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Journal of Virology, December 2003, p. 12753-12763, Vol. 77, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.23.12753-12763.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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

Tonia L. Symensma ,1,{dagger} DeeAnn Martinez-Guzman,1 Qingmei Jia,1 Eric Bortz,1 Ting-Ting Wu,1 Nandini Rudra-Ganguly,2 Steve Cole,3 Harvey Herschman,2 and Ren Sun1*

Department of Molecular and Medical Pharmacology, the UCLA AIDS Institute, the Jonsson Comprehensive Cancer Center, the Molecular Biology Institute, and the Dental Research Institute,1 Department of Biological Chemistry,2 Department of Medicine, University of California at Los Angeles, Los Angeles, California 900953

Received 14 July 2003/ Accepted 19 August 2003

The murine gammaherpesvirus 68 (MHV-68 or {gamma}HV-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.

* Corresponding author. Mailing address: Department of Molecular and Medical Pharmacology, University of California at Los Angeles, Los Angeles, CA 90095-1735. Phone: (310) 794-5557. Fax: (310) 825-6267. E-mail: rsun{at}mednet.ucla.edu.

{dagger} Present address: Department of Biological Sciences, Mount St. Mary’s College, Los Angeles, CA 90049.

Journal of Virology, December 2003, p. 12753-12763, Vol. 77, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.23.12753-12763.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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