The neonatal Fc receptor (FcRn) is a pan-arterivirus receptor

Teressa M. Shaw, Devra Huey, Makky Mousa-Makky, Jared Compaleo, Kylie Nennig, Aadit P. Shah, Fei Jiang, Xueer Qiu, Devon Klipsic, Raymond R. R. Rowland, Igor I. Slukvin, Meagan E. Sullender, Megan T. Baldridge, Haichang Li, Cody J. Warren () and Adam L. Bailey ()
Additional contact information
Teressa M. Shaw: University of Wisconsin–Madison School of Medicine and Public Health
Devra Huey: The Ohio State University
Makky Mousa-Makky: The Ohio State University
Jared Compaleo: The Ohio State University
Kylie Nennig: University of Wisconsin–Madison School of Medicine and Public Health
Aadit P. Shah: Stanford University School of Medicine
Fei Jiang: The Ohio State University
Xueer Qiu: University of Wisconsin–Madison School of Medicine and Public Health
Devon Klipsic: University of Wisconsin–Madison
Raymond R. R. Rowland: University of Illinois Urbana-Champaign
Igor I. Slukvin: University of Wisconsin–Madison School of Medicine and Public Health
Meagan E. Sullender: Washington University School of Medicine
Megan T. Baldridge: Washington University School of Medicine
Haichang Li: The Ohio State University
Cody J. Warren: The Ohio State University
Adam L. Bailey: University of Wisconsin–Madison School of Medicine and Public Health

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract Arteriviruses infect a variety of mammalian hosts, but the receptors used by these viruses to enter cells are poorly understood. We identified the neonatal Fc receptor (FcRn) as an important pro-viral host factor via comparative genome-wide CRISPR-knockout screens with multiple arteriviruses. Using a panel of cell lines and divergent arteriviruses, we demonstrate that FcRn is required for the entry step of arterivirus infection and serves as a molecular barrier to arterivirus cross-species infection. We also show that FcRn synergizes with another known arterivirus entry factor, CD163, to mediate arterivirus entry. Overexpression of FcRn and CD163 sensitizes non-permissive cells to infection and enables the culture of fastidious arteriviruses. Treatment of multiple cell lines with a pre-clinical anti-FcRn monoclonal antibody blocked infection and rescued cells from arterivirus-induced death. Altogether, this study identifies FcRn as a novel pan-arterivirus receptor, with implications for arterivirus emergence, cross-species infection, and host-directed pan-arterivirus countermeasure development.

Date: 2024
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DOI: 10.1038/s41467-024-51142-x

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