biosensors for monitoring amyloid formation during infection.
Metabolic flux analysis revealed key roles of ArcB in ADI pathway and IlvC in BCAA biosynthesis during anaerobic growth and infection.
Tang H, Zhang Q, Yang J … +10 more , Ruan Y, Zhang X, Pang S, Qiao Z, Huang J, Langford PR, Zhou R, Zhang H, Zhang Q, Li L
Virulence · 2026 Dec · PMID 41369137 · Full text
Critical metabolic enzymes and pathways specific to bacterial adaptation in different host microenvironments directly contribute to bacterial pathogenicity. In this study, a virulent strain of the important zoonotic path...
Critical metabolic enzymes and pathways specific to bacterial adaptation in different host microenvironments directly contribute to bacterial pathogenicity. In this study, a virulent strain of the important zoonotic pathogen was found to show enhanced growth under anaerobic conditions compared to aerobic conditions. Transcriptomic analysis found a significant suppression of many central metabolic genes during anaerobic growth of . The transcriptomic data were used to reconstruct a genome-scale metabolic network to assess the distribution of metabolic fluxes in under different conditions. Significant activation of the arginine deiminase (ADI) and branched-chain amino acid (BCAA) biosynthesis pathways was identified. Gene deletion mutants of and participating in these two pathways, respectively, were constructed. Compared to the wild-type strain, the Δ mutant showed more significant growth deficiency under anaerobic conditions than under aerobic conditions. Accumulation of ATP and NH, the metabolites of the ADI pathway, was significantly higher when was cultured under anaerobic conditions, and this effect was attenuated in the Δ mutant. The knockout of IlvC of the BCAA pathway disrupted the normal growth of in valine- and isoleucine-limited medium under anaerobic conditions. Both Δ and Δ showed attenuation in mice with decreased lethality, bacterial loads in tissues, and cytokine levels in serum, with the hypoxia-induced gene up-regulated in tissues. Therefore, ADI and BCAA pathways are critical for survival in response to hypoxia and infection , with ArcB and IlvC being promising drug targets.
DDX17 and viral infection.
Cheng Y, Wang R, Wang A … +5 more , Wu Z, Jia W, Lu H, Wu Q, Zhu S
Virulence · 2026 Dec · PMID 41367298 · Full text
DDX17 (DEAD-box RNA helicase 17) is an essential RNA helicase and regulatory ATPase in host cells, extensively involved in various cellular processes during viral infections, such as RNA splicing, transcriptional regulat...
DDX17 (DEAD-box RNA helicase 17) is an essential RNA helicase and regulatory ATPase in host cells, extensively involved in various cellular processes during viral infections, such as RNA splicing, transcriptional regulation, and post-transcriptional modification. DDX17 exhibits dual functionality in viral infections: it enhances the stability, packaging, and replication of viral RNA through interactions with viral ribonucleoprotein complexes, as evidenced in infections caused by influenza viruses and Hantaan virus (HTNV). Conversely, DDX17 can inhibit viral proliferation by disrupting viral RNA metabolism, as observed in hepatitis B virus (HBV) and Epstein-Barr virus (EBV) infections, where it suppresses replication by modulating viral RNA decapping and degradation. The dual role of DDX17 provides novel insights into host-virus interactions while also highlighting its significant potential as an antiviral therapeutic target. These findings are expected to establish a theoretical foundation for related research and offer valuable references for developing novel antiviral strategies.
The regulation of AsfR on tmRNA expression mediates bacterial motility and virulence in .
Chang H, Tong Y, Gao S … +8 more , Jiang X, Ma X, Li H, Tang Y, Li J, Tang H, Lin M, Liu Z
Virulence · 2026 Dec · PMID 41367294 · Full text
Transfer messenger RNA (tmRNA), a key component of the trans-translation system, plays an essential role on the virulence of pathogenic bacteria. However, the upstream regulatory mechanisms that regulate tmRNA expression...
