ArticleVirology2002
Communication between S1N330 and a region in S2 of murine coronavirus spike protein is important for virus entry into cells expressing CEACAM1b receptor.
Article in Virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 31 citations in OpenAlex.
- Evaluating the Immunogenicity of a RecombinantBiology · 2026Article
- Variable Expression of Opa Proteins by Neisseria gonorrhoeae Influences Bacterial Association and Phagocytic Killing by Human Neutrophils.Journal of bacteriology · 2022Article
- Reduction of Cell Fusion by Deletion in the Hypervariable Region of the Spike Protein of Mouse Hepatitis Virus.Viruses · 2022Article
- Identification of H209 as Essential for pH 8-Triggered Receptor-Independent Syncytium Formation by S Protein of Mouse Hepatitis Virus A59.Journal of virology · 2018Article
- Review
- Mutation in the cytoplasmic retrieval signal of porcine epidemic diarrhea virus spike (S) protein is responsible for enhanced fusion activity.Virus research · 2011Article
- Spongiform degeneration induced by neuropathogenic murine coronavirus infection.Pathology international · 2011Article
- Coronavirus pathogenesis.Advances in virus research · 2011Review
- Pathogenesis of murine coronavirus in the central nervous system.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Review
- Amino acid substitutions in the S2 subunit of mouse hepatitis virus variant V51 encode determinants of host range expansion.Journal of virology · 2008Article
- Amino acid substitutions in the s2 region enhance severe acute respiratory syndrome coronavirus infectivity in rat angiotensin-converting enzyme 2-expressing cells.Journal of virology · 2007Article
- Cooperative involvement of the S1 and S2 subunits of the murine coronavirus spike protein in receptor binding and extended host range.Journal of virology · 2006Article
- Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.Microbiology and molecular biology reviews : MMBR · 2005Review
- N-terminal domain of the murine coronavirus receptor CEACAM1 is responsible for fusogenic activation and conformational changes of the spike protein.Journal of virology · 2004Article
- Enhanced virulence mediated by the murine coronavirus, mouse hepatitis virus strain JHM, is associated with a glycine at residue 310 of the spike glycoprotein.Journal of virology · 2003Article
- Article
- The coronavirus spike protein is a class I virus fusion protein: structural and functional characterization of the fusion core complex.Journal of virology · 2003Article
- Receptor-induced conformational changes of murine coronavirus spike protein.Journal of virology · 2002Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The soluble receptor-resistant (srr) mutants, srr7 and srr11, isolated from a murine coronavirus, mouse hepatitis virus (MHV) JHMV, have an amino acid mutation at positions 1114 (Leu to Phe) and 65 (Leu to His), respectively, in the spike (S) protein. These mutants failed to efficiently infect BHK cells expressing CEACAM1b (BHK-R2), due to their low entry into this cell line, although they infected cells expressing CEACAM1a (BHK-R1) in a manner similar to that of wild-type (wt) JHMV cl-2 (Matsuyama and Taguchi, Virology 273, 80-89, 2000). Following the repeated passage of these mutants through BHK-R2 cells, viruses were no longer isolated from srr11-infected cells, while two distinct mutants, srr7A and srr7B, were obtained from srr7-infected cells. Srr7A and srr7B grew 2 log10 higher than srr7 and induced fusion in BHK-R2 cells, being similar to wt virus. In addition to the amino acid change at position 1114 that stemmed from parental srr7, srr7A and srr7B had mutations around position 280, corresponding to the third region of the S1N330 receptor-binding site (S1N330-III) common to all MHV strains examined thus far. Srr7A and srr7B S proteins showed high fusogenicity in both BHK-R1 and BHK-R2 cells, like the wt virus, while srr7Aa and srr7Ba S proteins, which had mutations in S1N330-III but not at amino acid 1114, exhibited profoundly reduced fusion activity in these cell lines. These findings suggest that communication between S1N330-III and the amino acid at position 1114 is important for efficient fusion activity in BHK-R2 cells. S1N330-III is a possible region in the S1 involved in viral entry into cells.
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