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Epstein‐barr virus and a tumour‐promoting phorbol ester use similar mechanisms in the stimulation of human b‐cell proliferation
Author(s) -
Guy Graeme R.,
Gordon John
Publication year - 1989
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910430427
Subject(s) - protein kinase c , phospholipid , signal transduction , biology , inositol , biochemistry , stimulation , receptor , kinase , inositol trisphosphate , microbiology and biotechnology , endocrinology , membrane
In marked contrast to ligands which activate B cells via their physiological receptors for antigen, transforming Epstein‐Barr virus (EBV) was found to be mitogenic for human B lymphocytes without increasing inositol phospholipid hydrolysis. B‐cell stimulation by EBV showed similar characteristics to those achieved by the tumour‐promoting phorbol ester TPA, in terms of the temporal appearance of surface activation antigens, the induction of RNA and DNA synthesis and the lower requirement for medium Ca ++ in comparison to agonists that lead to an increase in inositol phospholipid hydrolysis. The calcium‐ and phospholipid‐dependent kinase, protein kinase C (PKC), is activated by TPA and a proteolytically cleaved fragment (PKM) results. EBV induced the appearance of a calcium‐ and phospholipid‐independent activity that was chromatographically inseparable from PKM and this activity was capable of phosphorylating vimentin, a cell component that is thought to participate in the signal transduction cascade. These findings are discussed with special reference to the biochemical signalling pathways on which EBV might impinge to usurp growth control in B lymphocytes.