mBio
mBio(英文缩写 MBIO),ISSN 2150-7511,eISSN 2150-7511 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.786 | Q1 |
| 2022 | 6.400 | Q1 |
| 2023 | 5.100 | Q1 |
| 2024 | 4.700 | Q1 |
| 2025 | 5.400 | Q1 |
mBio 最新收录文献
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1. {"_":"Monoclonal antibodies raised against the Junín virus glycoprotein show broad reactivity and provide protection .","i":["in vivo"]}
PMID:日期:2026-09-25Argentine hemorrhagic fever (AHF) is a disease caused by the Junín virus (JUNV) that can be fatal in 15%-30% of untreated cases. Although JUNV is the only arenavirus for which efficient therapy and vaccination have been established, its administration is limited. In this study, hybridoma technology was used to generate 30 mouse monoclonal antibodies (mAbs) against the glycoprotein complex (GPC) of JUNV. Of these 30 mAbs, 26 showed strong cross-binding to GPCs from various arenaviruses. In addition, nine mAbs demonstrated potent neutralizing activity with a 50% inhibitory concentration of less than 1 µg/mL against a replication-competent chimeric vesicular stomatitis virus expressing JUNV GPC (rVSV-JUNV), as well as the live attenuated JUNV vaccine strain Candid#1. Furthermore, when tested using a challenge model of rVSV-JUNV in Stat2 mice, five select mAbs significantly reduced viral loads in the spleen when administered prophylactically. Humanized versions of JUNV-1A2, JUNV-1D5, and JUNV-5B12 mAbs, which showed protection in the Stat2 surrogate model, were produced. These antibodies were evaluated in a guinea pig challenge model of AHF and showed protective efficacy. Escape experiments with these humanized antibodies, as well as previously characterized antibodies, GB03 and JUN1, using rVSV-JUNV resulted in the acquisition of amino acid changes in the GP1 part of the GPC, which directly contacts host receptor transferrin receptor 1, indicating these sites could be key for future therapies. In summary, we generated mAbs that may be valuable for antibody-guided vaccine design and therapeutic development. Junín virus (JUNV) is a highly pathogenic virus that causes Argentine hemorrhagic fever (AHF) and is classified as a category A pathogen due to its potential for aerosol transmission and the significant number of annual infections and deaths associated with it. Although effective treatments exist, such as convalescent immune plasma, their availability is limited, and they are ineffective when given after the first week of symptoms. This study is significant because it focuses on developing therapeutic monoclonal antibodies against JUNV with strong neutralizing activity and protection in both a surrogate mouse model and a guinea pig challenge model of AHF. This has led to promising antibody candidates that could be used as therapeutics to combat ongoing outbreaks.
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2. {"_":"Establishment of an vascular tissue model to investigate bunyavirus-triggered vascular endothelial injury.","i":["ex vivo"]}
PMID:日期:2026-09-25Severe fever with thrombocytopenia syndrome, an emerging infectious disease caused by the tick-borne bunyavirus severe fever with thrombocytopenia syndrome virus (SFTSV), is associated with a high clinical fatality rate of 12%-50%. Vascular endothelial injury triggered by SFTSV infection has been linked to severe disease progression and mortality. Currently, a suitable model to investigate the underlying mechanisms of SFTSV-induced vascular damage is lacking. Here, we show that the human vascular tissue can be used as a model for studying bunyavirus-triggered endothelial injury. Both SFTSV and Rift Valley fever virus (RVFV) can successfully infect human vascular tissue, as evidenced by detection of viral nucleoprotein and viral amplification in the tissue. Histopathological analysis, TUNEL staining, and endothelial injury-associated transcriptional changes revealed irregular venous tissue structure, luminal endothelial disruption, and apoptosis following infection. This model enables evaluation of antiviral compound efficacy, demonstrating that niclosamide or 4'-fluorouridine significantly inhibits SFTSV and RVFV replication in vascular tissues. These findings establish the human vascular tissue as a valuable tool for investigating bunyavirus-induced vascular pathogenesis and for evaluating antiviral therapeutics. Severe fever with thrombocytopenia syndrome virus and other pathogenic bunyaviruses cause severe human diseases that are frequently associated with vascular dysfunction. However, the mechanisms underlying virus-induced vascular injury remain poorly defined due to the lack of physiologically relevant human tissue models. Here, we establish an human vascular tissue model that supports productive bunyavirus infection and enables quantitative assessment of endothelial injury, tissue damage, and antiviral efficacy. Using this model, we demonstrate that bunyavirus infection triggers endothelial disruption and that antiviral compounds can suppress viral replication and alleviate infection-associated tissue injury. This model provides a valuable experimental system for studying virus-vascular interactions and can support antiviral development against emerging bunyaviruses.
