Virulence最新文献

{"title":"The host protein CALCOCO2 interacts with bovine viral diarrhoea virus Npro, inhibiting type I interferon production and thereby promoting viral replication.","authors":"Song Wang, Ran Wei, Xiaomei Ma, Jin Guo, Muhammad Aizaz, Fangxu Li, Jun Wang, Hongmei Wang, Hongbin He","doi":"10.1080/21505594.2023.2289764","DOIUrl":"10.1080/21505594.2023.2289764","url":null,"abstract":"<p><p>Bovine viral diarrhoea-mucosal disease caused by bovine viral diarrhoea virus (BVDV) is a major infectious disease that affects the cattle industry. The nonstructural protein Npro of BVDV antagonizes the type I interferon (IFN-I) pathway, thereby escaping the host immune response. The exact mechanism by which Npro uses host proteins to inhibit IFN-I production is unclear. The host protein CALCOCO2 was identified as a binding partner of Npro using a yeast two-hybrid screen. The interaction between Npro and CALCOCO2 was confirmed by yeast co-transformation, co-immunoprecipitation assays, and GST pull-down assays. The stable overexpression of CALCOCO2 markedly promoted BVDV propagation, while the knockdown of CALCOCO2 significantly inhibited BVDV replication in MDBK cells. Interestingly, CALCOCO2 inhibited IFN-I and IFN-stimulated gene production in BVDV-infected cells. Ectopic expression of CALCOCO2 effectively reduced IRF3 protein levels via the proteasome pathway. CALCOCO2 was found to promote Npro-mediated ubiquitination degradation of IRF3 by interacting with IRF3. Our results demonstrate the molecular mechanism by which Npro recruits the CALCOCO2 protein to regulate IRF3 degradation to inhibit IFN-I production.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10730213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138478723","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}

{"title":"Unraveling the interplay between unicellular parasites and bacterial biofilms: Implications for disease persistence and antibiotic resistance.","authors":"Eva Zanditenas, Serge Ankri","doi":"10.1080/21505594.2023.2289775","DOIUrl":"10.1080/21505594.2023.2289775","url":null,"abstract":"<p><p>Bacterial biofilms have attracted significant attention due to their involvement in persistent infections, food and water contamination, and infrastructure corrosion. This review delves into the intricate interactions between bacterial biofilms and unicellular parasites, shedding light on their impact on biofilm formation, structure, and function. Unicellular parasites, including protozoa, influence bacterial biofilms through grazing activities, leading to adaptive changes in bacterial communities. Moreover, parasites like <i>Leishmania</i> and <i>Giardia</i> can shape biofilm composition in a grazing independent manner, potentially influencing disease outcomes. Biofilms, acting as reservoirs, enable the survival of protozoan parasites against environmental stressors and antimicrobial agents. Furthermore, these biofilms may influence parasite virulence and stress responses, posing challenges in disease treatment. Interactions between unicellular parasites and fungal-containing biofilms is also discussed, hinting at complex microbial relationships in various ecosystems. Understanding these interactions offers insights into disease mechanisms and antibiotic resistance dissemination, paving the way for innovative therapeutic strategies and ecosystem-level implications.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138499546","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}

{"title":"The pathogenicity and virulence of the opportunistic pathogen <i>Staphylococcus epidermidis</i>.","authors":"Órla Burke, Merve S Zeden, James P O'Gara","doi":"10.1080/21505594.2024.2359483","DOIUrl":"10.1080/21505594.2024.2359483","url":null,"abstract":"<p><p>The pervasive presence of <i>Staphylococcus epidermidis</i> and other coagulase-negative staphylococci on the skin and mucous membranes has long underpinned a casual disregard for the infection risk that these organisms pose to vulnerable patients in healthcare settings. Prior to the recognition of biofilm as an important virulence determinant in <i>S. epidermidis</i>, isolation of this microorganism in diagnostic specimens was often overlooked as clinically insignificant with potential delays in diagnosis and onset of appropriate treatment, contributing to the establishment of chronic infection and increased morbidity or mortality. While impressive progress has been made in our understanding of biofilm mechanisms in this important opportunistic pathogen, research into other virulence determinants has lagged <i>S. aureus</i>. In this review, the broader virulence potential of <i>S. epidermidis</i> including biofilm, toxins, proteases, immune evasion strategies and antibiotic resistance mechanisms is surveyed, together with current and future approaches for improved therapeutic interventions.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11178275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141311939","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}

