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Article: COX-2 Induction during Murine Gammaherpesvirus 68 Infection Leads to Enhancement of Viral Gene Expression

TitleCOX-2 Induction during Murine Gammaherpesvirus 68 Infection Leads to Enhancement of Viral Gene Expression
Authors
Issue Date2003
Citation
Journal of Virology, 2003, v. 77, n. 23, p. 12753-12763 How to Cite?
AbstractThe murine gammaherpesvirus 68 (MHV-68 or γHV-68) model provides many advantages for studying virus-host interactions involved in gammaherpesvirus replication, including the role of cellular responses to infection. We examined the effects of cellular cyclooxygenase-2 (COX-2) and its by-product prostaglandin E2 (PGE2) on MHV-68 gene expression and protein production following de novo infection of cultured cells. Western blot analyses revealed an induction of COX-2 protein in MHV-68-infected cells but not in cells infected with UV-irradiated MHV-68. Luciferase reporter assays demonstrated activation of the COX-2 promoter during MHV-68 replication. Two nonsteroidal anti-inflammatory drugs, a COX-2-specific inhibitor (NS-398) and a COX-1-COX-2 inhibitor (indomethacin), substantially reduced MHV-68 protein production in infected cells. Inhibition of viral protein expression and virion production by NS-398 was reversed in the presence of exogenous PGE2. Global gene expression analysis using an MHV-68 DNA array showed that PGE2 increased production of multiple viral gene products, and NS-398 inhibited production of many of the same genes. These studies suggest that COX-2 activity and PGE2 production may play significant roles during MHV-68 de novo infection.
Persistent Identifierhttp://hdl.handle.net/10722/285581
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSymensma, Tonia L.-
dc.contributor.authorMartinez-Guzman, Dee Ann-
dc.contributor.authorJia, Qingmei-
dc.contributor.authorBortz, Eric-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorRudra-Ganguly, Nandini-
dc.contributor.authorCole, Steve-
dc.contributor.authorHerschman, Harvey-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:07Z-
dc.date.available2020-08-18T04:56:07Z-
dc.date.issued2003-
dc.identifier.citationJournal of Virology, 2003, v. 77, n. 23, p. 12753-12763-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285581-
dc.description.abstractThe murine gammaherpesvirus 68 (MHV-68 or γHV-68) model provides many advantages for studying virus-host interactions involved in gammaherpesvirus replication, including the role of cellular responses to infection. We examined the effects of cellular cyclooxygenase-2 (COX-2) and its by-product prostaglandin E2 (PGE2) on MHV-68 gene expression and protein production following de novo infection of cultured cells. Western blot analyses revealed an induction of COX-2 protein in MHV-68-infected cells but not in cells infected with UV-irradiated MHV-68. Luciferase reporter assays demonstrated activation of the COX-2 promoter during MHV-68 replication. Two nonsteroidal anti-inflammatory drugs, a COX-2-specific inhibitor (NS-398) and a COX-1-COX-2 inhibitor (indomethacin), substantially reduced MHV-68 protein production in infected cells. Inhibition of viral protein expression and virion production by NS-398 was reversed in the presence of exogenous PGE2. Global gene expression analysis using an MHV-68 DNA array showed that PGE2 increased production of multiple viral gene products, and NS-398 inhibited production of many of the same genes. These studies suggest that COX-2 activity and PGE2 production may play significant roles during MHV-68 de novo infection.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleCOX-2 Induction during Murine Gammaherpesvirus 68 Infection Leads to Enhancement of Viral Gene Expression-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.77.23.12753-12763.2003-
dc.identifier.pmid14610197-
dc.identifier.pmcidPMC262602-
dc.identifier.scopuseid_2-s2.0-0242660903-
dc.identifier.volume77-
dc.identifier.issue23-
dc.identifier.spage12753-
dc.identifier.epage12763-
dc.identifier.isiWOS:000186612700036-
dc.identifier.issnl0022-538X-

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