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Papers In Press, published online ahead of print April 23, 2002
Centre de recherche en Rhumatologie et Immunologie, CHUL Research Center (CHUQ), Sainte-Foy, Québec G1V4G2
Corresponding Author: jean.gosselin{at}crchul.ulaval.ca
Infection of human monocytes by Epstein-Barr virus has been linked to a decrease in the production of pro-inflammatory 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 PMA-induced translocation of PKC isozymes a and b 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.
J. Biol. Chem, 10.1074/jbc.M109036200
Submitted on September 18, 2001
Revised on April 23, 2002
Accepted on April 23, 2002
Impaired protein kinase C activation/translocation in EBV-infected monocytes
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