Virulence[JOURNAL]
Sun
200 papers
Glutamate dehydrogenase 2 is required for virulence by facilitating fungal growth in the host hemocoel.
Lu Y, Wu D, Hu J … +6 more , Peng G, Zhong J, Liu Y, Li J, Gao Q, Yu XQ
Virulence · 2025 Dec · PMID 41298293 · Full text
, a fungal pathogen employed in pest biocontrol, can alkalize the surrounding environment, although the biological implications remain unclear. Here, we found that glutamate dehydrogenase 2 () was responsible for alkali...
, a fungal pathogen employed in pest biocontrol, can alkalize the surrounding environment, although the biological implications remain unclear. Here, we found that glutamate dehydrogenase 2 () was responsible for alkalization during fungal growth on insect wings or media containing cuticle powder. Loss of function resulted in significantly reduced virulence during both cuticle-passing and cuticle-bypassing infections but did not affect appressorium formation or cuticle penetration. Deletion of failed to alkalize amino acid-containing media under carbon deprivation, leading to impaired mycelia growth and conidiation. Hemolymph carbohydrates were decreased during infection, and the Δ mutant exhibited delayed fungal growth and impaired alkalization in hemolymph cultures. Notably, expression of , a pH-responsive transcription factor critical for virulence, was downregulated in hyphal bodies of the Δ mutant. Contrary to the established models in plant and human fungal pathogens, we demonstrate that Gdh2 activity is dispensable for appressorium formation but essential for fungal colonization in insect hemocoel during infection.
Colonization of the central nervous system as a key factor in the pathogenicity.
Cota Freitas GJ, Gouveia-Eufrasio L, Emidio ECP … +2 more , Aguiar Peres NT, Santos DA
Virulence · 2025 Dec · PMID 41284468 · Full text
The species complex is one of the main etiological agents of cryptococcosis, a fungal infection that affects the lungs and progresses to meningoencephalitis. Neurological infections caused by this species are associated...
The species complex is one of the main etiological agents of cryptococcosis, a fungal infection that affects the lungs and progresses to meningoencephalitis. Neurological infections caused by this species are associated with a higher incidence of cryptococcoma, sequelae, and relapse. Despite its clinical relevance, the mechanisms that sustain the infection and persistence of in the central nervous system (CNS) are still poorly understood. In this study, we performed a comprehensive phenotypic characterization of the virulence of five strains, focusing on the CNS infectious biology. Significant differences in virulence among the strains were found, highlighting intracellular survival within macrophages and growth in the CNS as determining factors of disease severity. The relative capsule size between 1-2, as opposed to a marked increase (> 2), was associated with increased virulence, a phenomenon we term optimized capsule enlargement. Considering the high energetic cost of capsule synthesis, this pattern favors the fungal reproductive fitness and replication within the host's tissues. These findings indicate that, in addition to the ability to reach the CNS, needs to colonize it efficiently to cause severe clinical manifestations, with optimized capsule enlargement being a key factor for its survival in this microenvironment.
Characterization of the pathogenicity and mechanisms underlying the pathogenesis of , a potential bacterial pathogen.
Tao Y, Zhang S, Qi K … +8 more , Luo W, Zhang S, Yang J, Jin D, Lu S, Huang Y, Zheng H, Xu J
Virulence · 2025 Dec · PMID 41274864 · Full text
is a Gram-negative bacterium isolated from the feces of bats, and there is a scarcity of information regarding its genomic and pathogenicity characteristics. This study systematically evaluated the pathogenic potential o...
is a Gram-negative bacterium isolated from the feces of bats, and there is a scarcity of information regarding its genomic and pathogenicity characteristics. This study systematically evaluated the pathogenic potential of . by comparing the survival rates, bacterial loads in the peripheral blood and organs, histopathological lesions, and the production of proinflammatory cytokines in C57BL/6 mice infected with strains HY037 and HY041 of . . The findings revealed that mice infected with . had low survival rates, with significant differences between the HY041 and HY037 strains. The mice infected with HY041 exhibited more severe pulmonary histopathological damage and higher levels of proinflammatory cytokines compared to those infected with HY037. These results demonstrated that . is lethal in mice, causing significant pulmonary histopathological damage accompanied by the dysregulated secretion of proinflammatory cytokines in lung tissues and blood. The molecular mechanisms underlying their virulence were investigated through comparative analyses of the genomic and transcriptional profiles of HY041 and HY037. The findings revealed that the genes encoding outer membrane protein A (OmpA), three peptidases, heat shock proteins, and proteins involved in lipopolysaccharide biosynthesis, and iron acquisition represent potential virulence factors of . . In conclusion, this study established . as a potential pathogen and identified significant differences in virulence across its strains, thereby enhancing our understanding of the pathogenesis of . .