Transfer messenger RNA (tmRNA), a key component of the trans-translation system, plays an essential role on the virulence of pathogenic bacteria. However, the upstream regulatory mechanisms that regulate tmRNA expression remain largely unexplored. In this study, AraC superfamily regulator (AsfR) was found to directly interact with the promoter of gene, which encodes tmRNA. Co-transformation of the reporter construct, consisting of tmRNA promoter fused to enhanced green fluorescent protein (eGFP), alongside an AsfR expression vector, resulted in increased fluorescence, indicating that AsfR positively regulates mRNA expression. Consistently, the transcription level of tmRNA was significantly decreased in Δ compared with WT of by quantitative real-time PCR (RT-qPCR) analyses. The Δ and Δ mutants exhibited significantly reduced motility and biofilm formation. Reduced transcription of the flagellar gene in both mutants suggests that the AsfR/tmRNA axis may regulate these processes via . Furthermore, deletion of and tmRNA impairs oxidant resistance and pathogenicity, resulting in growth inhibition in . This study elucidates the regulatory role of the AsfR-tmRNA pathway in flagellar motility, biofilm formation, and antioxidant capacity, all of which contribute to bacterial virulence and provide potential targets for the treatment of bacterial infections.
Evolving strategies of intracellular Hypervirulent during phage therapy: Reducing host autophagy and inflammation.
Chen H, Sun Y, Huang Z … +5 more , Zhao D, Kong J, Chen H, Zhou C, Zhou T
Virulence · 2025 Dec · PMID 41346207 · Full text
Hypervirulent (hvKp) presents challenges in infection management due to antibiotic resistance associated with its intracellular persistence. This study investigates the efficacy of phage therapy against intracellular hv...
Hypervirulent (hvKp) presents challenges in infection management due to antibiotic resistance associated with its intracellular persistence. This study investigates the efficacy of phage therapy against intracellular hvKp using a two-stage murine model. We assessed changes in virulence, host survival, and immune responses through phagocytosis assays, transmission electron microscopy, and Western blotting, complemented by transcriptomic and proteomic analyses. Results indicate that phage therapy reduces mortality and modulates bacterial virulence by downregulating capsule production. Following phage exposure, hvKp adapts by enhancing its oxidative stress resistance. Crucially, these adaptations weaken host inflammatory and autophagy responses, enabling better survival within host cells. These adaptations suggest that while phage therapy can mitigate infection severity, the capacity of hvKp to modulate host pathways underscores the complexity of treating intracellular infections and highlights the importance of targeting both bacterial and cellular responses.
induced ferroptosis by inhibition of the Nrf2/xCT/GPX4 pathway in bovine mastitis: and .
Mao P, Wang Z, Yuan C … +11 more , Liu K, Guo L, Dong J, Cui L, Li J, Zhu G, Meng X, Liu H, Zhang L, Wang R, Wang H
Virulence · 2025 Dec · PMID 41343264 · Full text
(), a prominent causative agent of mastitis in dairy cattle, remains enigmatic in its pathogenic mechanisms. This study aimed to reveal the effects of on mammary glands via the induction of ferroptosis, as well as the p...
(), a prominent causative agent of mastitis in dairy cattle, remains enigmatic in its pathogenic mechanisms. This study aimed to reveal the effects of on mammary glands via the induction of ferroptosis, as well as the protective role of Ferrostatin-1 (Fer-1) against this pathogen-mediated damage in bovine mammary epithelial cells (BMECs). Holstein cows were used to establish an intramammary infection model of . , primary BMECs were treated with 10 μM Fer-1 and alone or in combination. The results showed that mammary glands infected with exhibited increased transcriptional levels of (), , , and (). Concurrently, significant elevations in iron, 4-hydroxynonenal, and reactive oxygen species (ROS) levels were observed. Conversely, infection downregulated nuclear factor erythroid 2-related factor 2 (Nrf2), cystine/glutamate antiporter (xCT), glutathione peroxidase 4 (GPX4), and glutathione levels. Following invasion, intracellular Fe and lipid ROS accumulated in the BMECs, impeding activation of Nrf2/xCT/GPX4 signal transduction. Additionally, Fer-1 facilitated the nuclear translocation of Nrf2 protein, upregulating the protein levels of Nrf2/xCT/GPX4 while downregulation transcriptional levels of , , , and . In conclusion, Fer-1 alleviates -induced inflammatory factor activation and ferroptosis in BMECs via upregulation of the Nrf2/xCT/GPX4 pathway, supporting ferroptosis inhibition holds promise as a feasible therapeutic agent for the control of mastitis.
