ArticleJournal of virology2005
Murine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Evolutionary Insight into Fatal Human Coronaviruses (hCoVs) with a Focus on Circulating SARS-CoV-2 Variants Under Monitoring (VUMs).Biomedicines · 2025Review
- Adaptive variations in SARS-CoV-2 spike proteins: effects on distinct virus-cell entry stages.mBio · 2023Article
- Molecular Evolution of Human Coronavirus Genomes.Trends in microbiology · 2017Review
- Coronavirus Spike Protein and Tropism Changes.Advances in virus research · 2016Review
- The heptad repeat region is a major selection target in MERS-CoV and related coronaviruses.Scientific reports · 2015Article
- The nsp1, nsp13, and M proteins contribute to the hepatotropism of murine coronavirus JHM.WU.Journal of virology · 2015Article
- Contributions of the S2 spike ectodomain to attachment and host range of infectious bronchitis virus.Virus research · 2013Article
- Homologous 2',5'-phosphodiesterases from disparate RNA viruses antagonize antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Protective role of Toll-like Receptor 3-induced type I interferon in murine coronavirus infection of macrophages.Viruses · 2012Article
- Coronavirus pathogenesis.Advances in virus research · 2011Review
- Genetic determinants of mouse hepatitis virus strain 1 pneumovirulence.Journal of virology · 2010Article
- 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
- Antiviral effects of antisense morpholino oligomers in murine coronavirus infection models.Journal of virology · 2007Article
- Replicase genes of murine coronavirus strains A59 and JHM are interchangeable: differences in pathogenesis map to the 3' one-third of the genome.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
- Endosomal proteolysis by cathepsins is necessary for murine coronavirus mouse hepatitis virus type 2 spike-mediated entry.Journal of virology · 2006Article
- Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.Microbiology and molecular biology reviews : MMBR · 2005Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Murine coronavirus A59 strain causes mild to moderate hepatitis in mice. We have previously shown that mutants of A59, unable to induce hepatitis, may be selected by persistent infection of primary glial cells in vitro. These in vitro isolated mutants encoded two amino acids substitutions in the spike (S) gene: Q159L lies in the putative receptor binding domain of S, and H716D, within the cleavage signal of S. Here, we show that hepatotropic revertant variants may be selected from these in vitro isolated mutants (Q159L-H716D) by multiple passages in the mouse liver. One of these mutants, hr2, was chosen for more in-depth study based on a more hepatovirulent phenotype. The S gene of hr2 (Q159L-R654H-H716D-E1035D) differed from the in vitro isolates (Q159L-H716D) in only 2 amino acids (R654H and E1035D). Using targeted RNA recombination, we have constructed isogenic recombinant MHV-A59 viruses differing only in these specific amino acids in S (Q159L-R654H-H716D-E1035D). We demonstrate that specific amino acid substitutions within the spike gene of the hr2 isolate determine the ability of the virus to cause lethal hepatitis and replicate to significantly higher titers in the liver compared to wild-type A59. Our results provide compelling evidence of the ability of coronaviruses to rapidly evolve in vivo to highly virulent phenotypes by functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.
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Registered trials
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.