Mss2 shapes the virulence of through reactive oxygen species (ROS) and calcium signaling, independent of direct transcriptional control.
Ke CL, Tsai HY, Kulkarni A … +2 more , Bennett RJ, Lin CH
Virulence · 2025 Dec · PMID 41263677 · Full text
Mitochondrial function is essential for virulence in , yet the mechanism by which mitochondria influence pathogenesis remains largely undefined. Here, we reveal that the mitochondrial-associated factor Mss2 controls inva...
Mitochondrial function is essential for virulence in , yet the mechanism by which mitochondria influence pathogenesis remains largely undefined. Here, we reveal that the mitochondrial-associated factor Mss2 controls invasive growth through the regulation of calcium-reactive oxygen species (ROS) homeostasis. Deletion of results in impaired invasive growth on solid media without affecting hyphal formation in liquid media, indicating that Mss2 controls contact-specific responses. We demonstrate that the regulation of these processes by Mss2 is linked to the regulation of cytosolic calcium levels and cellular ROS production. Furthermore, transcriptomic profiling identified -regulated genes, including , , , and , whose expression is dependent on calcium and ROS levels. Restoration of invasive phenotypes through exogenous ROS confirms the functional significance of this calcium-ROS circuit. In systemic infection models, similar to , the Mss2 downstream genes exhibit severe virulence defects. Together, this work is the first to show that mitochondrial regulation of a coordinated calcium-ROS circuit is required for invasive hyphal growth and virulence in . These findings refine our understanding of fungal invasion and virulence and reveal that targeting mitochondrial signaling could be an important area for antifungal therapeutic interventions.
Surface proteome of plasma extracellular vesicles differentiates between SARS-CoV-2 and influenza infection.
Bertrams W, Roessler FK, Bæk R … +11 more , Jung AL, Laakmann K, Jørgensen MM, Lehmann M, Weckler B, Schulte LN, Rohde G, Bar N, Barten G, Schmeck B, CAPNETZ study group
Virulence · 2026 Dec · PMID 41263641 · Full text
Small extracellular vesicles (sEVs) play a role in the pathophysiology of viral respiratory infections and may be suitable biomarkers for COVID-19 and Influenza infections, or targets for treatment. We investigated diffe...
Small extracellular vesicles (sEVs) play a role in the pathophysiology of viral respiratory infections and may be suitable biomarkers for COVID-19 and Influenza infections, or targets for treatment. We investigated differences in the surface proteome of plasma sEVs in patients with COVID-19 and Influenza. In a discovery cohort with 117 patients, we used a random forest (RF) classifier in order to discriminate COVID-19 and Influenza patients based on routine clinical parameters. Furthermore, plasma samples from these patients were analyzed with an EV Array containing 33 antibodies to capture sEVs, which were then visualized with a combination of CD9, CD63, and CD81 antibodies. We applied an RF classifier and a random depth-first search (RDFS) approach to extract markers with the best discriminatory potential. Data were then validated in an independent set of patient samples on a chip-based ExoView platform.In the initial cohort of 117 patients, leukocyte numbers, and heart rate discriminated best between COVID-19 and Influenza infection. In the plasma samples, 32 EV surface markers could be detected. Feature panels containing CD9, CD81, and CD141 allowed a discrimination between COVID-19 and Influenza. Consecutively, increased CD9 abundance was validated in a second, independent cohort, with the ExoView technology. The increased CD9 signal in Influenza patients was confirmed and shown to be mostly driven by CD9/CD41a double positive sEVs, hinting at a thrombocyte origin.We identified leukocyte numbers and heart rate, as well as CD9 as a sEV surface marker to differentiate COVID-19 from Influenza patients.
Novel avian metapneumovirus subtype C variant is a newly emerged pathogen causing hydrosalpinx fluid syndrome in Sheldrake ducks in China.
