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

被引：337
作者：
Baldridge, Megan T. [1 ]
Nice, Timothy J. [1 ]
McCune, Broc T. [1 ]
Yokoyama, Christine C. [1 ]
Kambal, Amal [1 ]
Wheadon, Michael [1 ]
Diamond, Michael S. [1 ,2 ,3 ]
Ivanova, Yulia [1 ]
Artyomov, Maxim [1 ]
Virgin, Herbert W. [1 ]
机构：
[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA
[3] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA
来源：
SCIENCE | 2015年 / 347卷 / 6219期
关键词：
III INTERFERON; REPLICATION; SUSCEPTIBILITY; TRANSMISSION; SUFFICIENT; AUTOPHAGY; IMMUNITY; ATG16L1;
D O I：
10.1126/science.1258025
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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-lambda, 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
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页码：266 / 269
页数：4
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