Epstein-Barr virus (EBV), an oncovirus, has been shown to promote cancer cell metastasis – including such features and cell motility, migration, and invasiveness. We have demonstrated that lytic (but not latent) EBV-infected epithelial cells will migrate into an open space. High levels of active cellular Mnk1 have also been correlated to increased metastasis. As we have already shown that EBV lytic replication activates high levels of Mnk1, we are now studying how EBV lytic replication and Mnk1 work together to promote the migration of EBV-positive cells. We demonstrated that inhibition of Mnk1 prevents migration of lytic cells, and are now dissecting out the mechanism by which EBV lytic proteins and Mnk1 cooperate to drive metastasis.
