Receptor-independent spread of a highly neurotropic murine coronavirus JHMV strain from initially infected microglial cells in mixed neural cultures.
Identifieur interne : 004683 ( Main/Exploration ); précédent : 004682; suivant : 004684Receptor-independent spread of a highly neurotropic murine coronavirus JHMV strain from initially infected microglial cells in mixed neural cultures.
Auteurs : Keiko Nakagaki [Japon] ; Kazuhide Nakagaki ; Fumihiro TaguchiSource :
- Journal of virology [ 0022-538X ] ; 2005.
Descripteurs français
- KwdFr :
- Animaux, Anticorps de l'hépatite (immunologie), Astrocytes, Infections à coronavirus (métabolisme), Infections à coronavirus (virologie), Microglie (métabolisme), Microglie (virologie), Mutation, Neurones, Oligodendroglie, Récepteurs viraux (métabolisme), Réplication virale, Souris, Techniques de coculture, Virulence, Virus de l'hépatite murine (pathogénicité), Virus de l'hépatite murine (physiologie).
- MESH :
- immunologie : Anticorps de l'hépatite.
- métabolisme : Infections à coronavirus, Microglie, Récepteurs viraux.
- pathogénicité : Virus de l'hépatite murine.
- physiologie : Virus de l'hépatite murine.
- virologie : Infections à coronavirus, Microglie.
- Animaux, Astrocytes, Mutation, Neurones, Oligodendroglie, Réplication virale, Souris, Techniques de coculture, Virulence.
English descriptors
- KwdEn :
- Animals, Astrocytes, Coculture Techniques, Coronavirus Infections (metabolism), Coronavirus Infections (virology), Hepatitis Antibodies (immunology), Mice, Microglia (metabolism), Microglia (virology), Murine hepatitis virus (pathogenicity), Murine hepatitis virus (physiology), Mutation, Neurons, Oligodendroglia, Receptors, Virus (metabolism), Virulence, Virus Replication.
- MESH :
- chemical , immunology : Hepatitis Antibodies.
- metabolism : Coronavirus Infections, Microglia, Receptors, Virus.
- pathogenicity : Murine hepatitis virus.
- physiology : Murine hepatitis virus.
- virology : Coronavirus Infections, Microglia.
- Animals, Astrocytes, Coculture Techniques, Mice, Mutation, Neurons, Oligodendroglia, Virulence, Virus Replication.
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.
DOI: 10.1128/JVI.79.10.6102-6110.2005
PubMed: 15857995
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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