ArticleVirology1997
Altered pathogenesis of a mutant of the murine coronavirus MHV-A59 is associated with a Q159L amino acid substitution in the spike protein.
Article in Virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
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- Potential differences in cleavage of the S protein and type-1 interferon together control human coronavirus infection, propagation, and neuropathology within the central nervous system.Journal of virology · 2021Article
- A proline insertion-deletion in the spike glycoprotein fusion peptide of mouse hepatitis virus strongly alters neuropathology.The Journal of biological chemistry · 2019Article
- Effects of hypervariable regions in spike protein on pathogenicity, tropism, and serotypes of infectious bronchitis virus.Virus research · 2018Article
- Structure, Function, and Evolution of Coronavirus Spike Proteins.Annual review of virology · 2016Review
- Receptor recognition mechanisms of coronaviruses: a decade of structural studies.Journal of virology · 2015Review
- Cleavage of a Neuroinvasive Human Respiratory Virus Spike Glycoprotein by Proprotein Convertases Modulates Neurovirulence and Virus Spread within the Central Nervous System.PLoS pathogens · 2015Article
- Coronavirus cell entry occurs through the endo-/lysosomal pathway in a proteolysis-dependent manner.PLoS pathogens · 2014Article
- Middle East respiratory syndrome coronavirus (MERS-CoV): evidence and speculations.Archives of virology · 2014Review
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- Complete genome sequence of a Chinese virulent porcine epidemic diarrhea virus strain.Journal of virology · 2011Article
- Crystal structure of mouse coronavirus receptor-binding domain complexed with its murine receptor.Proceedings of the National Academy of Sciences of the United States of America · 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
- Article
- Organ-specific attenuation of murine hepatitis virus strain A59 by replacement of catalytic residues in the putative viral cyclic phosphodiesterase ns2.Journal of virology · 2009Article
- Article
- Genomic characterization of equine coronavirus.Virology · 2007Article
- Molecular analysis of Brazilian strains of bovine coronavirus (BCoV) reveals a deletion within the hypervariable region of the S1 subunit of the spike glycoprotein also found in human coronavirus OC43.Archives of virology · 2006Article
- Prevalence and genetic diversity of coronaviruses in bats from China.Journal of virology · 2006Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
C12, an attenuated, fusion delayed, very weakly hepatotropic mutant of mouse hepatitis virus strain A59 (MHV-A59( has been further characterized. We have previously shown that C12 has two amino acid substitutions relative to wild type virus in the spike protein, Q159L (within a region of S1 shown to bind to viral receptor in an in vitro assay) and H716D (in the proteolytic cleavage recognition site). We have sequenced the rest of the 31-kb genome of C-12 and compared it to wild type virus. Only three additional amino acids substitutions were found, all encoded within the replicase gene. Analysis of C12 in vivo in C57Bl/6 mice has shown that despite the fact that this virus replicates in the brain to titers at least as high as wild type and causes acute encephalitis similar to wild-type, this virus causes a minimal level of demyelination and only at very high levels of virus inoculation. Thus acute encephalitis is not sufficient for the induction of demyelination by MHV-A59. Analysis of mutants isolated at earlier times from the same persistently infected glial cell culture as C12, as well as mutants isolated from a second independent culture of persistently infected glial cells, suggests that both the weakly demyelinating and the weakly hepatotropic phenotypes of C12 are associated with the Q159L amino acid substitution.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.