ArticleJournal of virology1998
Targeted recombination within the spike gene of murine coronavirus mouse hepatitis virus-A59: Q159 is a determinant of hepatotropism.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
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- Reduction of Cell Fusion by Deletion in the Hypervariable Region of the Spike Protein of Mouse Hepatitis Virus.Viruses · 2022Article
- Spike glycoproteins: Their significance for corona viruses and receptor binding activities for pathogenesis and viral survival.Microbial pathogenesis · 2021Review
- A review of genetic methods and models for analysis of coronavirus-induced severe pneumonitis.The Journal of general virology · 2015Review
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- TNF receptor 1 mediates dendritic cell maturation and CD8 T cell response through two distinct mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 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
- A mechanism of virus-induced demyelination.Interdisciplinary perspectives on infectious diseases · 2010Article
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- Animal origins of the severe acute respiratory syndrome coronavirus: insight from ACE2-S-protein interactions.Journal of virology · 2006Review
- Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.Microbiology and molecular biology reviews : MMBR · 2005Review
- Contributions of the viral genetic background and a single amino acid substitution in an immunodominant CD8+ T-cell epitope to murine coronavirus neurovirulence.Journal of virology · 2005Article
- Development of a transgenic mouse model susceptible to human coronavirus 229E.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Murine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.Journal of virology · 2005Article
- Phylogenetic analysis and sequence comparisons of structural and non-structural SARS coronavirus proteins in Taiwan.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2005Article
- Article
- Reasoning of spike glycoproteins being more vulnerable to mutations among 158 coronavirus proteins from different species.Journal of molecular modeling · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies of a group of mutants of the murine coronavirus mouse hepatitis virus (MHV)-A59, isolated from persistently infected glial cells, have shown a strong correlation between a Q159L amino acid substitution in the S1 subunit of the spike gene and a loss in the ability to induce hepatitis and demyelination. To determine if Q159L alone is sufficient to cause these altered pathogenic properties, targeted RNA recombination was used to introduce a Q159L amino acid substitution into the spike gene of MHV-A59. Recombination was carried out between the genome of a temperature-sensitive mutant of MHV-A59 (Alb4) and RNA transcribed from a plasmid (pFV1) containing the spike gene as well as downstream regions, through the 3' end, of the MHV-A59 genome. We have selected and characterized two recombinant viruses containing Q159L. These recombinant viruses (159R36 and 159R40) replicate in the brains of C57BL/6 mice and induce encephalitis to a similar extent as wild-type MHV-A59. However, they exhibit a markedly reduced ability to replicate in the liver or produce hepatitis compared to wild-type MHV-A59. These viruses also exhibit reduced virulence and reduced demyelination. A recombinant virus containing the wild-type MHV-A59 spike gene, wtR10, behaved essentially like wild-type MHV-A59. This is the first report of the isolation of recombinant viruses containing a site-directed mutation, encoding an amino acid substitution, within the spike gene of any coronavirus. This technology will allow us to begin to map the molecular determinants of pathogenesis within the spike glycoprotein.
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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.