Emergence, function, and therapeutic strategies to target the PD-1/PD-L1 immune checkpoint during pathogenic fungal infections.
Zheng X, He X, Song Z … +2 more , Chen W, Liu F
Virulence · 2025 Dec · PMID 41343262 · Full text
Human pathogenic fungi are ubiquitous in the environment and induce an expanding repertoire of devastating diseases globally. Upon fungal invasion, the fungus adopts multiple strategies to adapt to, or eliminate, hostile...
Human pathogenic fungi are ubiquitous in the environment and induce an expanding repertoire of devastating diseases globally. Upon fungal invasion, the fungus adopts multiple strategies to adapt to, or eliminate, hostile environmental conditions, which immune checkpoints serve as one of the mechanism for fungal evasion. Programmed death receptor-1 (PD-1), an immunosuppressive molecule, transmits inhibitory signals upon binding to its ligand PD-L1. During infection, aberrant activation of the PD-1/PD-L1 pathway has been proven to facilitate immune evasion by the pathogen. In this review, we summarize the roles of PD-1/PD-L1 in fungal infection. First, the molecular structures and function of PD-1 and PD-L1 are described. Then, we highlight the dynamic expression patterns and regulatory mechanisms of PD-1/PD-L1 during fungal invasion. Potential therapeutics based on PD-1/PD-L1-blocking to enhance antifungal immunity and improve clinical outcomes are also discussed. These insights reveal future directions regarding PD-1/PD-L1 and immune checkpoint-based therapies for preventing pathogenic fungi infections.
Mapping evolutionary paradigm of Oropouche virus driven by dinucleotide bias and context-dependent codon bias.
Yang X, Liu Z, Ren X … +2 more , Wang C, Zhou J
Virulence · 2025 Dec · PMID 41343261 · Full text
Arthropod-borne viruses (arboviruses) pose significant public health threats, and understanding their evolutionary mechanisms can inform molecular diagnostics and vaccine design. Oropouche virus (OROV), a relatively unde...
Arthropod-borne viruses (arboviruses) pose significant public health threats, and understanding their evolutionary mechanisms can inform molecular diagnostics and vaccine design. Oropouche virus (OROV), a relatively understudied arbovirus, exhibits unique evolutionary dynamics in nucleotide composition. We analyzed 45 OROV strains across genotypes to assess selective pressures shaping nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase (RdRp) evolution. We utilized information entropy, dinucleotide odds ratios, relative synonymous codon usage values, and context-dependent codon bias (CDCB) to elucidate the genetic characteristics associated with mono-, di-, tri-, and tetranucleotide compositions. The extent of overall nucleotide usage bias, dinucleotide bias, and synonymous codon usage bias did not correlate with genotype-specific patterns, but rather exhibited a protein function-dependent pattern across the three proteins. Although dinucleotide bias and synonymous codon usage bias varied within a relatively broad range, the dinucleotide CpG, the over- and under-represented synonymous codons, and CDCB remained strongly influenced by natural selective pressures from both the host and the viral life cycle. Furthermore, the codon usage patterns, as indicated by the effective number of codons, suggest that the OROV nucleoprotein has been subject to stronger selective pressures in its evolutionary paradigm compared to the glycoprotein and RdRp, which appear to be primarily influenced by natural selection and mutation pressure. Additionally, analysis of relative codon deoptimization index (RCDI) and tRNA adaptation index (tAI) revealed suboptimal translational efficiency of OROV coding sequences in human hosts, suggesting limited codon usage adaptation.
YTHDC2 promotes sepsis-induced cardiomyopathy by activating apoptosis and NF-κB pathway.
Wang W, Zhang TN, Wang ZM … +2 more , Yang N, Liu CF
Virulence · 2025 Dec · PMID 41342228 · Full text
Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis, especially in children, and identification of novel therapeutic targets remains essential for improving patient outcomes. Recent studies have impli...
Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis, especially in children, and identification of novel therapeutic targets remains essential for improving patient outcomes. Recent studies have implicated N6-methyladenosine (mA), an RNA epigenetic modification, in SICM pathogenesis. However, the role of YTH domain-containing 2 (YTHDC2), an mA reader protein, in SICM remains unclear. This study used lipopolysaccharide (LPS)-treated adolescent rats, primary cardiomyocytes and H9c2 cardiomyocytes to mimic SICM and . We observed a significant upregulation of YTHDC2 and . Through comprehensive analyses including RNA sequencing (RNA-seq), Western blotting, and flow cytometry, we demonstrated that YTHDC2 promotes LPS-induced cardiomyocyte apoptosis. RNA immunoprecipitation sequencing (RIP-seq) and Western blotting further showed that YTHDC2 activates the LPS-induced NF-κB pathway. Mechanistic investigations using RIP-qPCR confirmed direct binding of YTHDC2 to mRNAs encoding the pro-apoptotic proteins BAX and BAK1, as well as the NF-κB subunit p65, with subsequent regulation of NF-κB transcriptional activity. Importantly, adeno-associated virus 9 (AAV9)-mediated cardiac-specific inhibition of YTHDC2 in adolescent rats effectively attenuated LPS-induced cardiomyocyte apoptosis and NF-κB pathway activation. Collectively, our findings establish YTHDC2 as a key regulator in SICM pathogenesis, promoting cardiomyocyte apoptosis and NF-κB signaling activation. These results highlight YTHDC2 as a promising therapeutic target for SICM.
Chronic viral infections impaired the growth process of splenic B cells by upregulating Bbc3 and Atf3 in LCMV-CL13 infected mouse model.
Li Z, Yang W, Cai F … +5 more , Li D, Chen Q, Zhang Y, Cui J, Wang W
Virulence · 2025 Dec · PMID 41329555 · Full text
Chronic persistent viral infections can lead to significant spleen damage, thus disrupting the host humoral immune response; however, the underlying mechanisms remain unclear. In this study, we employed a Lymphocytic cho...
Chronic persistent viral infections can lead to significant spleen damage, thus disrupting the host humoral immune response; however, the underlying mechanisms remain unclear. In this study, we employed a Lymphocytic choriomeningitis virus (LCMV) chronic infection model to investigate the effects of virus infection on spleen damage. Mice infected with Lymphocytic choriomeningitis virus clone 13 (LCMV-CL13) presented a series of pathological features, such as white pulp atrophy and reduced germinal center diameter, length, and area in the spleen. More importantly, we observed a diminished GC response alongside a weak antibody response in the chronic infection model. Single-cell RNA sequencing (scRNA-seq) further revealed the dysregulation of gene expression, including , , and , which inhibit B-cell differentiation during chronic viral infection. We verify that the upregulation of or , respectively, can promote apoptosis in BaF3 cells. Immune repertoire (IR) analysis revealed that the molecular diversity of the BCR repertoire after LCMV-CL13 infection, specifically manifested in BCR clonal diversity, gene segment usage preference, and CDR3 sequence changes. In conclusion, this study demonstrated that chronic LCMV-CL13 infection interrupted the development of splenic B cells by increasing the expression of apoptosis genes, thus enhancing our understanding of the underlying mechanisms of B-cell development interruption during chronic viral infection.
Genome-scale CRISPR screen identifies host factors associated with bovine parainfluenza virus 3 infection.
Geng Y, Jiang C, Zhang H … +9 more , Yang H, Peng Y, Chen Y, Hu C, Liu H, Li S, Chen H, Xie S, Guo A
Virulence · 2025 Dec · PMID 41328592 · Full text
Bovine parainfluenza virus type 3 (BPIV-3) is a major pathogen associated with the bovine respiratory disease complex. However, the limited understanding of host factors crucial for BPIV-3 replication has hindered the de...