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3. {"_":"The high protection of a novel chemo-attenuated sporozoite vaccine requires IL-15-mediated liver CD8 tissue-resident memory T-cell responses.","sup":["+"]}
PMID:日期:2026-09-24Chemo-attenuated sporozoite vaccines (SPZ-CVacs) are considered promising for malaria prevention, but safety concerns persist regarding antimalarial drugs targeting either liver- or blood-stage parasites. In this study, we found that nitroquine (CI-679), used to eliminate malaria blood-stage parasites, effectively rendered sporozoites attenuated by arresting late liver-stage development. A single vaccination with CI-679-attenuated () sporozoites conferred robust protection against sporozoite challenge in BALB/c mice. Using mouse models with distinct genetic backgrounds, we demonstrated that the robust protection conferred by the CI-679-attenuated vaccine was primarily associated with the frequency of parasite-specific CD8 tissue-resident memory (Trm) cells mediated by IL-15. Notably, the supplement of IL-15/IL-15Ra sushi complex remarkably increased Trm frequency and improved the protective efficacy of CI-679-attenuated vaccine. Our findings characterize a novel SPZ-CVac and provide mechanistic evidence supporting IL-15 as an adjuvant to enhance the efficacy of pre-erythrocytic stage vaccines.IMPORTANCEMalaria remains a devastating global disease. Chemo-attenuated sporozoite vaccines show promise, yet safety concerns persist as current drugs target only liver- or blood-stage parasites. Here, we found nitroquine (CI-679) has a potentially favorable safety profile because of its dual liver- and blood-stage activity, and a single vaccination with CI-679-attenuated sporozoites conferred robust protection against sporozoite challenge in BALB/c mice. Mechanistically, protection was associated with IL-15-mediated parasite-specific CD8 tissue-resident memory (Trm) cells. Notably, the supplement of IL-15/IL-15Ra sushi complex remarkably increased Trm frequency and enhanced protective efficacy. Therefore, we characterize a novel chemo-attenuated sporozoite vaccine and provide mechanistic evidence supporting IL-15 as an adjuvant for pre-erythrocytic stage vaccines.
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4. MinD-like ATPase FlhG synchronizes flagellation and cell division in spirochetes.
PMID:日期:2026-09-24Spirochetes are evolutionarily distinct bacteria defined by their spiral morphology, unique means of motility, and periplasmic flagella (PFs). Because these flagella reside within the periplasm and are mechanically integrated with the cell body, their assembly must be precisely coordinated with cell growth and cytokinesis. However, the mechanism coupling flagellar biogenesis to cell division in spirochetes remains unclear. Using the Lyme disease spirochete as a model, we identify FlhG (BB0269), a MinD-like ATPase, as a spatial regulator that links cell division to flagellar patterning. In wild-type cells, 7-11 long helical PFs form at each pole and form ribbon-like bundles that wrap around the cell cylinder to drive motility. Deletion of disrupts this ordered architecture, resulting in pronounced heterogeneity in flagellar number, defective ribbon formation, aberrant septation, and severe motility defects. Mechanistically, FlhG dynamically localizes to the poles and division site, where it spatially organizes FlhF, an SRP-type GTPase that controls flagellar number and positioning, and FliF, the MS-ring protein that is an essential early component for flagellar biogenesis. Through this spatial regulation, FlhG coordinates flagellar biogenesis with cytokinetic progression. Together, these findings uncover a spatial regulatory mechanism that couples cell division to flagellation, providing insight into how spirochetes coordinate morphogenesis and motility to maintain their distinctive cellular architecture. Spirochetes such as , the causative agent of Lyme disease, rely on periplasmic flagella for motility and cell shape, yet how these structures are coordinated with cell division has remained unclear. We identify a MinD-like ATPase, FlhG, as a spatial regulator that couples flagellar assembly to cytokinesis. In contrast to its homologs in most bacteria, FlhG does not regulate flagellar protein levels but instead directs subcellular positioning of key assembly factors. By dynamically redistributing between the cell poles and division site, FlhG synchronizes flagellar patterning with septum formation. These findings uncover a previously unrecognized mechanism linking cell morphogenesis to the cell cycle and reveal how conserved ATPases can be repurposed to organize complex bacterial architectures.