{"title":"Exogenous NADH promotes the bactericidal effect of aminoglycoside antibiotics against <i>Edwardsiella tarda</i>.","authors":"Yilin Zhong, Juan Guo, Ziyi Zhang, Yu Zheng, Manjun Yang, Yubin Su","doi":"10.1080/21505594.2024.2367647","DOIUrl":"10.1080/21505594.2024.2367647","url":null,"abstract":"<p><p>The global surge in multidrug-resistant bacteria owing to antibiotic misuse and overuse poses considerable risks to human and animal health. With existing antibiotics losing their effectiveness and the protracted process of developing new antibiotics, urgent alternatives are imperative to curb disease spread. Notably, improving the bactericidal effect of antibiotics by using non-antibiotic substances has emerged as a viable strategy. Although reduced nicotinamide adenine dinucleotide (NADH) may play a crucial role in regulating bacterial resistance, studies examining how the change of metabolic profile and bacterial resistance following by exogenous administration are scarce. Therefore, this study aimed to elucidate the metabolic changes that occur in <i>Edwardsiella tarda</i> (<i>E. tarda</i>), which exhibits resistance to various antibiotics, following the exogenous addition of NADH using metabolomics. The effects of these alterations on the bactericidal activity of neomycin were investigated. NADH enhanced the effectiveness of aminoglycoside antibiotics against <i>E. tarda</i> ATCC15947, achieving bacterial eradication at low doses. Metabolomic analysis revealed that NADH reprogrammed the ATCC15947 metabolic profile by promoting purine metabolism and energy metabolism, yielding increased adenosine triphosphate (ATP) levels. Increased ATP levels played a crucial role in enhancing the bactericidal effects of neomycin. Moreover, exogenous NADH promoted the bactericidal efficacy of tetracyclines and chloramphenicols. NADH in combination with neomycin was effective against other clinically resistant bacteria, including <i>Aeromonas hydrophila, Vibrio parahaemolyticus</i>, methicillin-resistant <i>Staphylococcus aureus</i>, and <i>Listeria monocytogenes</i>. These results may facilitate the development of effective approaches for preventing and managing <i>E. tarda</i>-induced infections and multidrug resistance in aquaculture and clinical settings.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11185186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331919","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}

{"title":"Streptococcal arginine deiminase system defences macrophage bactericidal effect mediated by XRE family protein XtrSs.","authors":"Yumin Zhang, Song Liang, Shidan Zhang, Qiankun Bai, Lei Dai, Jinxiu Wang, Huochun Yao, Wei Zhang, Guangjin Liu","doi":"10.1080/21505594.2024.2306719","DOIUrl":"10.1080/21505594.2024.2306719","url":null,"abstract":"<p><p>The arginine deiminase system (ADS) has been identified in various bacteria and functions to supplement energy production and enhance biological adaptability. The current understanding of the regulatory mechanism of ADS and its effect on bacterial pathogenesis is still limited. Here, we found that the XRE family transcriptional regulator XtrSs negatively affected <i>Streptococcus suis</i> virulence and significantly repressed ADS transcription when the bacteria were incubated in blood. Electrophoretic mobility shift (EMSA) and lacZ fusion assays further showed that XtrSs directly bind to the promoter of ArgR, an acknowledged positive regulator of bacterial ADS, to repress ArgR transcription. Moreover, we provided compelling evidence that <i>S. suis</i> could utilize arginine via ADS to adapt to acid stress, while Δ<i>xtrSs</i> enhanced this acid resistance by upregulating the ADS operon. Moreover, whole ADS-knockout <i>S. suis</i> increased arginine and antimicrobial NO in the infected macrophage cells, decreased intracellular survival, and even caused significant attenuation of bacterial virulence in a mouse infection model, while Δ<i>xtrSs</i> consistently presented the opposite results. Our experiments identified a novel ADS regulatory mechanism in <i>S. suis</i>, whereby XtrSs regulated ADS to modulate NO content in macrophages, promoting <i>S. suis</i> intracellular survival. Meanwhile, our findings provide a new perspective on how <i>Streptococci</i> evade the host's innate immune system.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10841013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139513787","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}

{"title":"<i>Coxiella burnetii</i> effector CvpE maintains biogenesis of <i>Coxiella</i>-containing vacuoles by suppressing lysosome tubulation through binding PI(3)P and perturbing PIKfyve activity on lysosomes.","authors":"Mingliang Zhao, Shan Zhang, Weiqiang Wan, Chunyu Zhou, Nana Li, Ruxi Cheng, Yonghui Yu, Xuan Ouyang, Dongsheng Zhou, Jun Jiao, Xiaolu Xiong","doi":"10.1080/21505594.2024.2350893","DOIUrl":"10.1080/21505594.2024.2350893","url":null,"abstract":"<p><p><i>Coxiella burnetii</i> (<i>C. burnetii</i>) is the causative agent of Q fever, a zoonotic disease. Intracellular replication of <i>C. burnetii</i> requires the maturation of a phagolysosome-like compartment known as the replication permissive <i>Coxiella</i>-containing vacuole (CCV). Effector proteins secreted by the Dot/Icm secretion system are indispensable for maturation of a single large CCV by facilitating the fusion of promiscuous vesicles. However, the mechanisms of CCV maintenance and evasion of host cell clearance remain to be defined. Here, we show that <i>C. burnetii</i> secreted <i>Coxiella</i> vacuolar protein E (CvpE) contributes to CCV biogenesis by inducing lysosome-like vacuole (LLV) enlargement. LLV fission by tubulation and autolysosome degradation is impaired in CvpE-expressing cells. Subsequently, we found that CvpE suppresses lysosomal Ca²⁺ channel transient receptor potential channel mucolipin 1 (TRPML1) activity in an indirect manner, in which CvpE binds phosphatidylinositol 3-phosphate [PI(3)P] and perturbs PIKfyve activity in lysosomes. Finally, the agonist of TRPML1, ML-SA5, inhibits CCV biogenesis and <i>C. burnetii</i> replication. These results provide insight into the mechanisms of CCV maintenance by CvpE and suggest that the agonist of TRPML1 can be a novel potential treatment that does not rely on antibiotics for Q fever by enhancing Coxiella-containing vacuoles (CCVs) fission.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11085968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899204","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}

