Divergent requirements for the MAPK(ERK) signal transduction pathway during initial virus infection of quiescent primary B cells and disruption of Epstein-Barr virus latency by phorbol esters

Quiescent primary B lymphocytes and Epstein-Barr virus (EBV)-immortalized l ymphoblastoid cell lines express components of the extracellular response k inase arm of the mitogen-activated protein kinase (MAPK(ERK)) Signal transd uction pathway and transmit signals through the pathway when exposed to app ropriate stimuli. Although the MAPK(ERK) pathway is activated following inf ection with EBV, MAPK/ERK kinase (MEK1) activity is not required to drive t he proliferation of infected cells. However, MEK1 contributes to EBV latenc y control.