Brain Invasion by Mouse Hepatitis Virus Depends on Impairment of Tight Junctions and Beta Interferon Production in Brain Microvascular Endothelial Cells.
Identifieur interne : 000127 ( France/Analysis ); précédent : 000126; suivant : 000128Brain Invasion by Mouse Hepatitis Virus Depends on Impairment of Tight Junctions and Beta Interferon Production in Brain Microvascular Endothelial Cells.
Auteurs : Christian Bleau [Canada] ; Aveline Filliol [France] ; Michel Samson [France] ; Lucie Lamontagne [Canada]Source :
- Journal of virology [ 1098-5514 ] ; 2015.
Descripteurs français
- KwdFr :
- Amorces ADN (génétique), Animaux, Barrière hémato-encéphalique (virologie), Cellules endothéliales (métabolisme), Encéphale (virologie), Femelle, Foie (virologie), Immunohistochimie, Impédance électrique, Interféron bêta (métabolisme), Jonctions serrées (virologie), Lignée cellulaire, Microvaisseaux (cytologie), Petit ARN interférent (génétique), Réaction de polymérisation en chaine en temps réel, Souris, Souris de lignée C57BL, Test ELISA, Tropisme viral (physiologie), Virulence, Virus de l'hépatite murine (pathogénicité), Virus de l'hépatite murine (physiologie).
- MESH :
- cytologie : Microvaisseaux.
- génétique : Amorces ADN, Petit ARN interférent.
- métabolisme : Cellules endothéliales, Interféron bêta.
- pathogénicité : Virus de l'hépatite murine.
- physiologie : Tropisme viral, Virus de l'hépatite murine.
- virologie : Barrière hémato-encéphalique, Encéphale, Foie, Jonctions serrées.
- Animaux, Femelle, Immunohistochimie, Impédance électrique, Lignée cellulaire, Réaction de polymérisation en chaine en temps réel, Souris, Souris de lignée C57BL, Test ELISA, Virulence.
English descriptors
- KwdEn :
- Animals, Blood-Brain Barrier (virology), Brain (virology), Cell Line, DNA Primers (genetics), Electric Impedance, Endothelial Cells (metabolism), Enzyme-Linked Immunosorbent Assay, Female, Immunohistochemistry, Interferon-beta (metabolism), Liver (virology), Mice, Mice, Inbred C57BL, Microvessels (cytology), Murine hepatitis virus (pathogenicity), Murine hepatitis virus (physiology), RNA, Small Interfering (genetics), Real-Time Polymerase Chain Reaction, Tight Junctions (virology), Viral Tropism (physiology), Virulence.
- MESH :
- chemical , genetics : DNA Primers, RNA, Small Interfering.
- cytology : Microvessels.
- metabolism : Endothelial Cells, Interferon-beta.
- pathogenicity : Murine hepatitis virus.
- physiology : Murine hepatitis virus, Viral Tropism.
- virology : Blood-Brain Barrier, Brain, Liver, Tight Junctions.
- Animals, Cell Line, Electric Impedance, Enzyme-Linked Immunosorbent Assay, Female, Immunohistochemistry, Mice, Mice, Inbred C57BL, Real-Time Polymerase Chain Reaction, Virulence.
Abstract
Coronaviruses (CoVs) have shown neuroinvasive properties in humans and animals secondary to replication in peripheral organs, but the mechanism of neuroinvasion is unknown. The major aim of our work was to evaluate the ability of CoVs to enter the central nervous system (CNS) through the blood-brain barrier (BBB). Using the highly hepatotropic mouse hepatitis virus type 3 (MHV3), its attenuated variant, 51.6-MHV3, which shows low tropism for endothelial cells, and the weakly hepatotropic MHV-A59 strain from the murine coronavirus group, we investigated the virus-induced dysfunctions of BBB in vivo and in brain microvascular endothelial cells (BMECs) in vitro. We report here a MHV strain-specific ability to cross the BBB during acute infection according to their virulence for liver. Brain invasion was observed only in MHV3-infected mice and correlated with enhanced BBB permeability associated with decreased expression of zona occludens protein 1 (ZO-1), VE-cadherin, and occludin, but not claudin-5, in the brain or in cultured BMECs. BBB breakdown in MHV3 infection was not related to production of barrier-dysregulating inflammatory cytokines or chemokines by infected BMECs but rather to a downregulation of barrier protective beta interferon (IFN-β) production. Our findings highlight the importance of IFN-β production by infected BMECs in preserving BBB function and preventing access of blood-borne infectious viruses to the brain.