Fu QL, Wang WW, Zeng T … +13 more , Cao S, Jiao WL, Lin L, Jiang NS, Liang QZ, Cheng LF, Chen HM, Liu JH, Liu RC, Wan CH, Fu GH, Lu LZ, Huang Y
Virulence · 2025 Dec · PMID 41261847 · Full text
Since 2021, an epidemic disease characterized with hydrosalpinx fluid syndrome (HFS) has been circulating in the laying Sheldrake ducks in China, which seriously endangers the healthy development of the duck industry. Th...
Since 2021, an epidemic disease characterized with hydrosalpinx fluid syndrome (HFS) has been circulating in the laying Sheldrake ducks in China, which seriously endangers the healthy development of the duck industry. The causative agent of this disease has been traced to avian metapneumovirus subtype C (aMPV/C), known to cause acute upper respiratory tract infections and egg-drop in poultry. To date, no reports have been made to isolate and characterize aMPV/C infection in Sheldrake ducks in China. Here, a strain of virus, designated aMPV-FJ21, was successfully isolated from the diseased ducks exhibiting HFS. Transmission electron microscopy revealed that the virus is an enveloped particle exhibiting a spherical or pleomorphic morphology. Indirect immunofluorescence assays demonstrated that the aMPV-FJ21 strain had an obvious reactive activity with the ploy-antibody against aMPV/C F protein. The complete genome of aMPV-FJ21 was determined to be 14,149 nucleotides in length. Notably, the amino acid sequence of the G protein was only 55.6%-78.7% identical to those of other aMPV/C reference strains. Phylogenetic analysis indicated that aMPV-FJ21 forms a distinct lineage within the aMPV/C group and is genetically distant from the North American and Eurasian lineages, suggesting that it may represent a novel genetic lineage. In challenge experiments, laying Sheldrake ducks with aMPV-FJ21 reproduced the typical clinical symptoms and pathological lesions observed in the field cases. Altogether, we had isolated a novel aMPV/C variant from Sheldrake ducks exhibiting HFS, distinct from previously reported strains, and provided the first evidence confirming its role as the causative agent of HFS in ducks.
Disruption of via RNA interference compromises antibacterial immunity in .
Bi J, Li Q, Liu P … +7 more , Li J, Gao R, Zhao T, Yuan X, Hao H, Wang Y, Li B
Virulence · 2025 Dec · PMID 41258869 · Full text
Gram-negative bacteria binding proteins (GNBPs) serve as essential pattern recognition receptors in insect innate immunity, detecting pathogen-associated molecular patterns to activate downstream immune responses. This m...
Gram-negative bacteria binding proteins (GNBPs) serve as essential pattern recognition receptors in insect innate immunity, detecting pathogen-associated molecular patterns to activate downstream immune responses. This molecular recognition mechanism presents a promising target for pest control strategies. However, the immunological functions of family members in remain poorly characterized, particularly for those with typical structural features. In this study, we identified and characterized a novel (designated ) from the cDNA library. Structural analysis revealed that TcGNBP3 exhibits the typical domain architecture characteristic of the family, comprising an N-terminal carbohydrate-binding module 39 (CBM39) domain and a C-terminal glycoside hydrolase family 16 (GH16) domain. Spatiotemporal expression profiling demonstrated peak transcript accumulation during the early pupal and late adult developmental stages, with predominant localization in immune-related tissues including the fat body and hemolymph. Bacterial challenges ( or ) induced significant upregulation of expression from 6 to 72 h. Molecular docking and ELISA analyses demonstrated TcGNBP3's binding affinity for lipopolysaccharide, peptidoglycan, and β-1,3-glucan, while functional assays confirmed its ability to bind and agglutinate five tested bacterial strains. RNAi-mediated silencing of severely compromised the beetles' immune response, suppressing immune-related genes (including transcription factors and antimicrobial peptides), disrupting prophenoloxidase cascade activation, and significantly reducing survival rates upon bacterial infection. These results identify as a key immune regulator in , supporting its development as an RNAi-based pest control target.
Oral L-Arginine treatment attenuates extrapulmonary dissemination and disease progression.
