EBV Activation By Anti-IgG-Triggered, Second Messenger Pathways

The Burkitt’s lymphoma cell line, Akata, demonstrates prompt and synchronous activation of latent EBV genomes following cross-linking of its membrane immunoglobulin G (mIgG) with anti-IgG (1). In B cells, activation from crosslinkage of mlg is initiated by a mlg-triggered phospholipase C (PLC), which cleaves phosphatidylinositol (PI) to inositol-1,4,5 trisphosphate (IP3) and diacylglycerol (DAG) (Fig. 1). IP3releases intracellular Ca++which can activate Ca++/calmodulin-dependent protein kinases, and DAG activates protein kinase C (PKC) (2). Adenylate cyclase can be activated, yielding cAMP which regulates protein kinase A (PKA). We have examined EBV activation in the Akata cells, the kinetics and synergy of these second messengers and the effect of cAMP, in the context of early antigen (EA) induction after anti-IgG crosslinking of mIgG (3).