This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Saydam, O.
Right arrow Articles by Schwyzer, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Saydam, O.
Right arrow Articles by Schwyzer, M.

Next Article 

Journal of Virology, April 2004, p. 3805-3810, Vol. 78, No. 8
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.8.3805-3810.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Transactivator Protein BICP0 of Bovine Herpesvirus 1 (BHV-1) Is Blocked by Prostaglandin D2 (PGD2), Which Points to a Mechanism for PGD2-Mediated Inhibition of BHV-1 Replication

Okay Saydam, Carlos Abril, Bernd Vogt, Mathias Ackermann, and Martin Schwyzer*

Faculty of Veterinary Medicine, Institute of Virology, University of Zurich, CH-8057 Zurich, Switzerland

Received 22 May 2003/ Accepted 17 December 2003

The immediate-early protein, BICP0, of bovine herpesvirus 1 (BHV-1) transactivates a variety of viral and cellular genes. In a yeast two-hybrid cDNA library screening, we found that lipocalin-type prostaglandin D synthase, which catalyzes the production of prostaglandin D2 (PGD2), is a cellular target of BICP0. We observed that, during wild-type BHV-1 infection, PGD2 levels were increased intracellularly and decreased in the medium. These effects were absent upon infection with recombinant BHV-1 expressing ß-galactosidase instead of BICP0 (A2G2). Transient-expression assays showed that BICP0 alone caused a significant increase in PGD2 levels in the cell. PGD2 repressed BHV-1 replication in cultured cells. Antiviral activities of prostaglandins have been documented long ago, but their mode of action remains to be clarified. Here we provide evidence that PGD2 impairs the transactivation ability of BICP0 that is necessary for efficient virus replication.

* Corresponding author. Mailing address: Institute of Virology, Faculty of Veterinary Medicine, University of Zurich, Winterthurerstrasse 266A, CH-8057 Zurich, Switzerland. Phone: 41-1-6358704. Fax: 41-1-6358911. E-mail: schwyzer{at}vetvir.unizh.ch.

Journal of Virology, April 2004, p. 3805-3810, Vol. 78, No. 8
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.8.3805-3810.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.





Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»