期刊
NATURE MICROBIOLOGY
卷 4, 期 7, 页码 1120-1128出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41564-019-0416-7
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资金
- Children's Discovery Institute of Washington University
- St Louis Children's Hospital Postdoctoral Research grant [MI-F-2018-712]
- Basic Science Research Program through the National Research Foundation of Korea - Ministry of Education [NRF-2016R1A6A3A03012352]
- Pediatric Infectious Diseases Society/St Jude Children's Research Hospital Fellowship Program in Basic Research
- NIH training grant [T32AI106688, T32AI007163]
- ALSAC
- NIH [R03 AI126101-01, K08 AR07091, K22 AI127846, R01 AI127552, R01 AI139314, R01 AI141478]
- Digestive Diseases Research Core Centers [P30 DK052574]
- Pew Biomedical Scholars Program
- Global Probiotics Council's Young Investigator Grant for Probiotics Research
Commensal microbes profoundly impact host immunity to enteric viral infections(1). We have shown that the bacterial microbiota and host antiviral cytokine interferon-lambda (IFN-lambda) determine the persistence of murine norovirus in the gut(2,3). However, the effects of the virome in modulating enteric infections remain unexplored. Here, we report that murine astrovirus can complement primary immunodeficiency to protect against murine norovirus and rotavirus infections. Protection against infection was horizontally transferable between immunocompromised mouse strains by co-housing and fecal transplantation. Furthermore, protection against enteric pathogens corresponded with the presence of a specific strain of murine astrovirus in the gut, and this complementation of immunodeficiency required IFN-lambda signalling in gut epithelial cells. Our study demonstrates that elements of the virome can protect against enteric pathogens in an immunodeficient host.
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