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Article: Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 RTA reactivates murine gammaherpesvirus 68 from latency

TitleKaposi's sarcoma-associated herpesvirus/human herpesvirus 8 RTA reactivates murine gammaherpesvirus 68 from latency
Authors
Issue Date2005
Citation
Journal of Virology, 2005, v. 79, n. 5, p. 3217-3222 How to Cite?
AbstractMurine gammaherpesvirus 68 (MHV-68), Kaposi's sarcoma-associated herpesvirus (HHV-8), and Epsiein-Barr virus (EBV) are all members of the gammaherpesvirus family, characterized by their ability to establish latency in lymphocytes. The RTA protein, conserved in all gammaherpesvinises, is known to play a critical role in reactivation from latency. Here we report that HHV-8 RTA, not EBV RTA, was able to induce MHV-68 lytic viral proteins and DNA replication and processing and produce viable MHV-68 virions from latently infected cells at levels similar to those for MHV-68 RTA. HHV-8 RTA was also able to activate two MHV-68 lytic promoters, whereas EBV RTA was not. In order to define the domains of RTA responsible for their functional differences in viral promoter activation and initiation of the MHV-68 lytic cycle, chimeric RTA proteins were constructed by exchanging the N-terminal and C-terminal domains of the RTA proteins. Our data suggest that the species specificity of MHV-68 RTA resides in the N-terminal DNA binding domain.
Persistent Identifierhttp://hdl.handle.net/10722/285584
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRickabaugh, Tammy M.-
dc.contributor.authorBrown, Helen J.-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorSong, Moon Jung-
dc.contributor.authorHwang, Seungmin-
dc.contributor.authorDeng, Hongyu-
dc.contributor.authorMitsouras, Katherine-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:07Z-
dc.date.available2020-08-18T04:56:07Z-
dc.date.issued2005-
dc.identifier.citationJournal of Virology, 2005, v. 79, n. 5, p. 3217-3222-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285584-
dc.description.abstractMurine gammaherpesvirus 68 (MHV-68), Kaposi's sarcoma-associated herpesvirus (HHV-8), and Epsiein-Barr virus (EBV) are all members of the gammaherpesvirus family, characterized by their ability to establish latency in lymphocytes. The RTA protein, conserved in all gammaherpesvinises, is known to play a critical role in reactivation from latency. Here we report that HHV-8 RTA, not EBV RTA, was able to induce MHV-68 lytic viral proteins and DNA replication and processing and produce viable MHV-68 virions from latently infected cells at levels similar to those for MHV-68 RTA. HHV-8 RTA was also able to activate two MHV-68 lytic promoters, whereas EBV RTA was not. In order to define the domains of RTA responsible for their functional differences in viral promoter activation and initiation of the MHV-68 lytic cycle, chimeric RTA proteins were constructed by exchanging the N-terminal and C-terminal domains of the RTA proteins. Our data suggest that the species specificity of MHV-68 RTA resides in the N-terminal DNA binding domain.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleKaposi's sarcoma-associated herpesvirus/human herpesvirus 8 RTA reactivates murine gammaherpesvirus 68 from latency-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.79.5.3217-3222.2005-
dc.identifier.pmid15709045-
dc.identifier.pmcidPMC548426-
dc.identifier.scopuseid_2-s2.0-13844324384-
dc.identifier.volume79-
dc.identifier.issue5-
dc.identifier.spage3217-
dc.identifier.epage3222-
dc.identifier.isiWOS:000227098400062-
dc.identifier.issnl0022-538X-

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