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dc.contributor.authorStempel, Markus
dc.contributor.authorChan, Baca
dc.contributor.authorJuranić Lisnić, Vanda
dc.contributor.authorKrmpotić, Astrid
dc.contributor.authorHartung, Josephine
dc.contributor.authorPaludan, Søren R
dc.contributor.authorFüllbrunn, Nadia
dc.contributor.authorLemmermann, Niels Aw
dc.contributor.authorBrinkmann, Melanie M
dc.date.accessioned2019-02-13T15:11:49Z
dc.date.available2019-02-13T15:11:49Z
dc.date.issued2019-01-29
dc.identifier.issn1460-2075
dc.identifier.pmid30696688
dc.identifier.doi10.15252/embj.2018100983
dc.identifier.urihttp://hdl.handle.net/10033/621687
dc.description.abstractCytomegaloviruses (CMVs) are master manipulators of the host immune response. Here, we reveal that the murine CMV (MCMV) protein m152 specifically targets the type I interferon (IFN) response by binding to stimulator of interferon genes (STING), thereby delaying its trafficking to the Golgi compartment from where STING initiates type I IFN signaling. Infection with an MCMV lacking m152 induced elevated type I IFN responses and this leads to reduced viral transcript levels both in vitro and in vivo. This effect is ameliorated in the absence of STING. Interestingly, while m152 inhibits STING‐mediated IRF signaling, it did not affect STING‐mediated NF‐κB signaling. Analysis of how m152 targets STING translocation reveals that STING activates NF‐κB signaling already from the ER prior to its trafficking to the Golgi. Strikingly, this response is important to promote early MCMV replication. Our results show that MCMV has evolved a mechanism to specifically antagonize the STING‐mediated antiviral IFN response, while preserving its pro‐viral NF‐κB response, providing an advantage in the establishment of an infection.en_US
dc.language.isoenen_US
dc.publisherWiley-Blackwellen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectSTINGen_US
dc.subjectIRF3en_US
dc.subjectNF‐κBen_US
dc.subjectherpesvirusen_US
dc.subjectinnate immunityen_US
dc.titleThe herpesviral antagonist m152 reveals differential activation of STING-dependent IRF and NF-κB signaling and STING's dual role during MCMV infection.en_US
dc.typeArticleen_US
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalEMBO Journalen_US
refterms.dateFOA2019-02-13T15:11:49Z
dc.source.journaltitleThe EMBO journal


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