Key result
CD300lf is an essential proteinaceous receptor for murine norovirus infection, and its expression in human cells breaks the species barrier for viral replication.
The identification of CD300lf as a proteinaceous receptor for murine norovirus reveals that receptor presence is the primary determinant of species tropism.
Receptor expression dictates MNoV species tropism; extends animal models but leaves open human norovirus translation.
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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Orchard et al. (2016) studied Norovirus infection. CD300lf expression or knockout vs. Wild-type cells/mice was evaluated on Murine norovirus binding, replication, and cell death. CD300lf is an essential proteinaceous receptor for murine norovirus infection, and its expression in human cells breaks the species barrier for viral replication.
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