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本文引用的文献

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Histo-blood group antigen-like substances of human enteric bacteria as specific adsorbents for human noroviruses.人类肠道细菌的组织血型抗原样物质作为人类诺如病毒的特异性吸附剂。
J Virol. 2013 Sep;87(17):9441-51. doi: 10.1128/JVI.01060-13. Epub 2013 Jun 26.
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Structure of human enterovirus 71 in complex with a capsid-binding inhibitor.人肠道病毒 71 结构与其衣壳结合抑制剂复合物。
Proc Natl Acad Sci U S A. 2013 Apr 2;110(14):5463-7. doi: 10.1073/pnas.1222379110. Epub 2013 Mar 18.
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Functional interactions between the gut microbiota and host metabolism.肠道微生物群与宿主代谢的功能相互作用。
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The gut microbiota in IBD.炎症性肠病中的肠道微生物群。
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A plate-based high-throughput assay for virus stability and vaccine formulation.基于平板的高通量病毒稳定性和疫苗配方检测方法。
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Glycan-modifying bacteria-derived soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei inhibit rotavirus infection in human intestinal cells.拟杆菌属和干酪乳杆菌来源的糖基修饰细菌衍生可溶性因子抑制人肠道细胞中的轮状病毒感染。
Microbes Infect. 2012 Mar;14(3):273-8. doi: 10.1016/j.micinf.2011.10.007. Epub 2011 Oct 25.
7
Intestinal microbiota promote enteric virus replication and systemic pathogenesis.肠道微生物促进肠道病毒复制和全身发病机制。
Science. 2011 Oct 14;334(6053):249-52. doi: 10.1126/science.1211057.
8
Successful transmission of a retrovirus depends on the commensal microbiota.逆转录病毒的成功传播取决于共生微生物菌群。
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Microbiota regulates immune defense against respiratory tract influenza A virus infection.微生物组调节免疫防御抵抗呼吸道流感 A 病毒感染。
Proc Natl Acad Sci U S A. 2011 Mar 29;108(13):5354-9. doi: 10.1073/pnas.1019378108. Epub 2011 Mar 14.
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Inadequately treated wastewater as a source of human enteric viruses in the environment.处理不充分的废水是环境中人类肠道病毒的来源之一。
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细菌脂多糖结合增强了病毒粒子的稳定性,并促进了肠道病毒的环境适应性。

Bacterial lipopolysaccharide binding enhances virion stability and promotes environmental fitness of an enteric virus.

机构信息

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

出版信息

Cell Host Microbe. 2014 Jan 15;15(1):36-46. doi: 10.1016/j.chom.2013.12.004.

DOI:10.1016/j.chom.2013.12.004
PMID:24439896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3920179/
Abstract

Enteric viruses, including poliovirus and reovirus, encounter a vast microbial community in the mammalian gastrointestinal tract, which has been shown to promote virus replication and pathogenesis. Investigating the underlying mechanisms, we find that poliovirus binds bacterial surface polysaccharides, which enhances virion stability and cell attachment by increasing binding to the viral receptor. Additionally, we identified a poliovirus mutant, VP1-T99K, with reduced lipopolysaccharide (LPS) binding. Although T99K and WT poliovirus cell attachment, replication, and pathogenesis in mice are equivalent, VP1-T99K poliovirus was unstable in feces following peroral inoculation of mice. Consequently, the ratio of mutant virus in feces is reduced following additional cycles of infection in mice. Thus, the mutant virus incurs a fitness cost when environmental stability is a factor. These data suggest that poliovirus binds bacterial surface polysaccharides, enhancing cell attachment and environmental stability, potentially promoting transmission to a new host.

摘要

肠道病毒,包括脊髓灰质炎病毒和呼肠孤病毒,在哺乳动物的胃肠道中遇到了庞大的微生物群落,这已被证明可促进病毒复制和发病机制。在研究潜在机制时,我们发现脊髓灰质炎病毒结合细菌表面多糖,通过增加与病毒受体的结合,提高了病毒粒子的稳定性和细胞附着性。此外,我们还鉴定出一种脊髓灰质炎病毒突变体 VP1-T99K,其与脂多糖 (LPS) 的结合减少。尽管 T99K 和 WT 脊髓灰质炎病毒在小鼠中的细胞附着、复制和发病机制相当,但 VP1-T99K 脊髓灰质炎病毒在经口接种小鼠的粪便中不稳定。因此,在小鼠中进行多次感染后,粪便中突变病毒的比例降低。因此,当环境稳定性成为一个因素时,突变病毒会产生适应性成本。这些数据表明,脊髓灰质炎病毒结合细菌表面多糖,增强了细胞附着和环境稳定性,可能促进了向新宿主的传播。