Hansakon A, Phucharoenrak P, Trachootham D … +6 more , Kaewrattana S, Jeerawattanawart S, Tangchang W, Chayakulkeeree M, Angkasekwinai N, Angkasekwinai P
Virulence · 2025 Dec · PMID 41258798 · Full text
is an opportunistic fungal pathogen causing severe infections in immunocompromised individuals. Arginine metabolism is critical for immune regulation, but its precise role in cryptococcal pathogenesis is not well underst...
is an opportunistic fungal pathogen causing severe infections in immunocompromised individuals. Arginine metabolism is critical for immune regulation, but its precise role in cryptococcal pathogenesis is not well understood. In this study, we investigated systemic and tissue-specific alterations in L-arginine metabolism during pulmonary infection and evaluated L-arginine supplementation as a potential therapy using a murine model. Key assessments included fungal burden quantification, inflammatory cell and cytokine characterization, brain gene expression analysis, histological examinations, and survival studies. We found significant depletion of serum L-arginine and its downstream metabolites, accompanied by increased arginase activity in infected tissues, indicating a disrupted metabolic balance. Gene expression analysis showed distinct metabolic shifts, including upregulation of arginase-1 (Arg1) and proline metabolism genes, with concurrent suppression of nitric oxide synthase 2 (Nos2) in the brain during the late infection phase. Oral L-arginine supplementation significantly reduced fungal burdens in the brain and spleen, suggesting its effectiveness in controlling cryptococcal dissemination from the lungs. Consequently, L-arginine administration improved survival and clinical scores while also reducing brain cryptococcoma in infected mice. Mechanistically, L-arginine enhanced protective immune responses within the mouse brain, facilitated microglial-mediated clearance of , and reduced cryptococcal invasion across brain endothelial cells . In summary, oral administration of L-arginine mitigates dissemination by augmenting brain's immune response. This study provides crucial insights into arginine metabolism in cryptococcal disease progression, supporting L-arginine as a promising immunomodulatory therapy.
Epidemiology, evolution, and biological characteristics of avian influenza A (H11) viruses from wild birds.
Zhao Z, Tian J, Bai X … +11 more , Li M, Song X, Li J, Shi J, Kong H, Zeng X, Tian G, Liu J, Li C, Chen H, Li Y
Virulence · 2025 Dec · PMID 41258791 · Full text
H11 subtype avian influenza viruses (AIVs) have been identified in both wild and domestic birds. H11N9 viruses from wild birds provided the NA gene to human H7N9 virus in 2013 in China, which caused five waves of human i...
H11 subtype avian influenza viruses (AIVs) have been identified in both wild and domestic birds. H11N9 viruses from wild birds provided the NA gene to human H7N9 virus in 2013 in China, which caused five waves of human infections. During active surveillance in wild birds in China, 17 H11 viruses were isolated between December 2022 and January 2024, including six H11N1, one H11N2, one H11N3, and nine H11N9. The epidemiology of H11 subtype viruses in public databases revealed that they distributed across seven continents, and more than 54.9% of H11 viruses originated from wild Anseriformes. Phylogenetic analysis of the HA genes indicated that H11 viruses were classified into Eurasian and North American lineages, and our isolates belonged to the Eurasian lineage. Bayesian phylogeographic analysis suggested that Bangladesh served as a crucial geographical transmission center for H11 viruses in Eurasian lineage. Reassortment indicated that the H11 isolates in the study underwent complex genomic recombination with various subtype AIVs circulating in wild and domestic birds, including the clade 2.3.4.4b H5N1 highly pathogenic viruses, and formed seven genotypes. Notably, 17 H11 isolates acquired several mutations associated with enhanced human-type receptor binding in HA (S137A) and increased mammalian virulence in PB1 (D3V, D622G), PB1-F2 (N66S), M1 (N30D, I43M, T215A), and NS1 (P42S, I106M). Seven representative viruses exhibited dual receptor binding specificity and could infect mice directly without prior adaptation. These findings highlight the potential public health risks posed by H11 viruses from wild birds and emphasize the necessity of enhancing routine surveillance.
Harnessing gut microbiota to mitigate Dublin: Lessons from . Typhimurium.
Moran M, Malmuthuge N, Guan LL
Virulence · 2025 Dec · PMID 41242340 · Full text
The emerging cattle-adapted pathogen, Dublin, threatens the global cattle industry by causing high mortality in calves and reduced production efficiency in cows. Due to limited therapeutic options, there is a need for n...
