ArticleJournal of virology1997
Identification of spike protein residues of murine coronavirus responsible for receptor-binding activity by use of soluble receptor-resistant mutants.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
- Reduction of Cell Fusion by Deletion in the Hypervariable Region of the Spike Protein of Mouse Hepatitis Virus.Viruses · 2022Article
- Membrane Protein of Human Coronavirus NL63 Is Responsible for Interaction with the Adhesion Receptor.Journal of virology · 2019Article
- IL-10 expression in pyramidal neurons after neuropathogenic coronaviral infection.Neuropathology : official journal of the Japanese Society of Neuropathology · 2017Article
- Formation of fibroblastic reticular network in the brain after infection with neurovirulent murine coronavirus.Neuropathology : official journal of the Japanese Society of Neuropathology · 2016Article
- Proteolytic processing of Middle East respiratory syndrome coronavirus spikes expands virus tropism.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Coronavirus Spike Protein and Tropism Changes.Advances in virus research · 2016Review
- Mice lacking α1,3-fucosyltransferase 9 exhibit modulation of in vivo immune responses against pathogens.Pathology international · 2014Article
- Contributions of the S2 spike ectodomain to attachment and host range of infectious bronchitis virus.Virus research · 2013Article
- The soluble form of the EIAV receptor encoded by an alternative splicing variant inhibits EIAV infection of target cells.PloS one · 2013Article
- Spongiform degeneration induced by neuropathogenic murine coronavirus infection.Pathology international · 2011Article
- Pathogenesis of neurotropic murine coronavirus is multifactorial.Trends in pharmacological sciences · 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
- Cytopathy of an infiltrating monocyte lineage during the early phase of infection with murinecoronavirus in the brain.Neuropathology : official journal of the Japanese Society of Neuropathology · 2010Article
- Conformational changes in the capsid of a calicivirus upon interaction with its functional receptor.Journal of virology · 2010Article
- Protease-mediated entry via the endosome of human coronavirus 229E.Journal of virology · 2009Article
- Amino acid substitutions in the S2 subunit of mouse hepatitis virus variant V51 encode determinants of host range expansion.Journal of virology · 2008Article
- Heparan sulfate is a binding molecule but not a receptor for CEACAM1-independent infection of murine coronavirus.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
- Receptor-independent infection of murine coronavirus: analysis by spinoculation.Journal of virology · 2006Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously demonstrated by site-directed mutagenesis analysis that the amino acid residues at positions 62 and 214 to 216 in the N-terminal region of mouse hepatitis virus (MHV) spike (S) protein are important for receptor-binding activity (H. Suzuki and F. Taguchi, J. Virol. 70:2632-2636, 1996). To further identify the residues responsible for the activity, we isolated the mutant viruses that were not neutralized with the soluble form of MHV receptor proteins, since such mutants were expected to have mutations in amino acids responsible for receptor-binding activity. Five soluble-receptor-resistant (srr) mutants isolated had mutations in a single amino acid at three different positions: one was at position 65 (Leu to His) (srr11) in the S1 subunit and three were at position 1114 (Leu to Phe) (srr3, srr4, and srr7) and one was at position 1163 (Cys to Phe) (srr18) in the S2 subunit. The receptor-binding activity examined by a virus overlay protein blot assay and by a coimmunoprecipitation assay showed that srr11 S protein had extremely reduced binding activity, while the srr7 and srr18 proteins had binding activity similar to that of wild-type cl-2 protein. However, when cell surface receptors were used for the binding assay, all srr mutants showed activity similar to that of the wild type or only slightly reduced activity. These results, together with our previous observations, suggest that amino acids located at positions 62 to 65 of S1, a region conserved among the MHV strains examined, are important for receptor-binding activity. We also discuss the mechanism by which srr mutants with a mutation in S2 showed high resistance to neutralization by a soluble receptor, despite their sufficient level of binding to soluble receptors.
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