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Journal of Virology, September 2004, p. 10187-10192, Vol. 78, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.18.10187-10192.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Role of Protein Kinase C {delta} in Reactivation of Kaposi's Sarcoma-Associated Herpesvirus

Einat Deutsch, Adina Cohen, Gila Kazimirsky, Sara Dovrat, Hadara Rubinfeld, Chaya Brodie, and Ronit Sarid*

Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, Israel

Received 30 December 2003/ Accepted 18 May 2004

TPA (12-O-tetradecanoylphorbol-13-acetate), a well-known activator of protein kinase C (PKC), can experimentally induce reactivation of Kaposi's sarcoma-associated herpesvirus (KSHV) in certain latently infected cells. We selectively blocked the activity of PKC isoforms by using GF 109203X or rottlerin and demonstrated that this inhibition largely decreased lytic KSHV reactivation by TPA. Translocation of the PKC{delta} isoform was evident shortly after TPA stimulation. Overexpression of the dominant-negative PKC{delta} mutant supported an essential role for the PKC{delta} isoform in virus reactivation, yet overexpression of PKC{delta} alone was not sufficient to induce lytic reactivation of KSHV, suggesting that additional signaling molecules participate in this pathway.

* Corresponding author. Mailing address: Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 52900, Israel. Phone: 972-3-5317853. Fax: 972-3-5351824. E-mail: saridr{at}mail.biu.ac.il.

Journal of Virology, September 2004, p. 10187-10192, Vol. 78, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.18.10187-10192.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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