The emerging cattle-adapted pathogen, Dublin, threatens the global cattle industry by causing high mortality in calves and reduced production efficiency in cows. Due to limited therapeutic options, there is a need for novel interventions to mitigate . Dublin. In the inflamed gut, Typhimurium, and possibly . Dublin, gain a metabolic advantage by utilizing niche nutrients during anaerobic respiration. . Dublin invades intestinal epithelial cells using genes encoded by Salmonella pathogenicity island 1 (SPI-1), initiating systemic disease and chronic infection. Propionate, a microbial fermentation product, inhibits SPI-1 transcription, presenting an opportunity to prevent infection. Lactobacilli endogenous to the small intestine of calves may be leveraged to inhibit . Dublin invasion and growth through propionate synthesis and nutrient blocking, respectively. Here, we discuss critical knowledge gaps of . Dublin pathogenesis while offering data-driven insights for the development of sustainable microbial-based interventions to mitigate . Dublin in cattle.
Liver-joint axis: Hepatitis B virus as a contributor to rheumatoid arthritis pathogenesis.
Wu H, Zhao N, Zhang X … +2 more , Zhang Y, Wang H
Virulence · 2025 Dec · PMID 41239737 · Full text
Hepatitis B virus (HBV) is increasingly recognized for its involvement in extrahepatic diseases, including rheumatological manifestations such as arthritis and joint pain. This review introduces the concept of the liver-...
Hepatitis B virus (HBV) is increasingly recognized for its involvement in extrahepatic diseases, including rheumatological manifestations such as arthritis and joint pain. This review introduces the concept of the liver-joint axis, hypothesizing that HBV may contribute to rheumatoid arthritis (RA) pathogenesis through immune and metabolic dysregulation. We emphasize the effect of HBV infection on fibroblast activation, metabolic reprogramming, and Th17/Treg imbalance. Transcriptome analysis further elucidates the complex signaling networks underlying HBV-associated RA. These findings support a pathogenic role for HBV in joint inflammation and suggest novel therapeutic opportunities for targeting HBV-driven RA.
Genome-wide identification and functional characterization of RxLR effectors in infecting Sarg.
Wang H, Fu Y, Peng X … +7 more , Li Z, Cao G, Song F, Zhou L, Wang Y, Lin H, Zhou X
Virulence · 2025 Dec · PMID 41236934 · Full text
is a globally distributed oomycete pathogen capable of infecting over 5,000 plant species, causing devastating root rot and stem canker diseases with significant agricultural and ecological impacts. Similar to other spe...
is a globally distributed oomycete pathogen capable of infecting over 5,000 plant species, causing devastating root rot and stem canker diseases with significant agricultural and ecological impacts. Similar to other species, secretes RxLR effectors to suppress host immunity and facilitate infection. Here, we present a high-quality genome assembly of strain ST402 isolated from an economically important Chinese hickory ( Sarg.), revealing 146 putative RxLR effectors. Transcriptomic profiling during the early infection stages (0-36 h post-inoculation) identified 66 differentially expressed RxLR effectors, with 4 highly induced candidates (PciRxLR1, PciRxLR21, PciRxLR57, and PciRxLR69) demonstrating cell death suppression activity against pathogen-associated molecular patterns (PAMPs) and promoting pathogenicity in . Subcellular localization revealed distinct nuclear and cytoplasmic targeting patterns of these effectors. Our findings provide critical insights into the molecular mechanisms underlying virulence and lay the foundation for developing targeted control strategies against this destructive pathogen.
Protoporphyrin IX targets viral spike glycoproteins to inactivate Akabane virus.
Li P, Zhang D, Deng M … +11 more , Zhao D, Zhang Y, Cai S, Zong W, Li C, Zhang M, Li Z, Zhao Y, Qin L, Gao H, Zhang K
Virulence · 2025 Dec · PMID 41236925 · Full text
Akabane virus (AKAV), an emerging arthropod-borne , is a significant pathogen of ruminants which causes severe congenital abnormalities and recurrent outbreaks in China and other Asian countries. However, no effective th...
