Brain Invasion by Mouse Hepatitis Virus Depends on Impairment of Tight Junctions and Beta Interferon Production in Brain Microvascular Endothelial Cells.
Identifieur interne : 000E51 ( PubMed/Checkpoint ); précédent : 000E50; suivant : 000E52Brain 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.
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
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:26202229Le document en format XML
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xml:lang="en"><term>Animals</term><term>Blood-Brain Barrier (virology)</term><term>Brain (virology)</term><term>Cell Line</term><term>DNA Primers (genetics)</term><term>Electric Impedance</term><term>Endothelial Cells (metabolism)</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Female</term><term>Immunohistochemistry</term><term>Interferon-beta (metabolism)</term><term>Liver (virology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Microvessels (cytology)</term><term>Murine hepatitis virus (pathogenicity)</term><term>Murine hepatitis virus (physiology)</term><term>RNA, Small Interfering (genetics)</term><term>Real-Time Polymerase Chain Reaction</term><term>Tight Junctions (virology)</term><term>Viral Tropism (physiology)</term><term>Virulence</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Amorces ADN (génétique)</term><term>Animaux</term><term>Barrière hémato-encéphalique (virologie)</term><term>Cellules endothéliales 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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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26202229</PMID><DateCompleted><Year>2015</Year><Month>12</Month><Day>07</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>89</Volume><Issue>19</Issue><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Brain Invasion by Mouse Hepatitis Virus Depends on Impairment of Tight Junctions and Beta Interferon Production in Brain Microvascular Endothelial Cells.</ArticleTitle><Pagination><MedlinePgn>9896-908</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01501-15</ELocationID><Abstract><AbstractText Label="UNLABELLED">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.</AbstractText><AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">Coronaviruses (CoVs) infect several mammals, including humans, and are associated with respiratory, gastrointestinal, and/or neurological diseases. There is some evidence that suggest that human respiratory CoVs may show neuroinvasive properties. Indeed, the severe acute respiratory syndrome coronavirus (SARS-CoV), causing severe acute respiratory syndrome, and the CoVs OC43 and 229E were found in the brains of SARS patients and multiple sclerosis patients, respectively. These findings suggest that hematogenously spread CoVs may gain access to the CNS at the BBB level. Herein we report for the first time that CoVs exhibit the ability to cross the BBB according to strain virulence. BBB invasion by CoVs correlates with virus-induced disruption of tight junctions on BMECs, leading to BBB dysfunction and enhanced permeability. We provide evidence that production of IFN-β by BMECs during CoV infection may prevent BBB breakdown and brain viral invasion.</AbstractText><CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bleau</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Département des Sciences Biologiques, Université du Québec à Montréal, Montréal, Québec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Filliol</LastName><ForeName>Aveline</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institut de Recherche en Santé-Environnement-Travail, Université de Rennes 1, Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Samson</LastName><ForeName>Michel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institut de Recherche en Santé-Environnement-Travail, Université de Rennes 1, Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lamontagne</LastName><ForeName>Lucie</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Département des Sciences Biologiques, Université du Québec à Montréal, Montréal, Québec, Canada lamontagne.lucie@uqam.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>07</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance></Chemical><Chemical><RegistryNumber>77238-31-4</RegistryNumber><NameOfSubstance UI="D016899">Interferon-beta</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="N">Blood-Brain Barrier</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017931" MajorTopicYN="N">DNA Primers</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017097" MajorTopicYN="N">Electric Impedance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004797" MajorTopicYN="N">Enzyme-Linked Immunosorbent Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016899" MajorTopicYN="N">Interferon-beta</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055806" MajorTopicYN="N">Microvessels</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006517" MajorTopicYN="N">Murine hepatitis virus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060888" MajorTopicYN="N">Real-Time Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019108" MajorTopicYN="N">Tight Junctions</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056189" MajorTopicYN="N">Viral Tropism</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>06</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>07</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>7</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>7</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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