Visualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1.

2.50
Hdl Handle:
http://hdl.handle.net/10033/297909
Title:
Visualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1.
Authors:
Kallfass, Carsten; Lienenklaus, Stefan; Weiss, Siegfried; Staeheli, Peter
Abstract:
The innate host defense against influenza virus is largely dependent on the type I interferon (IFN) system. However, surprisingly little is known about the cellular source of IFN in the infected lung. To clarify this question, we employed a reporter mouse that contains the firefly luciferase gene in place of the IFN-β-coding region. IFN-β-producing cells were identified either by simultaneous immunostaining of lungs for luciferase and cellular markers or by generating conditional reporter mice that express luciferase exclusively in defined cell types. Two different strains of influenza A virus were employed that either do or do not code for nonstructural protein 1 (NS1), which strongly suppresses innate immune responses of infected cells. We found that epithelial cells and lung macrophages, which represent the prime host cells for influenza viruses, showed vigorous IFN-β responses which, however, were severely reduced and delayed if the infecting virus was able to produce NS1. Interestingly, CD11c(+) cell populations that were either expressing or lacking macrophage markers produced the bulk of IFN-β at 48 h after infection with wild-type influenza A virus. Our results demonstrate that the virus-encoded IFN-antagonistic factor NS1 disarms specifically epithelial cells and lung macrophages, which otherwise would serve as main mediators of the early response against infection by influenza virus.
Affiliation:
Department of Virology, University of Freiburg, Freiburg, Germany.
Citation:
Visualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1. 2013, 87 (12):6925-30 J. Virol.
Journal:
Journal of virology
Issue Date:
Jun-2013
URI:
http://hdl.handle.net/10033/297909
DOI:
10.1128/JVI.00283-13
PubMed ID:
23576514
Type:
Article
Language:
en
ISSN:
1098-5514
Appears in Collections:
publications of the research group molecular Immunology (MOLI)

Full metadata record

DC FieldValue Language
dc.contributor.authorKallfass, Carstenen_GB
dc.contributor.authorLienenklaus, Stefanen_GB
dc.contributor.authorWeiss, Siegfrieden_GB
dc.contributor.authorStaeheli, Peteren_GB
dc.date.accessioned2013-08-12T14:14:26Z-
dc.date.available2013-08-12T14:14:26Z-
dc.date.issued2013-06-
dc.identifier.citationVisualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1. 2013, 87 (12):6925-30 J. Virol.en_GB
dc.identifier.issn1098-5514-
dc.identifier.pmid23576514-
dc.identifier.doi10.1128/JVI.00283-13-
dc.identifier.urihttp://hdl.handle.net/10033/297909-
dc.description.abstractThe innate host defense against influenza virus is largely dependent on the type I interferon (IFN) system. However, surprisingly little is known about the cellular source of IFN in the infected lung. To clarify this question, we employed a reporter mouse that contains the firefly luciferase gene in place of the IFN-β-coding region. IFN-β-producing cells were identified either by simultaneous immunostaining of lungs for luciferase and cellular markers or by generating conditional reporter mice that express luciferase exclusively in defined cell types. Two different strains of influenza A virus were employed that either do or do not code for nonstructural protein 1 (NS1), which strongly suppresses innate immune responses of infected cells. We found that epithelial cells and lung macrophages, which represent the prime host cells for influenza viruses, showed vigorous IFN-β responses which, however, were severely reduced and delayed if the infecting virus was able to produce NS1. Interestingly, CD11c(+) cell populations that were either expressing or lacking macrophage markers produced the bulk of IFN-β at 48 h after infection with wild-type influenza A virus. Our results demonstrate that the virus-encoded IFN-antagonistic factor NS1 disarms specifically epithelial cells and lung macrophages, which otherwise would serve as main mediators of the early response against infection by influenza virus.en_GB
dc.language.isoenen
dc.rightsArchived with thanks to Journal of virologyen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshAntigens, CD11cen_GB
dc.subject.meshEpithelial Cellsen_GB
dc.subject.meshImmunity, Innateen_GB
dc.subject.meshInfluenza A virusen_GB
dc.subject.meshInterferon-betaen_GB
dc.subject.meshLuciferasesen_GB
dc.subject.meshLungen_GB
dc.subject.meshMacrophagesen_GB
dc.subject.meshMiceen_GB
dc.subject.meshMice, Inbred C57BLen_GB
dc.subject.meshViral Nonstructural Proteinsen_GB
dc.titleVisualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1.en
dc.typeArticleen
dc.contributor.departmentDepartment of Virology, University of Freiburg, Freiburg, Germany.en_GB
dc.identifier.journalJournal of virologyen_GB

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