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Journal of Virology, November 2004, p. 12529-12536, Vol. 78, No. 22
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.22.12529-12536.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

A Cyclooxygenase-2 Homologue Encoded by Rhesus Cytomegalovirus Is a Determinant for Endothelial Cell Tropism

Cary A. Rue,1,{dagger} Michael A. Jarvis,1,{dagger} Amber J. Knoche,1 Heather L. Meyers,1 Victor R. DeFilippis,1 Scott G. Hansen,1 Markus Wagner,2 Klaus Früh,1 David G. Anders,3 Scott W. Wong,1 Peter A. Barry,4 and Jay A. Nelson1*

Vaccine and Gene Therapy Institute and Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, Oregon,1 Department of Pathology, Harvard Medical School, Boston, Massachusetts,2 The David Axelrod Institute, Wadsworth Center, Albany, New York,3 Center for Comparative Medicine, University of California at Davis, Davis, California4

Received 30 May 2004/ Accepted 3 August 2004

Cyclooxygenase-2 (COX-2) is a cellular enzyme in the eicosanoid synthetic pathway that mediates the synthesis of prostaglandins from arachidonic acid. The eicosanoids function as critical regulators of a number of cellular processes, including the acute and chronic inflammatory response, hemostasis, and the innate immune response. Human cytomegalovirus (HCMV), which does not encode a viral COX-2 isoform, has been shown to induce cellular COX-2 expression. Importantly, although the precise role of COX-2 in CMV replication is unknown, COX-2 induction was shown to be critical for normal HCMV replication. In an earlier study, we identified an open reading frame (Rh10) within the rhesus cytomegalovirus (RhCMV) genome that encoded a putative protein (designated vCOX-2) with high homology to cellular COX-2. In the current study, we show that vCOX-2 is expressed with early-gene kinetics during RhCMV infection, resulting in production of a 70-kDa protein. Consistent with the expression of a viral COX-2 isoform, cellular COX-2 expression was not induced during RhCMV infection. Finally, analysis of growth of recombinant RhCMV with vCOX-2 deleted identified vCOX-2 as a critical determinant for replication in endothelial cells.

* Corresponding author. Mailing address: Department of Molecular Microbiology and Immunology, 3181 SW Sam Jackson Rd., Oregon Health Sciences University, Portland, OR 97239. Phone: (503) 494-7768. Fax: (504) 494-6862. E-mail: nelsonj{at}ohsu.edu.

{dagger} C.A.R. and M.A.J. contributed equally to this study.

Journal of Virology, November 2004, p. 12529-12536, Vol. 78, No. 22
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.22.12529-12536.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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