CD300lf is the primary physiologic receptor of murine norovirus but not human norovirus.

Autor: Graziano VR; Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America., Walker FC; Department of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, Saint Louis, Missouri, United States of America., Kennedy EA; Department of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, Saint Louis, Missouri, United States of America., Wei J; Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America., Ettayebi K; Departments of Medicine and Molecular Virology & Microbiology, Baylor College of Medicine, Houston, Texas, United States of America., Strine MS; Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America., Filler RB; Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America., Hassan E; Department of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, Saint Louis, Missouri, United States of America., Hsieh LL; Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, United States of America., Kim AS; Department of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, Saint Louis, Missouri, United States of America., Kolawole AO; Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America., Wobus CE; Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America., Lindesmith LC; Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, United States of America., Baric RS; Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, United States of America., Estes MK; Departments of Medicine and Molecular Virology & Microbiology, Baylor College of Medicine, Houston, Texas, United States of America., Orchard RC; Department of Immunology, University of Texas Southwestern Medical School, Dallas, Texas, United States of America., Baldridge MT; Department of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, Saint Louis, Missouri, United States of America., Wilen CB; Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Jazyk: angličtina
Zdroj: PLoS pathogens [PLoS Pathog] 2020 Apr 06; Vol. 16 (4), pp. e1008242. Date of Electronic Publication: 2020 Apr 06 (Print Publication: 2020).
DOI: 10.1371/journal.ppat.1008242
Abstrakt: Murine norovirus (MNoV) is an important model of human norovirus (HNoV) and mucosal virus infection more broadly. Viral receptor utilization is a major determinant of cell tropism, host range, and pathogenesis. The bona fide receptor for HNoV is unknown. Recently, we identified CD300lf as a proteinaceous receptor for MNoV. Interestingly, its paralogue CD300ld was also sufficient for MNoV infection in vitro. Here we explored whether CD300lf is the sole physiologic receptor in vivo and whether HNoV can use a CD300 ortholog as an entry receptor. We report that both CD300ld and CD300lf are sufficient for infection by diverse MNoV strains in vitro. We further demonstrate that CD300lf is essential for both oral and parenteral MNoV infection and to elicit anti-MNoV humoral responses in vivo. In mice deficient in STAT1 signaling, CD300lf is required for MNoV-induced lethality. Finally, we demonstrate that human CD300lf (huCD300lf) is not essential for HNoV infection, nor does huCD300lf inhibit binding of HNoV virus-like particles to glycans. Thus, we report huCD300lf is not a receptor for HNoV.
Competing Interests: CBW and RCO are inventors on a patent application submitted by Washington University entitled “Receptor for norovirus and uses thereof” (U.S. Provisional Application 62/301,965).
Databáze: MEDLINE
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