Url:
DOI: 10.1128/JVI.01501-15
PubMed: 26202229
Affiliations:
- Canada, France
- Québec, Région Bretagne
- Montréal, Rennes
- Université de Rennes 1, Université du Québec à Montréal
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Links to Exploration step
pubmed:26202229Le document en format XML
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électrique</term><term>Interféron bêta (métabolisme)</term><term>Jonctions serrées (virologie)</term><term>Lignée cellulaire</term><term>Microvaisseaux (cytologie)</term><term>Petit ARN interférent (génétique)</term><term>Réaction de polymérisation en chaine en temps réel</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Test ELISA</term><term>Tropisme viral (physiologie)</term><term>Virulence</term><term>Virus de l'hépatite murine (pathogénicité)</term><term>Virus de l'hépatite murine (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA Primers</term><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Microvaisseaux</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Microvessels</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Amorces ADN</term><term>Petit ARN interférent</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Interferon-beta</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term><term>Interféron bêta</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Murine hepatitis virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Tropisme viral</term><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Murine hepatitis virus</term><term>Viral Tropism</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Barrière hémato-encéphalique</term><term>Encéphale</term><term>Foie</term><term>Jonctions serrées</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Blood-Brain Barrier</term><term>Brain</term><term>Liver</term><term>Tight Junctions</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Electric Impedance</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Female</term><term>Immunohistochemistry</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Real-Time Polymerase Chain Reaction</term><term>Virulence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Immunohistochimie</term><term>Impédance électrique</term><term>Lignée cellulaire</term><term>Réaction de polymérisation en chaine en temps réel</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Test ELISA</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Coronaviruses (CoVs) have shown neuroinvasive properties in humans and animals secondary to replication in peripheral organs, but the mechanism of neuroinvasion is unknown. The major aim of our work was to evaluate the ability of CoVs to enter the central nervous system (CNS) through the blood-brain barrier (BBB). Using the highly hepatotropic mouse hepatitis virus type 3 (MHV3), its attenuated variant, 51.6-MHV3, which shows low tropism for endothelial cells, and the weakly hepatotropic MHV-A59 strain from the murine coronavirus group, we investigated the virus-induced dysfunctions of BBB in vivo and in brain microvascular endothelial cells (BMECs) in vitro. We report here a MHV strain-specific ability to cross the BBB during acute infection according to their virulence for liver. Brain invasion was observed only in MHV3-infected mice and correlated with enhanced BBB permeability associated with decreased expression of zona occludens protein 1 (ZO-1), VE-cadherin, and occludin, but not claudin-5, in the brain or in cultured BMECs. BBB breakdown in MHV3 infection was not related to production of barrier-dysregulating inflammatory cytokines or chemokines by infected BMECs but rather to a downregulation of barrier protective beta interferon (IFN-β) production. Our findings highlight the importance of IFN-β production by infected BMECs in preserving BBB function and preventing access of blood-borne infectious viruses to the brain.</div></front></TEI><affiliations><list><country><li>Canada</li><li>France</li></country><region><li>Québec</li><li>Région Bretagne</li></region><settlement><li>Montréal</li><li>Rennes</li></settlement><orgName><li>Université de Rennes 1</li><li>Université du Québec à Montréal</li></orgName></list><tree><country name="Canada"><region name="Québec"><name sortKey="Bleau, Christian" sort="Bleau, Christian" uniqKey="Bleau C" first="Christian" last="Bleau">Christian Bleau</name></region><name sortKey="Lamontagne, Lucie" sort="Lamontagne, Lucie" uniqKey="Lamontagne L" first="Lucie" last="Lamontagne">Lucie Lamontagne</name></country><country name="France"><region name="Région Bretagne"><name sortKey="Filliol, Aveline" sort="Filliol, Aveline" uniqKey="Filliol A" first="Aveline" last="Filliol">Aveline Filliol</name></region><name sortKey="Samson, Michel" sort="Samson, Michel" uniqKey="Samson M" first="Michel" last="Samson">Michel Samson</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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