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Science. 2016 Aug 26;353(6302):933-6. doi: 10.1126/science.aaf1220. Epub 2016 Aug 18.

Discovery of a proteinaceous cellular receptor for a norovirus.

Author information

1
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
2
Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
3
Genome Engineering and iPSC Center, Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA.
4
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.

Abstract

Noroviruses (NoVs) are a leading cause of gastroenteritis globally, yet the host factors required for NoV infection are poorly understood. We identified host molecules that are essential for murine NoV (MNoV)-induced cell death, including CD300lf as a proteinaceous receptor. We found that CD300lf is essential for MNoV binding and replication in cell lines and primary cells. Additionally, Cd300lf(-/-) mice are resistant to MNoV infection. Expression of CD300lf in human cells breaks the species barrier that would otherwise restrict MNoV replication. The crystal structure of the CD300lf ectodomain reveals a potential ligand-binding cleft composed of residues that are critical for MNoV infection. Therefore, the presence of a proteinaceous receptor is the primary determinant of MNoV species tropism, whereas other components of cellular machinery required for NoV replication are conserved between humans and mice.

PMID:
27540007
PMCID:
PMC5484048
DOI:
10.1126/science.aaf1220
[Indexed for MEDLINE]
Free PMC Article

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