ArticleJournal of virology2006
Both spike and background genes contribute to murine coronavirus neurovirulence.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 61 citations in OpenAlex.
- Adaptive variations in SARS-CoV-2 spike proteins: effects on distinct virus-cell entry stages.mBio · 2023Article
- Ablation of microglia following infection of the central nervous system with a neurotropic murine coronavirus infection leads to increased demyelination and impaired remyelination.Journal of neuroimmunology · 2023Article
- ICU Delirium Is Associated with Cardiovascular Burden and Higher Mortality in Patients with Severe COVID-19 Pneumonia.Journal of clinical medicine · 2023Article
- Reverse Genetic Assessment of the Roles Played by the Spike Protein and ORF3 in Porcine Epidemic Diarrhea Virus Pathogenicity.Journal of virology · 2023Article
- Insights into coronavirus immunity taught by the murine coronavirus.European journal of immunology · 2021Review
- Clinical and molecular aspects of veterinary coronaviruses.Virus research · 2021Review
- Neurological Manifestations of COVID-19: Causality or Coincidence?Aging and disease · 2021Article
- COVID-19: ICU delirium management during SARS-CoV-2 pandemic.Critical care (London, England) · 2020Review
- Innate Immune Responses and Viral-Induced Neurologic Disease.Journal of clinical medicine · 2018Review
- Role of the inflammasome-related cytokines Il-1 and Il-18 during infection with murine coronavirus.Journal of neurovirology · 2017Article
- Porcine Hemagglutinating Encephalomyelitis Virus Enters Neuro-2a Cells via Clathrin-Mediated Endocytosis in a Rab5-, Cholesterol-, and pH-Dependent Manner.Journal of virology · 2017Article
- Locally Produced IL-10 Limits Cutaneous Vaccinia Virus Spread.PLoS pathogens · 2016Article
- Inducible Expression of CXCL1 within the Central Nervous System Amplifies Viral-Induced Demyelination.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- A small region of porcine hemagglutinating encephalomyelitis virus spike protein interacts with the neural cell adhesion molecule.Intervirology · 2015Article
- Human coronaviruses: viral and cellular factors involved in neuroinvasiveness and neuropathogenesis.Virus research · 2014Review
- Neutrophils are needed for an effective immune response against pulmonary rat coronavirus infection, but also contribute to pathology.The Journal of general virology · 2014Article
- Tropism and pathological findings associated with canine respiratory coronavirus (CRCoV).Veterinary microbiology · 2013Article
- Comparative evaluation of two hemagglutinating encephalomyelitis coronavirus vaccine candidates in mice.Clinical and vaccine immunology : CVI · 2012Article
- Roles of the fusion and hemagglutinin-neuraminidase proteins in replication, tropism, and pathogenicity of avian paramyxoviruses.Journal of virology · 2011Article
- Spongiform degeneration induced by neuropathogenic murine coronavirus infection.Pathology international · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Various strains of mouse hepatitis virus (MHV) exhibit different pathogenic phenotypes. Infection with the A59 strain of MHV induces both encephalitis and hepatitis, while the highly neurovirulent JHM strain induces a fatal encephalitis with little, if any, hepatitis. The pathogenic phenotype for each strain is determined by the genetic composition of the viral genome, as well as the host immune response. Using isogenic recombinant viruses with A59 background genes differing only in the spike gene, we have previously shown that high neurovirulence is associated with the JHM spike protein, the protein responsible for attachment to the host cell receptor (J. J. Phillips, M. M. Chua, G. F. Rall, and S. R. Weiss, Virology 301:109-120, 2002). Using another set of isogenic recombinant viruses with JHM background genes expressing either the JHM or A59 spike, we have further investigated the roles of viral genes in pathogenesis. Here, we demonstrate that the high neurovirulence of JHM is associated with accelerated spread through the brain and a heightened innate immune response that is characterized by high numbers of infiltrating neutrophils and macrophages, suggesting an immunopathogenic component to neurovirulence. While expression of the JHM spike is sufficient to confer a neurovirulent phenotype, as well as increased macrophage infiltration, background genes contribute to virulence as well, at least in part, by dictating the extent of the T-cell immune response.
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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.