Akabane virus (AKAV), an emerging arthropod-borne , is a significant pathogen of ruminants which causes severe congenital abnormalities and recurrent outbreaks in China and other Asian countries. However, no effective therapeutic options are available. In this study, structure-based virtual screening was performed using an FDA-approved compound library to identify potential compounds targeting the AKAV Gc protein. Ten candidate compounds were identified based on their high-affinity binding to the Gc protein. Among these ten candidates, Protoporphyrin IX (PPIX) demonstrated the most potent inhibitory effect on AKAV replication . Subsequent dose-response assays confirmed the antiviral efficacy of PPIX. Additionally, PPIX demonstrated antiviral activity at the pre-entry stage of infection. Notably, co-incubation of PPIX with AKAV virions resulted in rapid inactivation of the virus. Further experiments revealed that PPIX inactivates AKAV through direct binding to the Gc glycoprotein, leading to the disruption of its spike structure. experiments showed that pre-incubation of PPIX with AKAV can effectively inhibit the infectivity and pathogenicity of AKAV in sucking mice. Our findings demonstrate that PPIX exerts potent virucidal activity against AKAV both in vitro and in vivo, underscoring its potential potential use in preventing AKAV infection.
Carbon source-driven downregulation of the sRNA AmiL enhances virulence during acute lung infection.
Jing W, Li M, Huang S … +10 more , He X, Wu Y, Long J, Zhang S, Lin C, Xiao Q, Zeng J, Shen C, Chen C, Pu J
Virulence · 2025 Dec · PMID 41236921 · Full text
is a major opportunistic pathogen that causes severe acute lung infection. The ability of to precisely self-regulate its virulence factors is crucial for enhancing pathogenicity and establishing infection. However, how...
is a major opportunistic pathogen that causes severe acute lung infection. The ability of to precisely self-regulate its virulence factors is crucial for enhancing pathogenicity and establishing infection. However, how the bacterium dynamically adjusts virulence gene expression in response to host interaction remains to be elucidated. Here, transcriptome profiling revealed that infection of A549 alveolar epithelial cells significantly upregulated virulence genes associated with the type III secretion system (T3SS) and quorum sensing (QS) in PAO1, compared to a standard laboratory growth condition. In contrast, genes of the operon were markedly downregulated during infection. Notably, AmiL, the leader small RNA (sRNA) of the operon, exhibited consistently reduced expression across multiple infection models, including A549 cells, mouse lungs, and clinical isolates. AmiL expression was primarily repressed by succinate-mediated carbon catabolite repression (CCR) during the early stage of infection, and later by the transcription factor ArgR as succinate levels declined. Functional analyses showed AmiL bound to the mRNAs of the T3SS effector gene and the hydrogen cyanide synthesis gene , repressing their expression and thereby attenuating PAO1 virulence. Furthermore, deletion of gene enhanced the cytotoxicity of PAO1 in A549 cells, larvae, and a mouse lung infection model, resulting in more severe tissue damage and increased mortality. Therefore, our findings demonstrate that strategically downregulates AmiL in response to carbon source changes to enhance its virulence and pathogenicity during acute lung infection, and highlight a potential target for antibacterial therapy.
Cytochrome bd-II oxidase CyxA promotes the pathogenicity of by resisting oxidative stress.
Xiao X, Song G, Lu H … +9 more , Zheng W, Meng P, Peng W, Yang J, Wang M, Zhu J, Wang J, Li B, Li M
Virulence · 2025 Dec · PMID 41236911 · Full text
Adaptation to oxidative stress is crucial for survival of in external environments and within infected hosts. Cytochrome bd oxidase contributes to oxidative stress resistance and enhances the pathogenicity of several pa...
Adaptation to oxidative stress is crucial for survival of in external environments and within infected hosts. Cytochrome bd oxidase contributes to oxidative stress resistance and enhances the pathogenicity of several pathogens. In this study, we explored the role of cytochrome bd-II oxidase CyxA in 's response to oxidative stress and its overall pathogenicity. The expression level of was significantly increased in response to oxidative stress in the wild-type strain (WT). Deletion of reduced 's resistance to exogenous hydrogen peroxide (HO) and nitric oxide (NO). Additionally, the expression levels of at 37°C and 41°C were significantly higher compared to 30°C, and the Δ strain exhibited significantly lower viable counts, elevated intracellular reactive oxygen species (ROS) levels, and decreased total antioxidant capacity (T-AOC) relative to WT at 37°C and 41°C. Results from intraperitoneal and intestinal infection models in mice revealed that CyxA promotes pathogenicity by enhancing the invasiveness of into intra-abdominal tissues and confers a fitness advantage in the inflamed gut. Moreover, we provide preliminary evidence that CyxA exhibits catalase activity and increases the expression of catalase KatE. In summary, our results suggest that cytochrome bd-II oxidase CyxA enhances 's resistance to oxidative stress caused by exogenous ROS, elevated temperature, and inflammation, either by directly or indirectly metabolizing HO, thereby promoting its growth and pathogenicity.
