Show simple item record

dc.contributor.authorKochs, Georg
dc.contributor.authorMartínez-Sobrido, Luis
dc.contributor.authorLienenklaus, Stefan
dc.contributor.authorWeiss, Siegfried
dc.contributor.authorGarcía-Sastre, Adolfo
dc.contributor.authorStaeheli, Peter
dc.date.accessioned2010-02-01T15:32:02Z
dc.date.available2010-02-01T15:32:02Z
dc.date.issued2009-12
dc.identifier.citationStrong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene. 2009, 90 (Pt 12):2990-4 J. Gen. Virol.en
dc.identifier.issn1465-2099
dc.identifier.pmid19726611
dc.identifier.doi10.1099/vir.0.015727-0
dc.identifier.urihttp://hdl.handle.net/10033/90955
dc.description.abstractInfluenza viruses lacking the interferon (IFN)-antagonistic non-structural NS1 protein are strongly attenuated. Here, we show that mutants of a highly virulent variant of A/PR/8/34 (H1N1) carrying either a complete deletion or C-terminal truncations of NS1 were far more potent inducers of IFN in infected mice than NS1 mutants derived from standard A/PR/8/34. Efficient induction of IFN correlated with successful initial virus replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. As the new NS1 mutants can be handled in standard biosafety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshGene Deletionen
dc.subject.meshHumansen
dc.subject.meshInfluenza A Virus, H1N1 Subtypeen
dc.subject.meshInterferon-betaen
dc.subject.meshLungen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred BALB Cen
dc.subject.meshMutationen
dc.subject.meshOrthomyxoviridae Infectionsen
dc.subject.meshViral Nonstructural Proteinsen
dc.subject.meshVirulenceen
dc.subject.meshVirus Replicationen
dc.titleStrong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene.en
dc.typeArticleen
dc.contributor.departmentDepartment of Virology, University of Freiburg, D-79008 Freiburg, Germany. georg.kochs@uniklinik-freiburg.deen
dc.identifier.journalThe Journal of general virologyen
refterms.dateFOA2010-12-15T00:00:00Z
html.description.abstractInfluenza viruses lacking the interferon (IFN)-antagonistic non-structural NS1 protein are strongly attenuated. Here, we show that mutants of a highly virulent variant of A/PR/8/34 (H1N1) carrying either a complete deletion or C-terminal truncations of NS1 were far more potent inducers of IFN in infected mice than NS1 mutants derived from standard A/PR/8/34. Efficient induction of IFN correlated with successful initial virus replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. As the new NS1 mutants can be handled in standard biosafety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.


Files in this item

Thumbnail
Name:
Kochs et al_final.pdf
Size:
252.6Kb
Format:
PDF
Description:
allowed pdf

This item appears in the following Collection(s)

Show simple item record