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Article: Inhibition of the phosphatidylinositol 3-kinase-Akt pathway enhances gamma-2 herpesvirus lytic replication and facilitates reactivation from latency

TitleInhibition of the phosphatidylinositol 3-kinase-Akt pathway enhances gamma-2 herpesvirus lytic replication and facilitates reactivation from latency
Authors
Issue Date2010
Citation
Journal of General Virology, 2010, v. 91, n. 2, p. 463-469 How to Cite?
AbstractCellular signalling pathways are critical in regulating the balance between latency and lytic replication of herpesviruses. Here, we investigated the effect of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway on replication of two gamma-2 herpesviruses, murine gammaherpesvirus-68 (MHV-68) and human herpesvirus-8/Kaposi's sarcoma-associated herpesvirus (HHV-8/KSHV). We found that de novo infection of MHV-68 induced PI3K-dependent Akt activation and the lytic replication of MHV-68 was enhanced by inhibiting the PI3K-Akt pathway with both chemical inhibitors and RNA interference technology. Inhibiting the activity of Akt using Akt inhibitor VIII also facilitated the reactivation of KSHV from latency. Both lytic replication and latency depend on the activity of viral transactivator RTA and we further show that the activity of RTA is increased by reducing Akt1 expression. The data suggest that the PI3K-Akt pathway suppresses the activity of RTA and thereby contributes to the maintenance of viral latency and promotes tumorigenesis. © 2010 SGM.
Persistent Identifierhttp://hdl.handle.net/10722/285662
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 0.990
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPeng, Li-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorTchieu, Jason H.-
dc.contributor.authorFeng, Jun-
dc.contributor.authorBrown, Helen J.-
dc.contributor.authorFeng, Jiaying-
dc.contributor.authorLi, Xudong-
dc.contributor.authorQi, Jing-
dc.contributor.authorDeng, Hongyu-
dc.contributor.authorVivanco, Igor-
dc.contributor.authorMelinghoff, Ingo K.-
dc.contributor.authorJamieson, Christina-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:19Z-
dc.date.available2020-08-18T04:56:19Z-
dc.date.issued2010-
dc.identifier.citationJournal of General Virology, 2010, v. 91, n. 2, p. 463-469-
dc.identifier.issn0022-1317-
dc.identifier.urihttp://hdl.handle.net/10722/285662-
dc.description.abstractCellular signalling pathways are critical in regulating the balance between latency and lytic replication of herpesviruses. Here, we investigated the effect of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway on replication of two gamma-2 herpesviruses, murine gammaherpesvirus-68 (MHV-68) and human herpesvirus-8/Kaposi's sarcoma-associated herpesvirus (HHV-8/KSHV). We found that de novo infection of MHV-68 induced PI3K-dependent Akt activation and the lytic replication of MHV-68 was enhanced by inhibiting the PI3K-Akt pathway with both chemical inhibitors and RNA interference technology. Inhibiting the activity of Akt using Akt inhibitor VIII also facilitated the reactivation of KSHV from latency. Both lytic replication and latency depend on the activity of viral transactivator RTA and we further show that the activity of RTA is increased by reducing Akt1 expression. The data suggest that the PI3K-Akt pathway suppresses the activity of RTA and thereby contributes to the maintenance of viral latency and promotes tumorigenesis. © 2010 SGM.-
dc.languageeng-
dc.relation.ispartofJournal of General Virology-
dc.titleInhibition of the phosphatidylinositol 3-kinase-Akt pathway enhances gamma-2 herpesvirus lytic replication and facilitates reactivation from latency-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1099/vir.0.015073-0-
dc.identifier.pmid19864499-
dc.identifier.pmcidPMC2888311-
dc.identifier.scopuseid_2-s2.0-76249099841-
dc.identifier.volume91-
dc.identifier.issue2-
dc.identifier.spage463-
dc.identifier.epage469-
dc.identifier.eissn1465-2099-
dc.identifier.isiWOS:000274806600017-
dc.identifier.issnl0022-1317-

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