ArticleJournal of virology2005
Receptor-independent spread of a highly neurotropic murine coronavirus JHMV strain from initially infected microglial cells in mixed neural cultures.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
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- SARS-CoV-2 Infection of Ocular Cells from Human Adult Donor Eyes and hESC-Derived Eye Organoids.SSRN · 2020Article
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- Contribution of porcine aminopeptidase N to porcine deltacoronavirus infection.Emerging microbes & infections · 2018Article
- Extracellular matrix in the CNS induced by neuropathogenic viral infection.Neuropathology : official journal of the Japanese Society of Neuropathology · 2017Article
- Formation of fibroblastic reticular network in the brain after infection with neurovirulent murine coronavirus.Neuropathology : official journal of the Japanese Society of Neuropathology · 2016Article
- Structure, Function, and Evolution of Coronavirus Spike Proteins.Annual review of virology · 2016Review
- Mice lacking α1,3-fucosyltransferase 9 exhibit modulation of in vivo immune responses against pathogens.Pathology international · 2014Article
- T cell mediated suppression of neurotropic coronavirus replication in neural precursor cells.Virology · 2014Article
- Human coronavirus HKU1 infection of primary human type II alveolar epithelial cells: cytopathic effects and innate immune response.PloS one · 2013Article
- Review
- Spongiform degeneration induced by neuropathogenic murine coronavirus infection.Pathology international · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although neurovirulent mouse hepatitis virus (MHV) strain JHMV multiplies in a variety of brain cells, expression of its receptor carcinoembryonic antigen cell adhesion molecule 1 (CEACAM 1) (MHVR) is restricted only in microglia. The present study was undertaken to clarify the mechanism of an extensive JHMV infection in the brain by using neural cells isolated from mouse brain. In contrast to wild-type (wt) JHMV, a soluble-receptor-resistant mutant (srr7) infects and spreads solely in an MHVR-dependent fashion (F. Taguchi and S. Matsuyama, J. Virol. 76:950-958, 2002). In mixed neural cell cultures, srr7 infected a limited number of cells and infection did not spread, although wt JHMV induced syncytia in most of the cells. srr7-infected cells were positive for GS-lectin, a microglia marker. Fluorescence-activated cell sorter analysis showed that about 80% of the brain cells stained with anti-MHVR antibody (CC1) were also positive for GS-lectin. Pretreatment of those cells with CC1 prevented virus attachment to the cell surface and also blocked virus infection. These results show that microglia express functional MHVR that mediates JHMV infection. As expected, in microglial cell-enriched cultures, both srr7and wt JHMV produced syncytia in a majority of cells. Treatment with CC1 of mixed neural cell cultures and microglia cultures previously infected with wt virus failed to block the spread of infection, indicating that wt infection spreads in an MHVR-independent fashion. Thus, the present study indicates that microglial cells are the major population of the initial target for MHV infection and that the wt spreads from initially infected microglia to a variety of cells in an MHVR-independent fashion.
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