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5. {"_":"Altered physiology of drug-resistant restricts adaptation to host-relevant conditions and produces condition-dependent collateral vulnerabilities.","i":["Mycobacterium tuberculosis"]}
PMID:日期:2026-09-24Antibiotic resistance mutations often disrupt essential cellular processes; however, the physiological consequences of these mutations under host-relevant conditions remain poorly understood in many bacterial pathogens. Here, we have used a combination of phenotypic growth assays and metabolomics to investigate how drug resistance affects the metabolism of and its ability to adapt to different host-relevant conditions. This work shows that (i) the fitness costs of antibiotic resistance in are highly variable and can be exacerbated or alleviated depending on the media carbon source, (ii) genetically unrelated resistance mutations have overlapping phenotypes and metabolic dysregulation, (iii) the growth of bedaquiline- and rifampicin-resistant mutants was impaired on host-relevant carbon sources, and (iv) resistance mutants have condition-specific collateral antibiotic susceptibilities, with rifampicin-resistant mutants being hypersusceptible to ATP synthase inhibitors when grown under conditions that require propionate metabolism. Collectively, this study highlights how drug resistance impacts bacterial physiology and places metabolic constraints on the ability of to adapt to changes in host-relevant conditions. This work has major implications for our understanding of how resistance evolves within the host context and reinforces the importance of how physiological variation in might affect the outcomes of new treatment regimens. Mutations that provide antibiotic resistance in bacterial pathogens often disrupt key cellular processes. The effects of these disruptions on cellular physiology are poorly understood, especially within the context of a host environment. In this article, we investigated how antibiotic resistance mutations affect the ability of , the causative agent of tuberculosis, to grow under host-relevant conditions. Using techniques that characterize growth and metabolism, we demonstrate that antibiotic-resistant can have both increased and decreased growth depending on the media carbon source, highlighting how interactions between drug resistance traits and the environment affect the ability of to adapt to changing conditions. We also show that unrelated antibiotic-resistant strains share similar metabolic defects, which can be exploited to improve antimicrobial susceptibility. Overall, this work demonstrates that drug resistance reshapes the physiology of in growth-dependent ways, having major implications for our understanding of how drug resistance evolves within the host context and for the design of new treatment strategies against antibiotic-resistant .
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6. Pangolin-derived sarbecoviruses show attenuated pathogenicity and transmissibility than SARS-CoV-2 in human ACE2 transgenic hamsters.