Bovine parainfluenza virus type 3 (BPIV-3) is a major pathogen associated with the bovine respiratory disease complex. However, the limited understanding of host factors crucial for BPIV-3 replication has hindered the development of effective preventive and therapeutic strategies. To tackle this critical issue, we constructed a bovine genome-wide CRISPR/Cas9 knockout library in Madin-Darby bovine kidney cells, which was then used to systematically identify and characterize the host genes essential for BPIV-3a replication. Subsequently, 10 genes were validated using both RT-qPCR and viral titration assays. Furthermore, through gene knockout or knockdown and rescue experiments, we identified three key genes required for BPIV-3a replication: Wnt family member 5A (WNT5A), solute carrier family 16 member 13 (SLC16A13), and selenoprotein N (SELENON). However, their effects on viral adhesion and internalization varied. WNT5A was involved in both processes, SLC16A13 participated solely in internalization, while SELENON had no significant impact on either. Beyond BPIV-3a, these three genes were also found to be essential for the infection of BPIV-3c and Bovine enterovirus. In conclusion, this study offers novel insights into the molecular mechanisms governing the replication and pathogenesis of BPIV-3a, BPIV-3c, and bovine enterovirus within host cells, thereby providing a foundation for identifying potential targets in the development of novel antiviral strategies.
The virulence function of RXLR effector of is coupled with its cell death-inducing activity.
Huang G, Hu Y, Lu N … +2 more , Meng Y, Shan W
Virulence · 2025 Dec · PMID 41321044 · Full text
RXLR effectors secreted by pathogens are important virulence factors in suppressing plant immunity and facilitating pathogen infection. In addition to possessing a variety of functions, some RXLR effectors have been fou...
RXLR effectors secreted by pathogens are important virulence factors in suppressing plant immunity and facilitating pathogen infection. In addition to possessing a variety of functions, some RXLR effectors have been found to trigger host cell death with different underlying mechanisms. was previously reported as a virulent RXLR effector secreted by and triggers cell death in various plants. However, it is uncertain whether this type of cell death promotes or restricts the colonization of this hemibiotrophic pathogen. Here, we explored the correlation between the cell death activity of and its contribution to the infection of . Sequencing data revealed that exhibited both point mutations and presence/absence polymorphisms in the population under positive selection. , one of four alleles, lost its cell death-inducing ability, also lost its ability to increase plant susceptibility to pathogen infection. Furthermore, could compromise the cell death-inducing and virulence functions of the other three alleles. truncated mutants deficient in cell death-inducing activity showed abolished ability to increase plant susceptibility. Finally, was unable to increase the susceptibility of TRV- plants, which showed abolished cell death. Taken together, the cell death-inducing activity of is essential for its virulence function during colonization of hemibiotrophic pathogen, suggesting that exploits the cell death triggered by to facilitate the transition from biotrophy to necrotrophy. These findings provide a new perspective for understanding the role of RXLR effectors triggered cell death in the pathogenesis of hemibiotrophic pathogens.
Fluorescence-based biosensors for West Nile virus detection.
Blázquez AB, Saiz JC, Herrero L … +5 more , Sánchez-Céspedes J, Vázquez A, Cisneros JM, Martin-Acebes MA, Jiménez de Oya N
Virulence · 2025 Dec · PMID 41319272 · Full text
Flaviviruses are emerging pathogens, mostly transmitted by arthropod vectors, responsible for human, animal, and zoonotic diseases. The emergence of flaviviruses has been favored in recent decades by factors related to c...
Flaviviruses are emerging pathogens, mostly transmitted by arthropod vectors, responsible for human, animal, and zoonotic diseases. The emergence of flaviviruses has been favored in recent decades by factors related to climate change and globalization, which contribute to the arrival and establishment of their vectors in new geographic areas, thus promoting epidemic outbreaks and facilitating these viruses to become endemic in these areas. This is the case of the West Nile virus (WNV) in Europe, which affects its natural bird host populations and also accidental hosts such as humans and horses. Flaviviruses are antigenically related, which induces cross-reactivity, making their serological diagnosis difficult, especially in areas where several flaviviruses co-circulate. Here, we have developed WNV biosensors in which the enzymatic activity of the viral protease, expressed during infection, allows its detection using fluorescence-based techniques. These biosensors carry WNV-specific protease cleavage sites and show high specificity for the detection of both lineages 1 and 2, with limits of detection (LODs) ranging from 0.001-0.0001 MOI at 48 hours post-infection (h.p.i.). These LODs are even lower at 72 h.p.i. reaching as low as an MOI of 2.5 × 10. They are also capable of detecting, although with lower sensitivity, other flaviviruses such as dengue, Zika, and Usutu viruses, without showing reactivity against unrelated viruses. These biosensors have been validated in viral neutralization assays with sera from infected mice and humans, as well as in antiviral screening, with results comparable to those of currently used systems, showing significant potential as clinical and laboratory tools.