ROS-induced allosteric modulation of NikR promotes biofilm formation by attenuating FlgR-dependent inhibition of the molybdate transport system.
Zheng Y, Li S, Xue J … +8 more , Zhang L, Wang L, Zhao Y, Zhang W, Ma W, Liu J, Sun Y, Sun Y
Virulence · 2025 Dec · PMID 41225722 · Full text
biofilm formation is crucial for its persistence and transmission, constituting a notable public health concern. Understanding the regulatory mechanisms driving biofilm initiation is vital for developing effective contro...
biofilm formation is crucial for its persistence and transmission, constituting a notable public health concern. Understanding the regulatory mechanisms driving biofilm initiation is vital for developing effective control strategies. This study reveals a previously uncharacterized regulatory mechanism where reactive oxygen species (ROS) promote biofilm formation by modulating the key flagellar regulator FlgR and the molybdate transport system ModABD. We demonstrate that FlgR acts as a repressor of biofilm development. Mechanistically, FlgR inhibits the transcription of the operon, essential for biofilm formation, by suppressing the activity of sigma factor σ. Crucially, we identify the nickel-responsive regulator NikR as a repressor of expression. ROS induces a conformational change in NikR, converting it to its DNA-binding holo-form, which directly binds the promoter and represses its expression. This repression alleviates FlgR-mediated inhibition of σ, thereby de-repressing the operon and facilitating the transition from planktonic to biofilm growth. Our findings uncover a previously unknown ROS-NikR-FlgR-σ-ModABD signaling axis governing biofilm formation.
Orthobunyaviruses: Epidemiology, innate immune escape, and intervention strategies.
Li P, Zhao D, Fu J … +8 more , Zhang Y, Cai S, Deng M, Li C, Huang J, Qin L, Gao H, Zhang K
Virulence · 2025 Dec · PMID 41217955 · Full text
Orthobunyaviruses, including La Crosse virus (LACV), Oropouche virus (OROV), Schmallenberg virus (SBV), and Akabane virus (AKAV), pose substantial threats to global public health and livestock industries. This review foc...
Orthobunyaviruses, including La Crosse virus (LACV), Oropouche virus (OROV), Schmallenberg virus (SBV), and Akabane virus (AKAV), pose substantial threats to global public health and livestock industries. This review focuses on the interplay between these viruses and the host immune systems, highlighting key mechanisms of viral entry and immune evasion. The viruses exploit vulnerabilities in host innate immunity, particularly through nonstructural protein NSs, which disrupts type I interferon signaling and transcriptional machinery. Additionally, this review delineates how host restriction factors counteract viral proliferation through compartmentalized defense mechanisms including BST-2 and MxA. The review also discusses antiviral strategies, including vaccines and inhibitors. Hence, this review synthesizes current knowledge on host recognition, immune evasion, and therapies for Orthobunyaviruses infections (focusing on LACV, OROV, AKAV, SBV) to guide targeted antiviral and broad-spectrum countermeasure development against emerging Orthobunyaviruses threats.
Effectiveness of antiviral, immunomodulatory and platelet-enhancing agents for treatment of dengue infection: A systematic review.
Aynekulu Mersha DG, Duijff F, Langerak T … +6 more , Hakim MS, Martina B, Goeijenbier M, Dalm VASH, van Lelyveld SFL, van Gorp ECM
Virulence · 2025 Dec · PMID 41214477 · Full text
Dengue is a vector-borne infectious disease, caused by dengue virus (DENV), with a rapidly increasing incidence worldwide. With no feasible, widely applicable prevention method available in the near term, the need for an...