PMID:日期:2026-09-24Genetic diversity of sarbecoviruses phylogenetically related to SARS-CoV-2 has been identified in Malayan pangolins. However, their potential pathogenicity and risk of cross-species transmission to humans remain largely unknown. In the present study, we performed comparative characterization of SARS-CoV-2 and two pangolin SARS-CoV-2-related viruses, named MpCoV-GD and MpCoV-GX, respectively, in human cell lines and organoids and human ACE2 (hACE2) transgenic hamsters. The cell-to-cell fusion assay showed that the Spike (S) protein of MpCoV-GD induces a stronger membrane fusion than the MpCoV-GX S protein, though weaker than the SARS-CoV-2 S protein. In human cells and organoids, both MpCoV-GX and MpCoV-GD replicated well but less efficiently than SARS-CoV-2. In K18-hACE2 hamsters, MpCoV-GD induced lung pathology comparable to SARS-CoV-2 by showing extensive damage to the alveolar parenchyma, while MpCoV-GX mainly caused alveolar wall thickening due to mild inflammatory cell infiltration. Similar to SARS-CoV-2, the two pangolin coronaviruses were capable of transmitting through direct contact and aerosol exposure, but their infectivity was largely attenuated during aerosol transmission. This study expands our understanding of the biological and infection features of the pangolin-derived sarbecoviruses. It demonstrates that current SARS-CoV-2-related therapeutics and pre-existing immunity can elicit cross-protection against the pangolin sarbecoviruses. Although their pathogenicity and transmissibility are relatively low, our findings suggest the necessity of continuing sarbecovirus surveillance in pangolins and other wildlife for prevention of future disease emergence.IMPORTANCEPangolin-derived sarbecoviruses capable of infecting human cells underscore the role of wildlife as reservoirs for potential zoonotic emergence. MpCoV-GD induces lung pathology comparable to SARS-CoV-2 in hACE2 hamsters, highlighting the need for proactive assessment of novel coronaviruses. Although aerosol transmission of MpCoV-GD and MpCoV-GX is attenuated, their ability to spread via direct contact and airborne routes indicates a tangible risk of cross-species transmission. Importantly, cross-neutralizing activity or inhibition conferred by existing SARS-CoV-2 immunity and therapeutics suggests that current preparedness strategies may help mitigate their impact. These findings reinforce the necessity of sustained surveillance of sarbecoviruses in pangolins and other wildlife to enable early detection and prevention of future outbreaks with significant public health consequences.
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7. {"_":" contributes to human neutrophil evasion via mechanisms independent of β-glucan unmasking.","i":["Candida auris MNN1"]}
PMID:日期:2026-09-24Systemic () infections can have mortality rates up to 60%, and little is known about immune responses to this fungal pathogen. Neutrophils play a major role in immunity to many fungal pathogens, including species. However, neutrophils internalize at a lower rate than . We previously found that the cell wall mannan blocks access to β-glucan, an immunostimulatory motif. Here, we analyzed the immune-evasion properties of mannan separate from glucan masking. We generated eight mannosylation mutants and identified two with increased rates of phagocytosis by human neutrophils. One of these mutants, Δ, did not exhibit increased exposure of β-glucan. Nuclear magnetic resonance analysis of Δ mannan showed decreased α-1,3-mannose linkages and acid-labile side chains. These structural changes increased the affinity of human Dectin-2 and Mincle for mannans , and Fab blocking of Dectin-2 decreased human neutrophil phagocytosis of Δ. Overall, our work provides insight into human neutrophil recognition of mannans and further understanding of mechanisms of immune evasion for this fungal pathogen.IMPORTANCECell surface glycan recognition plays an important role in the innate immune response to fungal pathogens. Here, we use mannosylation mutants to identify genes that contribute to its neutrophil evasion properties. We identify a mannosylation gene, , that contributes to human and murine peripheral blood neutrophil evasion without significantly impacting beta-glucan masking. We attribute to the alteration of cell surface mannans that leads to decreased Dectin-2-binding affinity. While mannan has been associated with masking β-glucan in the cell wall, the impact of specific mannan structures on receptor binding presents an additional mechanism of neutrophil evasion for .
