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Article: Murine gamma-herpesvirus 68 hijacks MAVS and IKKβ to initiate lytic replication

TitleMurine gamma-herpesvirus 68 hijacks MAVS and IKKβ to initiate lytic replication
Authors
Issue Date2010
Citation
PLoS Pathogens, 2010, v. 6, n. 7, article no. e1001001 How to Cite?
AbstractUpon viral infection, the mitochondrial antiviral signaling (MAVS)-IKKβ pathway is activated to restrict viral replication. Manipulation of immune signaling events by pathogens has been an outstanding theme of host-pathogen interaction. Here we report that the loss of MAVS or IKKβ impaired the lytic replication of gamma-herpesvirus 68 (γHV68), a model herpesvirus for human Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus. γHV68 infection activated IKKβ in a MAVS-dependent manner; however, IKKβ phosphorylated and promoted the transcriptional activation of the γHV68 replication and transcription activator (RTA). Mutational analyses identified IKKβ phosphorylation sites, through which RTAmediated transcription was increased by IKKβ, within the transactivation domain of RTA. Moreover, the lytic replication of recombinant γHV68 carrying mutations within the IKKβ phosphorylation sites was greatly impaired. These findings support the conclusion that γHV68 hijacks the antiviral MAVS-IKKβ pathway to promote viral transcription and lytic infection, representing an example whereby viral replication is coupled to host immune activation. © 2010 Dong et al.
Persistent Identifierhttp://hdl.handle.net/10722/285883
ISSN
2019 Impact Factor: 6.218
2015 SCImago Journal Rankings: 5.185
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorDong, Xiaonan-
dc.contributor.authorFeng, Hao-
dc.contributor.authorSun, Qinmiao-
dc.contributor.authorLi, Haiyan-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorSun, Ren-
dc.contributor.authorTibbetts, Scott A.-
dc.contributor.authorChen, Zhijian J.-
dc.contributor.authorFeng, Pinghui-
dc.date.accessioned2020-08-18T04:56:54Z-
dc.date.available2020-08-18T04:56:54Z-
dc.date.issued2010-
dc.identifier.citationPLoS Pathogens, 2010, v. 6, n. 7, article no. e1001001-
dc.identifier.issn1553-7366-
dc.identifier.urihttp://hdl.handle.net/10722/285883-
dc.description.abstractUpon viral infection, the mitochondrial antiviral signaling (MAVS)-IKKβ pathway is activated to restrict viral replication. Manipulation of immune signaling events by pathogens has been an outstanding theme of host-pathogen interaction. Here we report that the loss of MAVS or IKKβ impaired the lytic replication of gamma-herpesvirus 68 (γHV68), a model herpesvirus for human Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus. γHV68 infection activated IKKβ in a MAVS-dependent manner; however, IKKβ phosphorylated and promoted the transcriptional activation of the γHV68 replication and transcription activator (RTA). Mutational analyses identified IKKβ phosphorylation sites, through which RTAmediated transcription was increased by IKKβ, within the transactivation domain of RTA. Moreover, the lytic replication of recombinant γHV68 carrying mutations within the IKKβ phosphorylation sites was greatly impaired. These findings support the conclusion that γHV68 hijacks the antiviral MAVS-IKKβ pathway to promote viral transcription and lytic infection, representing an example whereby viral replication is coupled to host immune activation. © 2010 Dong et al.-
dc.languageeng-
dc.relation.ispartofPLoS Pathogens-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleMurine gamma-herpesvirus 68 hijacks MAVS and IKKβ to initiate lytic replication-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.ppat.1001001-
dc.identifier.pmid20686657-
dc.identifier.pmcidPMC2912392-
dc.identifier.scopuseid_2-s2.0-77957661741-
dc.identifier.volume6-
dc.identifier.issue7-
dc.identifier.spagearticle no. e1001001-
dc.identifier.epagearticle no. e1001001-
dc.identifier.eissn1553-7374-

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