ArticleVirology2003
Amino acid substitutions within the heptad repeat domain 1 of murine coronavirus spike protein restrict viral antigen spread in the central nervous system.
Article in Virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- The Reassessed Potential of SARS-CoV-2 Attenuation for COVID-19 Vaccine Development-A Systematic Review.Viruses · 2022Pooled it
- A Systematic Review of the Neuropathologic Findings of Post-Viral Olfactory Dysfunction: Implications and Novel Insight for the COVID-19 Pandemic.American journal of rhinology & allergy · 2021Pooled it
- Adaptive variations in SARS-CoV-2 spike proteins: effects on distinct virus-cell entry stages.mBio · 2023Article
- Coronavirus Spike Protein and Tropism Changes.Advances in virus research · 2016Review
- The nsp1, nsp13, and M proteins contribute to the hepatotropism of murine coronavirus JHM.WU.Journal of virology · 2015Article
- Coronavirus pathogenesis.Advances in virus research · 2011Review
- Pathogenesis of neurotropic murine coronavirus is multifactorial.Trends in pharmacological sciences · 2011Article
- 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
- Synthetic reconstruction of zoonotic and early human severe acute respiratory syndrome coronavirus isolates that produce fatal disease in aged mice.Journal of virology · 2007Article
- Endosomal proteolysis by cathepsins is necessary for murine coronavirus mouse hepatitis virus type 2 spike-mediated entry.Journal of virology · 2006Article
- Murine encephalitis caused by HCoV-OC43, a human coronavirus with broad species specificity, is partly immune-mediated.Virology · 2006Article
- Human angiotensin-converting enzyme 2 (ACE2) is a receptor for human respiratory coronavirus NL63.Advances in experimental medicine and biology · 2006Article
- Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.Microbiology and molecular biology reviews : MMBR · 2005Review
- Expression of hemagglutinin esterase protein from recombinant mouse hepatitis virus enhances neurovirulence.Journal of virology · 2005Article
- 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
- Viral expression of CCL2 is sufficient to induce demyelination in RAG1-/- mice infected with a neurotropic coronavirus.Journal of virology · 2005Article
- Increased epitope-specific CD8+ T cells prevent murine coronavirus spread to the spinal cord and subsequent demyelination.Journal of virology · 2005Article
- Human respiratory coronavirus OC43: genetic stability and neuroinvasion.Journal of virology · 2004Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Targeted recombination was carried out to select mouse hepatitis viruses (MHVs) in a defined genetic background, containing an MHV-JHM spike gene encoding either three heptad repeat 1 (HR1) substitutions (Q1067H, Q1094H, and L1114R) or L1114R alone. The recombinant virus, which expresses spike with the three substitutions, was nonfusogenic at neutral pH. Its replication was significantly inhibited by lysosomotropic agents, and it was highly neuroattenuated in vivo. In contrast, the recombinant expressing spike with L1114R alone mediated cell-to-cell fusion at neutral pH and replicated efficiently despite the presence of lysosomotropic agents; however, it still caused only subclinical morbidity and no mortality in animals. Thus, both recombinant viruses were highly attenuated and expressed viral antigen which was restricted to the olfactory bulbs and was markedly absent from other regions of the brains at 5 days postinfection. These data demonstrate that amino acid substitutions, in particular L1114R, within HR1 of the JHM spike reduced the ability of MHV to spread in the central nervous system. Furthermore, the requirements for low pH for fusion and viral entry are not prerequisites for the highly attenuated phenotype.
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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.