ArticleFrontiers in cellular neuroscience2015
Gliopathy of Demyelinating and Non-Demyelinating Strains of Mouse Hepatitis Virus.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Neurotropic Murine β-Coronavirus Infection Causes Differential Expression of Connexin 47 in Oligodendrocyte Subpopulations Associated with Demyelination.Molecular neurobiology · 2025Article
- Isolation and Enrichment of Major Primary Neuroglial Cells from Neonatal Mouse Brain.Bio-protocol · 2024Article
- Article
- Electrically-evoked oscillating calcium transients in mono- and co-cultures of iPSC glia and sensory neurons.Frontiers in cellular neuroscience · 2023Article
- Article
- Spike Glycoprotein Is Central to Coronavirus Pathogenesis-Parallel Between m-CoV and SARS-CoV-2.Annals of neurosciences · 2021Review
- Murine-β-coronavirus-induced neuropathogenesis sheds light on CNS pathobiology of SARS-CoV2.Journal of neurovirology · 2021Review
- A proline insertion-deletion in the spike glycoprotein fusion peptide of mouse hepatitis virus strongly alters neuropathology.The Journal of biological chemistry · 2019Article
- Connexin 43/47 channels are important for astrocyte/ oligodendrocyte cross-talk in myelination and demyelination.Journal of biosciences · 2018Review
- Microtubule-assisted altered trafficking of astrocytic gap junction protein connexin 43 is associated with depletion of connexin 47 during mouse hepatitis virus infection.The Journal of biological chemistry · 2017Article
- Demyelinating strain of mouse hepatitis virus infection bridging innate and adaptive immune response in the induction of demyelination.Clinical immunology (Orlando, Fla.) · 2016Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Demyelination in the central nervous system induced by neurovirulent strains of Mouse Hepatitis Virus (MHV) is mediated by the viral spike glycoprotein, but it is not clear whether the mechanism of this disease pathology involves direct viral infection of oligodendrocytes. Detailed studies of glial cell tropism of MHV are presented, demonstrating that direct MHV infection of oligodendrocytes differs between demyelinating (RSA59) and non-demyelinating (RSMHV2) viral strains both in vitro and in vivo. Our results indicate that direct injury of mature oligodendrocytes is an important mechanism of virus-induced demyelination. In vivo, RSA59 infection was identified in spinal cord gray and white matter, but infected oligodendrocytes were restricted to white matter. In contrast, RSMHV2 infection was restricted to gray matter neurons and was not localized to oligodendrocytes. In vitro, RSA59 can infect both oligodendrocyte precursors and differentiated oligodendrocytes, whereas RSMHV2 can infect oligodendrocyte precursors but not differentiated oligodendrocytes. Viral spreading through axonal means to white matter and release of the demyelinating strain MHV at the nerve end is critical for oligodendrocytes infection and subsequent demyelination. Understanding the mechanisms by which known viruses effect demyelination in this animal model has important therapeutic implications in the treatment of human demyelinating disease.
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