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dc.contributor.authorSchwanke, Hella
dc.contributor.authorStempel, Markus
dc.contributor.authorBrinkmann, Melanie M
dc.date.accessioned2020-07-23T10:56:10Z
dc.date.available2020-07-23T10:56:10Z
dc.date.issued2020-07-07
dc.identifier.citationViruses. 2020;12(7):E733. Published 2020 Jul 7. doi:10.3390/v12070733.en_US
dc.identifier.pmid32645843
dc.identifier.doi10.3390/v12070733
dc.identifier.urihttp://hdl.handle.net/10033/622359
dc.description.abstractThe type I interferon (IFN) response is a principal component of our immune system that allows to counter a viral attack immediately upon viral entry into host cells. Upon engagement of aberrantly localised nucleic acids, germline-encoded pattern recognition receptors convey their find via a signalling cascade to prompt kinase-mediated activation of a specific set of five transcription factors. Within the nucleus, the coordinated interaction of these dimeric transcription factors with coactivators and the basal RNA transcription machinery is required to access the gene encoding the type I IFN IFNβ (IFNB1). Virus-induced release of IFNβ then induces the antiviral state of the system and mediates further mechanisms for defence. Due to its key role during the induction of the initial IFN response, the activity of the transcription factor interferon regulatory factor 3 (IRF3) is tightly regulated by the host and fiercely targeted by viral proteins at all conceivable levels. In this review, we will revisit the steps enabling the trans-activating potential of IRF3 after its activation and the subsequent assembly of the multi-protein complex at the IFNβ enhancer that controls gene expression. Further, we will inspect the regulatory mechanisms of these steps imposed by the host cell and present the manifold strategies viruses have evolved to intervene with IFNβ transcription downstream of IRF3 activation in order to secure establishment of a productive infection.en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectIRF3en_US
dc.subjectNF-κBen_US
dc.subjectantagonisten_US
dc.subjectantiviral responseen_US
dc.subjectenhanceosomeen_US
dc.subjectimmune modulationen_US
dc.subjectinnate immunityen_US
dc.subjectinterferon betaen_US
dc.subjectinterferon regulatory factoren_US
dc.subjectviral evasionen_US
dc.titleOf Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent Expression.en_US
dc.typeReviewen_US
dc.typeOtheren_US
dc.identifier.eissn1999-4915
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalVirusesen_US
dc.source.volume12
dc.source.issue7
refterms.dateFOA2020-07-23T10:56:11Z
dc.source.journaltitleViruses
dc.source.countrySwitzerland


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