期刊
SCIENCE
卷 353, 期 6302, 页码 933-936出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf1220
关键词
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资金
- National Cancer Institute Cancer Center [P30 CA091842]
- NIH [U19 AI109725, 1F31CA177194, 5T32CA009547]
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.
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