Abstract
Human norovirus is a major human pathogen causing the majority of cases of viral gastroenteritis globally. Viral entry is the first step of the viral life cycle and is a significant determinant of cell tropism, host range, immune interactions, and pathogenesis. Bile salts and histo-blood group antigens are key mediators of norovirus entry; however, the molecular mechanisms by which these molecules promote infection and the identity of a potential human norovirus receptor remain unknown. Recently, there have been several important advances in norovirus entry biology including the identification of CD300lf as the receptor for murine norovirus and of the role of the minor capsid protein VP2 in viral genome release. Here, we will review the current understanding about norovirus attachment and entry and highlight important future directions.
Highlights
Human norovirus (HNoV) is the leading cause of acute gastroenteritis worldwide causing roughly700 million infections and 200,000 deaths annually [1,2]
Recent genome-wide CRISPR screens identified CD300lf as the proteinaceous receptor for mouse norovirus (MNoV), the first receptor described of any norovirus [26,33], while recent cryo-electron microscopy studies revealed insight into the molecular mechanism of feline calicivirus (FCV) entry and viral genome delivery [34,35,36]
Non-enveloped virus entry is a multi-step process starting with viral attachment to target cells, followed by receptor engagement, endocytosis, cell membrane penetration, and uncoating that culminates in the delivery of the viral genome into the cytoplasm [5] (Figure 1)
Summary
Human norovirus (HNoV) is the leading cause of acute gastroenteritis worldwide causing roughly. Recent genome-wide CRISPR screens identified CD300lf as the proteinaceous receptor for MNoV, the first receptor described of any norovirus [26,33], while recent cryo-electron microscopy studies revealed insight into the molecular mechanism of FCV entry and viral genome delivery [34,35,36]. These studies have important implications in understanding HNoV entry and pathogenesis
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