Pathogenicity and virulence of .
Zhang Y, Jiang P, Yin J … +1 more , Zhu G
Virulence · 2025 Dec · PMID 41319271 · Full text
is a genus of apicomplexan parasites that causes diarrheal disease in humans and animals worldwide. The primary species affecting humans are and , while other species may also infect humans, specially immunocompromised...
is a genus of apicomplexan parasites that causes diarrheal disease in humans and animals worldwide. The primary species affecting humans are and , while other species may also infect humans, specially immunocompromised individuals. Infections are particularly severe in people with weakened immune systems and malnourished children in developing countries. In livestock, especially young ruminants, leads to significant economic losses. The parasite occupies a unique epicellular niche and undergoes a complex life cycle involving both asexual and sexual stages. While the mechanisms of parasite invasion, replication, immune evasion, and tissue damage have been challenging to unravel due to earlier technical limitations and lack of genetic tools, recent advances have transformed our understanding. Innovations in genomics, transcriptomics, and molecular genetics have identified key virulence factors and clarified intricate host-parasite interactions. The parasite's secretory organelles (micronemes, rhoptries, dense granules, and small granules) play central roles by releasing molecules that facilitate host cell attachment, invasion, and modulation of host defenses. This review provides an up-to-date overview of the biology and pathogenic mechanisms of , highlighting structural features, invasion strategies, and host immune responses. It also covers recent progress in experimental models, vaccine development, and identification of new molecular targets for treatment and prevention. By synthesizing recent discoveries with previous research, this review offers a current perspective linking fundamental biology to disease outcomes and potential control strategies.
Negative regulation of reassortant canine influenza virus replication and key site identification in porcine and ferret bronchial epithelial cell lines.
Guo J, Jung B, Yoon SW … +11 more , Liu Y, Feng Z, Yeom M, Na W, Xu Q, Lim JW, Pang M, Hao F, Chen R, Song D, Xie X
Virulence · 2025 Dec · PMID 41307451 · Full text
The segmented nature and high mutability of the influenza virus RNA genome facilitate rapid mutation and reassortment, allowing the virus to breach host barriers and migrate between different species, potentially leading...
The segmented nature and high mutability of the influenza virus RNA genome facilitate rapid mutation and reassortment, allowing the virus to breach host barriers and migrate between different species, potentially leading to unpredictable influenza outbreaks. With dogs emerging as new natural hosts for influenza virus, vigilant surveillance and scientific prevention strategies are imperative. Here, based on our previous isolation of 21 strains, which are reassortments of the canine influenza virus (CIV) H3N2 (KR/07) with gene segments from the influenza A pandemic (H1N1) 2009 virus strain (CA/09), the replication kinetics of these reassortants in immortalized mammalian respiratory epithelial cell lines from swine and ferret named hTERT-PBECs and hTERT-FBECs, alongside induced changes in cytokine expression, were investigated. Reverse genetics was utilized to generate the reassortment H3N2 canine influenza rKR/07-PB2/NP, which contains the PB2 and NP segments from CA/09. The viral titer of rKR/07-PB2/NP was significantly lower than those of the parental viruses KR/07 and CA/09. In addition, rKR/07-PB2/NP notably decreased expression levels of interleukin-1β (IL-1β) and interleukin-10 (IL-10) in both immortal cells, particularly in hTERT-PBECs. Our findings not only contribute to the understanding and exploring cross-species transmission mechanisms of influenza virus, but also provide new ideas for prevention and treatment of CIV.
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