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Article: Conserved Herpesviral Kinase Promotes Viral Persistence by Inhibiting the IRF-3-Mediated Type I Interferon Response

TitleConserved Herpesviral Kinase Promotes Viral Persistence by Inhibiting the IRF-3-Mediated Type I Interferon Response
Authors
KeywordsMICROBIO
MOLIMMUNO
Issue Date2009
Citation
Cell Host and Microbe, 2009, v. 5, n. 2, p. 166-178 How to Cite?
AbstractA conserved herpesviral kinase, designated ORF36 in murine γ-herpesvirus 68 (MHV-68), plays multiple vital roles in the viral life cycle. Here, we show by screening mutant viruses that ORF36 counteracts the antiviral type I interferon (IFN) response. ORF36 specifically binds to the activated form of interferon regulatory factor 3 (IRF-3) in the nucleus, inhibiting IRF-3 interaction with the cotranscriptional activator CBP and thereby suppressing the recruitment of RNA polymerase II to the interferon β promoter. The anti-IFN function of ORF36 is conserved among herpesvirus subfamilies, although the conserved kinase activity is not absolutely required for this function. MHV-68 lacking ORF36 induces a greater interferon response and is attenuated in vitro and in vivo, where acute viral infection in the lung and latency in the spleen are compromised. Our data suggest that herpesviruses have evolved within their conserved kinase an anti-IFN activity critical for evasion of host immunity and for persistence. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/285648
ISSN
2023 Impact Factor: 20.6
2023 SCImago Journal Rankings: 7.760
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHwang, Seungmin-
dc.contributor.authorKim, Kyeong Seon-
dc.contributor.authorFlano, Emilio-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorTong, Leming M.-
dc.contributor.authorPark, Ann N.-
dc.contributor.authorSong, Moon Jung-
dc.contributor.authorSanchez, David Jesse-
dc.contributor.authorO'Connell, Ryan M.-
dc.contributor.authorCheng, Genhong-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:17Z-
dc.date.available2020-08-18T04:56:17Z-
dc.date.issued2009-
dc.identifier.citationCell Host and Microbe, 2009, v. 5, n. 2, p. 166-178-
dc.identifier.issn1931-3128-
dc.identifier.urihttp://hdl.handle.net/10722/285648-
dc.description.abstractA conserved herpesviral kinase, designated ORF36 in murine γ-herpesvirus 68 (MHV-68), plays multiple vital roles in the viral life cycle. Here, we show by screening mutant viruses that ORF36 counteracts the antiviral type I interferon (IFN) response. ORF36 specifically binds to the activated form of interferon regulatory factor 3 (IRF-3) in the nucleus, inhibiting IRF-3 interaction with the cotranscriptional activator CBP and thereby suppressing the recruitment of RNA polymerase II to the interferon β promoter. The anti-IFN function of ORF36 is conserved among herpesvirus subfamilies, although the conserved kinase activity is not absolutely required for this function. MHV-68 lacking ORF36 induces a greater interferon response and is attenuated in vitro and in vivo, where acute viral infection in the lung and latency in the spleen are compromised. Our data suggest that herpesviruses have evolved within their conserved kinase an anti-IFN activity critical for evasion of host immunity and for persistence. © 2009 Elsevier Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofCell Host and Microbe-
dc.subjectMICROBIO-
dc.subjectMOLIMMUNO-
dc.titleConserved Herpesviral Kinase Promotes Viral Persistence by Inhibiting the IRF-3-Mediated Type I Interferon Response-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.chom.2008.12.013-
dc.identifier.pmid19218087-
dc.identifier.pmcidPMC2749518-
dc.identifier.scopuseid_2-s2.0-60649109368-
dc.identifier.volume5-
dc.identifier.issue2-
dc.identifier.spage166-
dc.identifier.epage178-
dc.identifier.isiWOS:000263814000008-
dc.identifier.issnl1931-3128-

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