{"title":"Alkaloids solenopsins from fire ants display <i>in vitro</i> and <i>in vivo</i> activity against the yeast <i>Candida auris</i>.","authors":"Leandro Honorato, Jhon Jhamilton Artunduaga Bonilla, Larissa Ribeiro da Silva, Julio Kornetz, Daniel Zamith-Miranda, Alessandro F Valdez, Joshua D Nosanchuk, Eduardo Gonçalves Paterson Fox, Leonardo Nimrichter","doi":"10.1080/21505594.2024.2413329","DOIUrl":"10.1080/21505594.2024.2413329","url":null,"abstract":"<p><p>The urgency surrounding <i>Candida auris</i> as a public health threat is highlighted by both the Center for Disease Control (CDC) and World Health Organization (WHO) that categorized this species as a priority fungal pathogen. Given the current limitations of antifungal therapy for <i>C. auris</i>, particularly due to its multiple resistance to the current antifungals, the identification of new drugs is of paramount importance. Some alkaloids abundant in the venom of the red invasive fire ant (<i>Solenopsis invicta</i>), known as solenopsins, have garnered attention as potent inhibitors of bacterial biofilms, and there are no studies demonstrating such effects against fungal pathogens. Thus, we herein investigated the antibiotic efficacy of solenopsin alkaloids against <i>C. auris</i> biofilms and planktonic cells. Both natural and synthetic solenopsins inhibited the growth of <i>C. auris</i> strains from different clades, including fluconazole and amphotericin B-resistant isolates. Such alkaloids also inhibited matrix deposition and altered cellular metabolic activity of <i>C. auris</i> in biofilm conditions. Mechanistically, the alkaloids compromised membrane integrity as measured by propidium iodide uptake in exposed planktonic cells. Additionally, combining the alkaloids with AMB yielded an additive antifungal effect, even against AMB-resistant strains. Finally, both extracted solenopsins and the synthetic analogues demonstrated protective effect <i>in vivo</i> against <i>C. auris</i> infection in the invertebrate model <i>Galleria mellonella</i>. These findings underscore the potent antifungal activities of solenopsins against <i>C. auris</i> and suggest their inclusion in future drug development. Furthermore, exploring derivatives of solenopsins could reveal novel compounds with therapeutic promise.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381760","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}

{"title":"Re-emergence of Chandipura virus infection in India.","authors":"Naveen Kumar, Vijay P Bondre","doi":"10.1080/21505594.2024.2421218","DOIUrl":"10.1080/21505594.2024.2421218","url":null,"abstract":"","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523231","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}

{"title":"Correction.","authors":"","doi":"10.1080/21505594.2024.2363658","DOIUrl":"10.1080/21505594.2024.2363658","url":null,"abstract":"","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11168232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141296879","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}

{"title":"M1-type polarized macrophage contributes to brain damage through CXCR3.2/CXCL11 pathways after RGNNV infection in grouper.","authors":"Kaishan Liang, Minlin Zhang, Jiantao Liang, Xiaoling Zuo, Xianze Jia, Jinhong Shan, Zongyang Li, Jie Yu, Zijie Xuan, Liyuan Luo, Huihong Zhao, Songyong Gan, Ding Liu, Qiwei Qin, Qing Wang","doi":"10.1080/21505594.2024.2355971","DOIUrl":"10.1080/21505594.2024.2355971","url":null,"abstract":"<p><p>The vertebrate central nervous system (CNS) is the most complex system of the body. The CNS, especially the brain, is generally regarded as immune-privileged. However, the specialized immune strategies in the brain and how immune cells, specifically macrophages in the brain, respond to virus invasion remain poorly understood. Therefore, this study aimed to examine the potential immune response of macrophages in the brain of orange-spotted groupers (<i>Epinephelus coioides</i>) following red-spotted grouper nervous necrosis virus (RGNNV) infection. We observed that RGNNV induced macrophages to produce an inflammatory response in the brain of orange-spotted grouper, and the macrophages exhibited M1-type polarization after RGNNV infection. In addition, we found RGNNV-induced macrophage M1 polarization via the CXCR3.2- CXCL11 pathway. Furthermore, we observed that RGNNV triggered M1 polarization in macrophages, resulting in substantial proinflammatory cytokine production and subsequent damage to brain tissue. These findings reveal a unique mechanism for brain macrophage polarization, emphasizing their role in contributing to nervous tissue damage following viral infection in the CNS.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11123556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140923264","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}