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.
|
Authors | T M Gallagher, M J Buchmeier, S Perlman |
Journal | Advances in experimental medicine and biology
(Adv Exp Med Biol)
Vol. 342
Pg. 279-84
( 1993)
ISSN: 0065-2598 [Print] United States |
PMID | 8209743
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
|
Chemical References |
- Membrane Glycoproteins
- Receptors, Coronavirus
- Receptors, Virus
- Recombinant Fusion Proteins
- Spike Glycoprotein, Coronavirus
- Viral Envelope Proteins
- spike glycoprotein, SARS-CoV
- spike protein, mouse hepatitis virus
|
Topics |
- Animals
- Astrocytoma
- Cell Fusion
- Cell Line
(microbiology)
- Cricetinae
- Cytopathogenic Effect, Viral
- Genetic Vectors
- Kidney
- Membrane Glycoproteins
(chemistry, physiology)
- Mesocricetus
- Murine hepatitis virus
(physiology)
- Rats
- Receptors, Coronavirus
- Receptors, Virus
(deficiency, physiology)
- Recombinant Fusion Proteins
(metabolism)
- Species Specificity
- Spike Glycoprotein, Coronavirus
- Tumor Cells, Cultured
(microbiology)
- Viral Envelope Proteins
(chemistry, physiology)
- Virus Replication
|