自引率: 4.6%
被引量: 3060
通过率: 暂无数据
审稿周期: 6
版面费用: 暂无数据
国人发稿量: 10
投稿须知/期刊简介:
In conformance with the aims of the Japanese Society for Bacteriology, the Japanese Society for Virology, and the Japanese Society for Immunology, this journal is devoted to the world-wide dissemination of advanced knowledge in bacteriology, virology, immunology, and related fields.
期刊描述简介:
Microbiology and Immunology is a multidisciplinary journal aimed at providing insight into the study of microbes and the host immune, biological and physiological responses, and therapeutics. The journal publishes reports of significant results as high quality original articles and notes dealing with advanced research in all fields of bacteriology, virology, and immunology, and related fields; pathogenic infections in humans, various animals including invertebrates, and plants; pathogenicity and virulence factors such as microbial toxins and cell-surface components; factors involved in host defense, inflammation, development of vaccines; antimicrobial agents and drug resistance of microbes; genomics and proteomics. Microbiology and Immunology also features review and mini-review articles targeted broader audience, not limited to researchers in these fields.
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Analysis of neuraminidase activity of human parainfluenza viruses using enzyme-linked lectin assay and BTP3-Neu5Ac assay.
被引量：- 发表：1970
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A single amino acid substitution in the Borna disease virus glycoprotein enhances the infectivity titer of vesicular stomatitis virus pseudotyped virus by altering membrane fusion activity.
被引量：- 发表：1970
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Development of a double-antibody sandwich ELISA for detection of SARS-CoV-2 variants based on nucleocapsid protein-specific antibodies.
被引量：- 发表：1970
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Neutralization mechanism of human monoclonal antibodies against type B botulinum neurotoxin.
Botulism is a deadly neuroparalytic condition caused by the botulinum neurotoxin (BoNT) produced by Clostridium botulinum and related species. Toxin-neutralizing antibodies are the most effective treatments for BoNT intoxication. We generated human monoclonal antibodies neutralizing type B botulinum neurotoxin (BoNT/B), designated M2 and M4. The combination of these antibodies exhibited a strong neutralizing effect against BoNT/B toxicity. In this study, we analyzed the mechanisms of action of these antibodies in vitro. M4 binds to the C-terminus of the heavy chain (the receptor-binding domain) and inhibits BoNT/B binding to neuronal PC12 cells. Although M2 recognized the light (L) chain (the metalloprotease domain), it did not inhibit substrate (VAMP2) cleavage in the cleavage assay. M2 increased the surface localization of BoNT/B in PC12 cells at a later time point, suggesting that M2 inhibits the translocation of the L chain from synaptic vesicles to the cytosol. These results indicate that M2 and M4 inhibit the different processes of BoNT/B individually and that multistep inhibition is important for the synergistic effect of the combination of monoclonal antibodies. Our findings may facilitate the development of effective therapeutic antibodies against BoNTs.
被引量：- 发表：1970
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Statins enhance extracellular release of hepatitis C virus particles through ERK5 activation.
Statins, such as lovastatin, have been known to inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Statins were reported to moderately suppress hepatitis C virus (HCV) replication in cultured cells harboring HCV RNA replicons. We report here using an HCV cell culture (HCVcc) system that high concentrations of lovastatin (5-20 μg/mL) markedly enhanced the release of HCV infectious particles (virion) in the culture supernatants by up to 40 times, without enhancing HCV RNA replication, HCV protein synthesis, or HCV virion assembly in the cells. We also found that lovastatin increased the phosphorylation (activation) level of extracellular-signal-regulated kinase 5 (ERK5) in both the infected and uninfected cells in a dose-dependent manner. The lovastatin-mediated increase of HCV virion release was partially reversed by selective ERK5 inhibitors, BIX02189 and XMD8-92, or by ERK5 knockdown using small interfering RNA (siRNA). Moreover, we demonstrated that other cholesterol-lowering statins, but not dehydrolovastatin that is incapable of inhibiting HMG-CoA reductase and activating ERK5, enhanced HCV virion release to the same extent as observed with lovastatin. These results collectively suggest that statins markedly enhance HCV virion release from infected cells through HMG-CoA reductase inhibition and ERK5 activation.
被引量：- 发表：1970
