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肠道微生物促进肠道病毒复制和全身发病机制。

Intestinal microbiota promote enteric virus replication and systemic pathogenesis.

机构信息

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

出版信息

Science. 2011 Oct 14;334(6053):249-52. doi: 10.1126/science.1211057.

Abstract

Intestinal bacteria aid host health and limit bacterial pathogen colonization. However, the influence of bacteria on enteric viruses is largely unknown. We depleted the intestinal microbiota of mice with antibiotics before inoculation with poliovirus, an enteric virus. Antibiotic-treated mice were less susceptible to poliovirus disease and supported minimal viral replication in the intestine. Exposure to bacteria or their N-acetylglucosamine-containing surface polysaccharides, including lipopolysaccharide and peptidoglycan, enhanced poliovirus infectivity. We found that poliovirus binds lipopolysaccharide, and exposure of poliovirus to bacteria enhanced host cell association and infection. The pathogenesis of reovirus, an unrelated enteric virus, also was more severe in the presence of intestinal microbes. These results suggest that antibiotic-mediated microbiota depletion diminishes enteric virus infection and that enteric viruses exploit intestinal microbes for replication and transmission.

摘要

肠道细菌有助于宿主健康并限制细菌病原体的定植。然而,细菌对肠道病毒的影响在很大程度上尚不清楚。我们在用脊髓灰质炎病毒(一种肠道病毒)接种前用抗生素耗尽了小鼠的肠道菌群。经抗生素处理的小鼠对脊髓灰质炎病毒病的易感性降低,并且在肠道中支持最小的病毒复制。暴露于细菌或其含有 N-乙酰葡萄糖胺的表面多糖,包括脂多糖和肽聚糖,增强了脊髓灰质炎病毒的感染力。我们发现脊髓灰质炎病毒结合脂多糖,并且脊髓灰质炎病毒暴露于细菌会增强宿主细胞的关联和感染。肠道微生物的存在也会加重与肠道病毒无关的呼肠孤病毒的发病机制。这些结果表明,抗生素介导的微生物组耗竭可减少肠道病毒感染,并且肠道病毒利用肠道微生物进行复制和传播。

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