Commensal microbes and interferon-λ determine persistence of enteric murine norovirus infection.

Commensal microbes and interferon-λ determine persistence of enteric murine norovirus infection.
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DOI:
10.1126/science.1258025
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发表时间:
2015-01-16
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Virgin HW
Virgin HW
中科院分区:
其他
文献类型:
--
作者:
Baldridge MT;Nice TJ;McCune BT;Yokoyama CC;Kambal A;Wheadon M;Diamond MS;Ivanova Y;Artyomov M;Virgin HW

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人类诺如病毒(NoV)导致全球90%以上的流行性非细菌性胃肠炎,其持续感染一部分人的能力可能有助于其传播。这种肠道病毒如何建立持续感染还不清楚。我们发现抗生素可以预防持续性鼠诺如病毒(MNoV)感染,这种效果可以通过补充细菌微生物群来逆转。抗生素不能预防组织感染或影响系统性病毒复制,但在肠道中有特异性作用。抗病毒细胞因子干扰素-λ的受体Ifnlr 1以及转录因子Stat 1和Irf 3是抗生素预防病毒持续存在所必需的。因此,细菌微生物组以被先天免疫系统的特定组分抵消的方式促进肠道病毒持续存在。
The capacity of human norovirus (NoV), which causes >90% of global epidemic nonbacterial gastroenteritis, to infect a subset of people persistently may contribute to its spread. How such enteric viruses establish persistent infections is not well understood. We found that antibiotics prevented persistent murine norovirus (MNoV) infection, an effect that was reversed by replenishment of the bacterial microbiota. Antibiotics did not prevent tissue infection or affect systemic viral replication but acted specifically in the intestine. The receptor for the antiviral cytokine interferon-λ, Ifnlr1, as well as the transcription factors Stat1 and Irf3, were required for antibiotics to prevent viral persistence. Thus, the bacterial microbiome fosters enteric viral persistence in a manner counteracted by specific components of the innate immune system.
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