Abstract
In this report, we demonstrate the syncytial spread of MHV4 (strain JHM) infection through non-murine cell cultures which lack a specific MHV4 receptor and are therefore resistant to infection by free virions. This was achieved by allowing infected murine cells to settle onto confluent monolayers of non-murine cells in a straightforward infectious center assay. Receptor-independent syncytium formation induced by cells expressing the MHV4 spike (S) from recombinant vaccinia viruses (VV) indicated that spread was mediated by this coronavirus glycoprotein. We conclude that the S protein of MHV4 is so potently fusogenic that it does not require prior binding to a virus-specific surface receptor to induce fusion of closely-opposed plasma membranes.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Astrocytoma
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Cell Fusion
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Cell Line / microbiology
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Cricetinae
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Cytopathogenic Effect, Viral
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Genetic Vectors
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Kidney
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Membrane Glycoproteins / chemistry
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Membrane Glycoproteins / physiology*
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Mesocricetus
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Murine hepatitis virus / physiology*
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Rats
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Receptors, Coronavirus
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Receptors, Virus / deficiency
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Receptors, Virus / physiology*
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Recombinant Fusion Proteins / metabolism
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Species Specificity
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Spike Glycoprotein, Coronavirus
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Tumor Cells, Cultured / microbiology
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Viral Envelope Proteins / chemistry
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Viral Envelope Proteins / physiology*
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Virus Replication*
Substances
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Membrane Glycoproteins
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Receptors, Coronavirus
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Receptors, Virus
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Recombinant Fusion Proteins
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Spike Glycoprotein, Coronavirus
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Viral Envelope Proteins
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spike glycoprotein, SARS-CoV
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spike protein, mouse hepatitis virus