ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2010
Pathogenesis of murine coronavirus in the central nervous system.
Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 116 citations in OpenAlex.
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- Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025Review
- Comparative transcriptome profiling of the lumbosacral dorsal root ganglia reveals sexually dimorphic gene expression in a murine model of coronavirus-induced neurodegeneration.American journal of clinical and experimental urology · 2025Article
- Multiple sclerosis: etiology in the context of neurovascular unit and immune system involvement and advancements withFrontiers in immunology · 2025Review
- COVID-AMD database for coronavirus-infected animal models with comparative analysis tools.Scientific reports · 2024Article
- Host response to Aplysia Abyssovirus 1 in nervous system and gill.Developmental and comparative immunology · 2024Article
- Evolution of SARS-CoV-2 in the murine central nervous system drives viral diversification.Nature microbiology · 2024Article
- Neurons cytoskeletal architecture remodeling during the replication cycle of mouse coronavirus MHV-JHM: a morphological in vitro study.BMC veterinary research · 2024Article
- The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model.Viruses · 2023Review
- Neurovirulent cytokines increase neuronal excitability in a model of coronavirus-induced neuroinflammation.Intensive care medicine experimental · 2023Article
- Antiviral Activity of Anthranilamide Peptidomimetics against Herpes Simplex Virus 1 and a Coronavirus.Antibiotics (Basel, Switzerland) · 2023Article
- Assessment of GO-Based Protein Interaction Affinities in the Large-Scale Human-Coronavirus Family Interactome.Vaccines · 2023Article
- Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.Frontiers in molecular neuroscience · 2023Review
- B cells going viral in the CNS: Dynamics, complexities, and functions of B cells responding to viral encephalitis.Immunological reviews · 2022Review
- Potential Utility of Natural Products against Oxidative Stress in Animal Models of Multiple Sclerosis.Antioxidants (Basel, Switzerland) · 2022Review
- Sustained Infiltration of Neutrophils Into the CNS Results in Increased Demyelination in a Viral-Induced Model of Multiple Sclerosis.Frontiers in immunology · 2022Article
18 more citing papers are in PubMed but not listed here.
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) is a collection of strains that induce disease in several organ systems of mice. Infection with neurotropic strains JHM and A59 causes acute encephalitis, and in survivors, chronic demyelination, the latter of which serves as an animal model for multiple sclerosis. The MHV receptor is a carcinoembryonic antigen-related cell adhesion molecule, CEACAM1a; paradoxically, CEACAM1a is poorly expressed in the central nervous system (CNS), leading to speculation of an additional receptor. Comparison of highly neurovirulent JHM isolates with less virulent variants and the weakly neurovirulent A59 strain, combined with the use of reverse genetics, has allowed mapping of pathogenic properties to individual viral genes. The spike protein, responsible for viral entry, is a major determinant of tropism and virulence. Other viral proteins, both structural and nonstructural, also contribute to pathogenesis in the CNS. Studies of host responses to MHV indicate that both innate and adaptive responses are crucial to antiviral defense. Type I interferon is essential to prevent very early mortality after infection. CD8 T cells, with the help of CD4 T cells, are crucial for viral clearance during acute disease and persist in the CNS during chronic disease. B cells are necessary to prevent reactivation of virus in the CNS following clearance of acute infection. Despite advances in understanding of coronavirus pathogenesis, questions remain regarding the mechanisms of viral entry and spread in cell types expressing low levels of receptor, as well as the unique interplay between virus and the host immune system during acute and chronic disease.
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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.