Genome-wide CRISPR screen demonstrates β4GALNT2 restricts human parainfluenza virus 3 infection in host cells, indicating a glycan-based defense mechanism against respiratory viruses.
Human respirovirus 3 (also known as human parainfluenza virus 3; hPIV3) is a major cause of severe acute respiratory infections in vulnerable populations. Here we conducted a genome-wide CRISPR/Cas9 library screen to identify key host factors for hPIV3 infection. In addition to identifying several host proteins involved in glycosylation as proviral factors, we identified β-1,4-N-Acetyl-Galactosaminyltransferase 2 (β4GALNT2) as a potent restriction factor. Further investigation demonstrated that the addition of a GalNAc residue to α2-3-sialylated glycans by β4GALNT2, resulting in the Sda glycotope, disrupted the interaction between the viral hemagglutinin-neuraminidase (HN) attachment protein and sialoglycan receptors. Specifically, the additional GalNAc residue interfered with the interaction of residue W371 in HN with sub-terminal glycan moieties. β4GALNT2-mediated Sda epitope expression also negatively affected infection by other respiroviruses, with the strongest effect being observed for hPIV3.
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