ReviewJournal of neurovirology2010
Murine coronavirus neuropathogenesis: determinants of virulence.
Review in Journal of neurovirology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Endolysosome-targeted nanoparticle delivery of antiviral therapy for coronavirus infections.Life science alliance · 2025Article
- CD6 regulates CD4 T follicular helper cell differentiation and humoral immunity during murine coronavirus infection.Journal of virology · 2025Article
- CD6 Regulates CD4 T Follicular Helper Cell Differentiation and Humoral Immunity During Murine Coronavirus Infection.bioRxiv : the preprint server for biology · 2024Article
- Antiviral Activity of Graphene Oxide-Silver Nanocomposites Against Murine Betacoronavirus.International journal of nanomedicine · 2024Article
- A suitable model to investigate acute neurological consequences of coronavirus infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Selective visuoconstructional impairment following mild COVID-19 with inflammatory and neuroimaging correlation findings.Molecular psychiatry · 2023Article
- Non-SARS Coronaviruses in Individuals with Psychiatric Disorders.Current topics in behavioral neurosciences · 2023Article
- Micronutrient Improvement of Epithelial Barrier Function in Various Disease States: A Case for Adjuvant Therapy.International journal of molecular sciences · 2022Review
- Neuropathies and neurological dysfunction induced by coronaviruses.Journal of neurovirology · 2021Review
- Animal Coronaviruses Induced Apoptosis.Life (Basel, Switzerland) · 2021Review
- SARS-CoV-2 and nervous system: From pathogenesis to clinical manifestation.Journal of neuroimmunology · 2021Review
- Evidence of Microglial Immune Response Following Coronavirus PHEV Infection of CNS.Frontiers in immunology · 2021Article
- The Role of Extracellular Vesicles in Demyelination of the Central Nervous System.International journal of molecular sciences · 2020Review
- How SARS-Cov-2 can involve the central nervous system. A systematic analysis of literature of the department of human neurosciences of Sapienza University, Italy.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2020Review
- Review
- Central nervous system involvement by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2).Journal of medical virology · 2020Article
- Involvement of the Nervous System in SARS-CoV-2 Infection.Neurotoxicity research · 2020Review
- Unraveling the Possible Routes of SARS-COV-2 Invasion into the Central Nervous System.Current treatment options in neurology · 2020Review
- Human Coronaviruses and Other Respiratory Viruses: Underestimated Opportunistic Pathogens of the Central Nervous System?Viruses · 2019Review
- Immune Relevant and Immune Deficient Mice: Options and Opportunities in Translational Research.ILAR journal · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Murine coronavirus, mouse hepatitis virus (MHV), causes various diseases depending on the strain and route of inoculation. Both the JHM and A59 strains, when inoculated intracranially or intranasally, are neurovirulent. Comparison of the highly virulent JHM isolate, JHM.SD, with less virulent JHM isolates and with A59 has been used to determine the mechanisms and genes responsible for high neuropathogenicity of MHV. The focus of this review is on the contributions of viral spread, replication, and innate and adaptive immunity to MHV neuropathogenesis. JHM.SD spreads more quickly among neurons than less neurovirulent MHVs, and is able to spread in the absence of the canonical MHV receptor, CEACAM1a. The observation that JHM.SD infects more cells and expresses more antigen, but produces less infectious virus per cell than A59, implies that efficient replication is not always a correlate of high neurovirulence. This is likely due to the unstable nature of the JHM.SD spike protein (S). JHM.SD induces a generally protective innate immune response; however, the strong neutrophil response may be more pathogenic than protective. In addition, JHM.SD induces only a minimal T-cell response, whereas the strong T-cell response and the concomitant interferon-γ (IFN-γ) induced by the less neurovirulent A59 is protective. Differences in the S and nucleocapsid (N) proteins between A59 and JHM.SD contribute to JHM.SD neuropathogenicity. The hemmagglutinin-esterase (HE) protein may enhance neuropathogenicity of some MHV isolates, but is unlikely a major contributor to the high neuroviruence of JHM.SD. Further data suggest that neither the internal (I) protein nor nonstructural proteins ns4, and ns2 are significant contributors to neurovirulence.
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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.