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Originally published In Press as doi:10.1074/jbc.M109036200 on April 23, 2002

J. Biol. Chem., Vol. 277, Issue 27, 24148-24154, July 5, 2002
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Impaired Protein Kinase C Activation/Translocation in Epstein-Barr Virus-infected Monocytes*

Mélanie Tardif, Martin Savard, Louis FlamandDagger §, and Jean Gosselin

From the Laboratory of Viral Immunology, Dagger  Laboratory of Virology, Centre de Recherche en Rhumatologie et Immunologie, Centre de Recherche du Centre Hospitalier de l'Université Laval, and Université Laval, Québec G1V 4G2, Canada

Infection of human monocytes by Epstein-Barr virus (EBV) has been linked to a decrease in the production of proinflammatory mediators as well as an impairment of phagocytosis. Considering the key role of protein kinases C (PKCs) in many biological functions of monocytes, including phagocytosis, we investigated the effects of EBV on the PKC activity in infected monocytes. Our results indicate that infection of monocytes by EBV impairs both phorbol 12-myristate 13-acetate (PMA)-induced translocation of PKC isozymes alpha  and beta  from cytosol to membrane as well as the PKC enzymatic activity. Similarly, the subcellular distribution of the receptor for activated C kinase (RACK), an anchoring protein essential to PKC translocation, was also found to be reduced in EBV-infected monocytes. Transfection of 293T cells with an expression vector coding for the immediate-early protein ZEBRA of EBV resulted in impaired PMA-induced translocation and activity of PKC. Using co-immunoprecipitation assays, the ZEBRA protein was found to physically interact with the RACK1 protein. Thus interaction of ZEBRA with RACK likely results in the inhibition of PKC activity, which in turn affects functions of monocytes, such as phagocytosis.

* This work was supported by a grant from the Canadian Institutes of Health Research (CIHR) (to J. G.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ CIHR Young Investigator awardee.

Senior Scholar from the Fonds de la Recherche en Santé du Quebéc. To whom correspondence should be addressed: Laboratory of Viral Immunology, Centre de Recherche en Rhumatologie et Immunologie, CHUL Research Center (CHUQ), 2705 boul. Laurier, Rm. T 1-49, Sainte-Foy, Québec G1V 4G2, Canada. Tel.: 418-654-2772; Fax: 418-654-2127; E-mail: Jean.Gosselin@crchul. ulaval.ca.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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