Upon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis.

2.50
Hdl Handle:
http://hdl.handle.net/10033/346454
Title:
Upon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis.
Authors:
Detje, Claudia N; Lienenklaus, Stefan; Chhatbar, Chintan; Spanier, Julia; Prajeeth, Chittappen K; Soldner, Claudia; Tovey, Michael G; Schlüter, Dirk; Weiss, Siegfried; Stangel, Martin; Kalinke, Ulrich ( 0000-0003-0503-9564 )
Abstract:
Previously we found that following intranasal (i.n.) infection with neurotropic vesicular stomatitis virus (VSV) type I interferon receptor (IFNAR) triggering of neuroectodermal cells was critically required to constrain intracerebral virus spread. To address whether locally active IFN-β was induced proximally, we studied spatiotemporal conditions of VSV-mediated IFN-β induction. To this end, we performed infection studies with IFN-β reporter mice. One day after intravenous (i.v.) VSV infection, luciferase induction was detected in lymph nodes. Upon i.n. infection, luciferase induction was discovered at similar sites with delayed kinetics, whereas on days 3 and 4 postinfection enhanced luciferase expression additionally was detected in the foreheads of reporter mice. A detailed analysis of cell type-specific IFN-β reporter mice revealed that within the olfactory bulb IFN-β was expressed by neuroectodermal cells, primarily by astrocytes and to a lesser extent by neurons. Importantly, locally induced type I IFN triggered distal parts of the brain as indicated by the analysis of ISRE-eGFP mice which after i.n. VSV infection showed enhanced green fluorescent protein (eGFP) expression throughout the brain. Compared to wild-type mice, IFN-β(-/-) mice showed increased mortality to i.n. VSV infection, whereas upon i.v. infection no such differences were detected highlighting the biological significance of intracerebrally expressed IFN-β. In conclusion, upon i.n. VSV instillation, IFN-β responses mounted by astrocytes within the olfactory bulb critically contribute to the antiviral defense by stimulating distal IFN-β-negative brain areas and thus arresting virus spread.
Affiliation:
Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany.
Citation:
Upon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis. 2015, 89 (5):2731-8 J. Virol.
Journal:
Journal of virology
Issue Date:
1-Mar-2015
URI:
http://hdl.handle.net/10033/346454
DOI:
10.1128/JVI.02044-14
PubMed ID:
25540366
Type:
Article
Language:
en
ISSN:
1098-5514
Appears in Collections:
publications of the department of experimental infection research ([TC] EXPI)

Full metadata record

DC FieldValue Language
dc.contributor.authorDetje, Claudia Nen
dc.contributor.authorLienenklaus, Stefanen
dc.contributor.authorChhatbar, Chintanen
dc.contributor.authorSpanier, Juliaen
dc.contributor.authorPrajeeth, Chittappen Ken
dc.contributor.authorSoldner, Claudiaen
dc.contributor.authorTovey, Michael Gen
dc.contributor.authorSchlüter, Dirken
dc.contributor.authorWeiss, Siegfrieden
dc.contributor.authorStangel, Martinen
dc.contributor.authorKalinke, Ulrichen
dc.date.accessioned2015-03-10T10:25:33Zen
dc.date.available2015-03-10T10:25:33Zen
dc.date.issued2015-03-01en
dc.identifier.citationUpon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis. 2015, 89 (5):2731-8 J. Virol.en
dc.identifier.issn1098-5514en
dc.identifier.pmid25540366en
dc.identifier.doi10.1128/JVI.02044-14en
dc.identifier.urihttp://hdl.handle.net/10033/346454en
dc.description.abstractPreviously we found that following intranasal (i.n.) infection with neurotropic vesicular stomatitis virus (VSV) type I interferon receptor (IFNAR) triggering of neuroectodermal cells was critically required to constrain intracerebral virus spread. To address whether locally active IFN-β was induced proximally, we studied spatiotemporal conditions of VSV-mediated IFN-β induction. To this end, we performed infection studies with IFN-β reporter mice. One day after intravenous (i.v.) VSV infection, luciferase induction was detected in lymph nodes. Upon i.n. infection, luciferase induction was discovered at similar sites with delayed kinetics, whereas on days 3 and 4 postinfection enhanced luciferase expression additionally was detected in the foreheads of reporter mice. A detailed analysis of cell type-specific IFN-β reporter mice revealed that within the olfactory bulb IFN-β was expressed by neuroectodermal cells, primarily by astrocytes and to a lesser extent by neurons. Importantly, locally induced type I IFN triggered distal parts of the brain as indicated by the analysis of ISRE-eGFP mice which after i.n. VSV infection showed enhanced green fluorescent protein (eGFP) expression throughout the brain. Compared to wild-type mice, IFN-β(-/-) mice showed increased mortality to i.n. VSV infection, whereas upon i.v. infection no such differences were detected highlighting the biological significance of intracerebrally expressed IFN-β. In conclusion, upon i.n. VSV instillation, IFN-β responses mounted by astrocytes within the olfactory bulb critically contribute to the antiviral defense by stimulating distal IFN-β-negative brain areas and thus arresting virus spread.en
dc.language.isoenen
dc.titleUpon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis.en
dc.typeArticleen
dc.contributor.departmentInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany.en
dc.identifier.journalJournal of virologyen

Related articles on PubMed

This item is licensed under a Creative Commons License
Creative Commons
All Items in HZI are protected by copyright, with all rights reserved, unless otherwise indicated.