Dengue is a vector-borne infectious disease, caused by dengue virus (DENV), with a rapidly increasing incidence worldwide. With no feasible, widely applicable prevention method available in the near term, the need for an effective treatment is of great importance. This systematic review aims to provide a comprehensive overview of potential antiviral, immunomodulatory, and platelet-enhancing therapies for the treatment of DENV. This systematic review was conducted according to the PRISMA guidelines. Clinical trials that investigate treatment options for DENV in the general population were included. Twenty-six studies were included, investigating length of hospital stay ( = 10), platelet count ( = 16), interleukin (IL)-6 levels ( = 4), virological log reduction (VLR) ( = 2), and non-structural (NS)-1 clearance time ( = 4). Focusing on potential antiviral agents, four studies showed a significant reduction regarding length of hospital stay, of which two used doxycycline. The most profound reduction of hospital stay was observed when doxycycline was combined with herbal extract (7.3 days vs 9.1 days). This combination was also able to achieve a significant rise in platelet count (+154.1 × 10/L vs + 66.0 × 10/L in 7 days). Immunomodulatory therapies did not demonstrate efficacy against DENV, although some evidence suggests that rupatadine may increase platelet count. The platelet-enhancing agents recombinant human IL-11, anti-rhD immunoglobulin (anti-D), and eltrombopag all showed a significant rise in platelet count. Small sample sizes make it challenging to draw definitive conclusions out of the included studies. Larger clinical trials are needed to evaluate treatments for DENV, with particular focus on doxycycline, , rupatadine, and platelet-enhancing agents.
Rapid detection of Seneca Valley virus based on reverse transcription recombinase polymerase amplification and CRISPR-Cas13a.
Wu Y, Su J, Sun J … +11 more , Li Z, Yang J, Wu C, Liu Z, Wang J, Wang Y, Liu J, Duan L, Wang C, Zhu G, Wen X
Virulence · 2025 Dec · PMID 41212595 · Full text
The Seneca Valley virus (SVV) is an emerging novel etiological agent that triggers vesicular stomatitis in pigs. SVV leads to considerable financial detriment to the global swine industry. Availability of expeditious, si...
The Seneca Valley virus (SVV) is an emerging novel etiological agent that triggers vesicular stomatitis in pigs. SVV leads to considerable financial detriment to the global swine industry. Availability of expeditious, simple, and precise detection techniques would aid in the diagnosis and control of Seneca Valley disease. In this study, we developed a novel SVV detection assay based on reverse transcription recombinase polymerase amplification (RT-RPA)/CRISPR-Cas13a. This technique can specifically identify SVV with no cross-reactivity with other viruses, such as the porcine reproductive and respiratory syndrome virus, pseudorabies virus, classical swine fever virus, and foot-and-mouth disease virus. It boasts a detection threshold as sensitive as 2.43 copies/μL, matching the proficiency of reverse transcriptase quantitative PCR in clinical diagnostics. The streamlined RT-RPA/CRISPR-Cas13a assay for SVV minimizes procedural complexity and the likelihood of contamination. Integrating this method with nucleic acid acquisition via nucleic acid releaser enables a turnaround time of only 40 min from sample acquisition to result determination, underscoring its suitability for on-site diagnostics and affirming its role as a robust instrument for the monitoring and detection of SVV.
Pathogenicity and virulence of : Strategies for metabolic adaptation and immune evasion.
Guimarães ES, Gomes MTR, de Araujo ACVSC … +2 more , Ramos KKS, Oliveira SC
Virulence · 2025 Dec · PMID 41212588 · Full text
species are facultative intracellular pathogens that have evolved sophisticated mechanisms to evade host immune responses and establish chronic infections. This review provides an analysis of virulence and pathogenicity...
species are facultative intracellular pathogens that have evolved sophisticated mechanisms to evade host immune responses and establish chronic infections. This review provides an analysis of virulence and pathogenicity, with particular emphasis on the intricate interactions between the pathogen and its host. We examine the molecular and cellular mechanisms underlying pathogenesis, detailing the processes by which the bacterium invades, survives, and replicates within host cells. An in-depth discussion of the key virulence factors and their roles in immune evasion is provided, including strategies that enable the pathogen to circumvent immune detection, subvert host immune signaling pathways, and manipulate intracellular trafficking. Furthermore, we explore ability to modulate host cellular functions, particularly through the induction of the unfolded protein response and its implications for bacterial persistence. The review also highlights the influence of type I interferon responses on host susceptibility to infection, shedding light on their role in disease progression. Additionally, we discuss metabolic adaptations, including its ability to exploit host-derived nutrients and reprogram metabolic pathways to sustain long-term persistence. Finally, we address emerging research directions and future perspectives in the field, emphasizing the need for novel therapeutic and vaccine strategies. A deeper understanding of these complex host-pathogen interactions will be instrumental in developing more effective approaches for the control, prevention, and treatment of brucellosis.
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