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8. {"_":"Discovery and characterization of a pigment produced by .","i":["Streptococcus pyogenes"]}
PMID:日期:2026-09-23is a major human-restricted pathogen capable of both localized and systemic diseases, as well as causing post-infectious acute and chronic rheumatological conditions. Despite its well-documented clinical importance and over a century of extensive research, gaps persist in understanding this pathogen. We report the discovery of a novel pigment produced by when cultured in a replete, chemically defined medium. Color development accumulates during growth, requires exposure to oxygen, and remains associated with the bacterial cell. Though only 20% of a small strain collection produced the pigment (8 of 40), positive cultures were overrepresented by M1 and M89 serotypes. Given that pigments are critical virulence and fitness determinants in pathogens like , here, we describe initial attempts to characterize pigment biosynthesis, regulation, and potential benefits to the organism. A total of 20,405 transposon mutants were screened for pigment loss in liquid culture, and we identified 94 independent hits enriched in pathways associated with isoprenoid biosynthesis, purine biosynthesis, guanosine transport, and mixed acid fermentation. Although color development requires oxygen, the extracted pigment did not provide antioxidative activity as compared with non-pigmented extracts. Pigment production was inhibited when the Rgg2/Rgg3 quorum-sensing system was active, though by an unknown mechanism. Treatment of RAW-Blue macrophages with the extracted pigment significantly reduced NFκB activation, suggesting a potential anti-inflammatory effect. Overall, this study describes a previously uncharacterized pigment produced by and provides insights into its oxygen-dependent production and associated metabolic pathways. is a ubiquitous pathogen responsible for ~1.8 million severe infections and 500,000 deaths annually. This organism has not been recognized as a pigment-producing bacterium, but here we identify and characterize the production of a previously unreported colorful compound generated when cultured in a chemically defined medium. This finding reveals an underexplored aspect of biology and raises the question of its contribution to pathogenesis. Given the established roles of microbial pigments in virulence and immune modulation in other pathogens, this work provides a foundation for future investigations into its functional significance and potential as a target for therapeutic or vaccine development.
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9. {"_":"mGem: The two-decade evolution of coral microbiome manipulations.","i":["in vivo"]}
PMID:日期:2026-09-22Over the past two decades, microbiome manipulations have emerged as a strategy to bolster coral fitness. Here, we provide a timeline of two decades of research on coral microbiome manipulation studies aimed at improving coral health. A summary of coral hosts, probiotic taxa, and how experimental design varies across studies is synthesized to identify commonly used taxa and research gaps. This review highlights methodological challenges and identifies opportunities to advance probiotic development and translate microbial interventions into practical tools for coral restoration and reef management.
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10. HCMV US30 induces TMED10-DRP1-mediated mitochondrial fission and apoptosis to promote viral multiplication.
PMID:日期:2026-09-22Human cytomegalovirus (HCMV) hijacks host components to modulate cell death for its optimized replication and dissemination. We identified HCMV US30 as a viral factor that induces caspase-dependent apoptosis. US30 induces both DRP1-dependent mitochondrial fission and subsequent apoptosis, as well as IRE1α-mediated unfolded protein responses (UPR). Mechanistically, US30 interacts with NPL4 to impair ER-associated protein degradation and subsequently induce UPR. In parallel, US30 associates with the Endoplasmic reticulum-Golgi intermediate compartment (ERGIC) protein TMED10 and promotes its translocation to the cytoplasm, where it activates DRP1 to initiate mitochondrial fission and subsequent caspase-dependent apoptosis. US30 induces UPR and mitochondrial fission/apoptosis via distinct domains, and the two distinct effects are uncoupled. We also show that US30-induced mitochondrial fission and apoptosis, but not UPR, contribute to the multiplication and dissemination of HCMV. These findings reveal that HCMV US30 induces mitochondrial fission and apoptosis to promote viral replication and dissemination and provide potential targets for intervention of HCMV-induced diseases.IMPORTANCEHuman cytomegalovirus (HCMV) is a human pathogenic herpesvirus that causes global epidemics. HCMV hijacks cellular compartments to maintain its replication and dissemination, which is associated with host cell fate. Here, we identified HCMV US30 as a viral factor to induce caspase-dependent apoptosis. Proteomics analysis revealed that US30 disrupts both ER and mitochondrial homeostasis. We further found that US30-induced mitochondrial fission, but not UPR, mediates apoptosis. Mechanistically, our results indicate that US30 interacts with NPL4 to activate UPR and associates with TMED10 to trigger mitochondrial fission, which are dependent on distinct domains of US30. Most importantly, we found that US30 alters the localization of TMED10 from ERGIC to the cytosol to activate DRP1. Finally, our results showed that US30-induced mitochondrial fission and apoptosis, but not UPR, contribute to the multiplication and dissemination of HCMV. These findings enhance our understanding of HCMV-host interplay and provide potential targets for intervention of HCMV-induced diseases.