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Science. 2018 Apr 13;360(6385):204-208. doi: 10.1126/science.aar3799.

Tropism for tuft cells determines immune promotion of norovirus pathogenesis.

Author information

1
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
2
Department of Microbiology and Immunology, University of Illinois at Chicago College of Medicine, Chicago, IL, USA.
3
Department of Immunology and Infectious Disease, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
4
Kimmel Center for Biology and Medicine at the Skirball Institute and Department of Microbiology, New York University School of Medicine, New York, NY 10016, USA.
5
Department of Immunology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.
6
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
7
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.

Abstract

Complex interactions between host immunity and the microbiome regulate norovirus infection. However, the mechanism of host immune promotion of enteric virus infection remains obscure. The cellular tropism of noroviruses is also unknown. Recently, we identified CD300lf as a murine norovirus (MNoV) receptor. In this study, we have shown that tuft cells, a rare type of intestinal epithelial cell, express CD300lf and are the target cell for MNoV in the mouse intestine. We found that type 2 cytokines, which induce tuft cell proliferation, promote MNoV infection in vivo. These cytokines can replace the effect of commensal microbiota in promoting virus infection. Our work thus provides insight into how the immune system and microbes can coordinately promote enteric viral infection.

Comment in

PMID:
29650672
PMCID:
PMC6039974
DOI:
10.1126/science.aar3799
[Indexed for MEDLINE]
Free PMC Article

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