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dc.contributor.authorKoch, Sandra
dc.contributor.authorDamas, Modester
dc.contributor.authorFreise, Anika
dc.contributor.authorHage, Elias
dc.contributor.authorDhingra, Akshay
dc.contributor.authorRückert, Jessica
dc.contributor.authorGallo, Antonio
dc.contributor.authorKremmer, Elisabeth
dc.contributor.authorTegge, Werner
dc.contributor.authorBrönstrup, Mark
dc.contributor.authorBrune, Wolfram
dc.contributor.authorSchulz, Thomas F
dc.date.accessioned2019-05-21T11:47:57Z
dc.date.available2019-05-21T11:47:57Z
dc.date.issued2019-05-01
dc.identifier.citationPLoS Pathog. 2019 May 6;15(5):e1007743. doi: 10.1371/journal.ppat.1007743. eCollection 2019 May.en_US
dc.identifier.issn1553-7374
dc.identifier.pmid31059555
dc.identifier.doi10.1371/journal.ppat.1007743
dc.identifier.urihttp://hdl.handle.net/10033/621790
dc.description.abstractKaposi's sarcoma-associated herpesvirus (KSHV; human herpesvirus 8) belongs to the subfamily of Gammaherpesvirinae and is the etiological agent of Kaposi's sarcoma as well as of two lymphoproliferative diseases: primary effusion lymphoma and multicentric Castleman disease. The KSHV life cycle is divided into a latent and a lytic phase and is highly regulated by viral immunomodulatory proteins which control the host antiviral immune response. Among them is a group of proteins with homology to cellular interferon regulatory factors, the viral interferon regulatory factors 1-4. The KSHV vIRFs are known as inhibitors of cellular interferon signaling and are involved in different oncogenic pathways. Here we characterized the role of the second vIRF protein, vIRF2, during the KSHV life cycle. We found the vIRF2 protein to be expressed in different KSHV positive cells with early lytic kinetics. Importantly, we observed that vIRF2 suppresses the expression of viral early lytic genes in both newly infected and reactivated persistently infected endothelial cells. This vIRF2-dependent regulation of the KSHV life cycle might involve the increased expression of cellular interferon-induced genes such as the IFIT proteins 1, 2 and 3, which antagonize the expression of early KSHV lytic proteins. Our findings suggest a model in which the viral protein vIRF2 allows KSHV to harness an IFN-dependent pathway to regulate KSHV early gene expression.en_US
dc.language.isoenen_US
dc.publisherPLOSen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleKaposi's sarcoma-associated herpesvirus vIRF2 protein utilizes an IFN-dependent pathway to regulate viral early gene expression.en_US
dc.typeArticleen_US
dc.contributor.departmentHZI, Helmholtz Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.en_US
dc.identifier.journalPLOS Pathogensen_US
refterms.dateFOA2019-05-21T11:47:57Z
dc.source.journaltitlePLoS pathogens


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