Stemming from our mTOR work, we have identified Mnk1/2 (MAPK-interacting kinase 1/2) as an interesting cellular modulator of EBV lytic replication. This kinase, activated by the MAPKs ERK and p38, is best known for its promotion of cap-dependent translation through phosphorylation of the translation initiation factor eIF4E. We have found, that in addition to this function, Mnk1/2 participates in the regulation of EBV lytic replication, insomuch as Mnk1/2 becomes highly phosphorylated/activated during early lytic replication within EBV-infected cells, and that treatment with a Mnk inhibitor alters subsequent lytic replication – in a cell-type dependent manner. Mnk1/2, a known mediator of metastasis of cancer cells, also plays a role in the migration of lytic EBV-infected epithelial cells. All in all, this makes Mnk1/2 an interesting cellular protein to focus on in terms of suppressing EBV lytic replication and metastatic potential.
