Epstein-Barr virus lytic cycle activation (EBV lytic induction)

Epstein-Barr virus (EBV) lytic cycle activation is a biological process and therapeutic strategy rather than a single molecular target. It involves the transition of EBV from a latent state to a replicative (lytic) state, primarily driven by the expression of the viral immediate-early transcription factors BZLF1 (Zta) and BRLF1 (Rta) (PMID: 28630100). In EBV-associated malignancies like Burkitt lymphoma, the virus typically remains in a latent state, allowing the tumor to evade the immune system and standard antiviral therapies. Lytic induction therapy utilizes pharmacological agents, such as histone deacetylase (HDAC) inhibitors or certain cytotoxic drugs, to trigger the expression of these viral master switches (PMID: 31434317, PMID: 25405790). This activation leads to direct oncolysis and the expression of viral kinases, such as thymidine kinase, which can then phosphorylate antiviral prodrugs like ganciclovir into their active, cytotoxic forms to kill the host cancer cell (PMID: 21148614). While this strategy offers a way to specifically target EBV-positive tumor cells, therapeutic challenges include ensuring uniform induction across the tumor and managing the potential for systemic viral dissemination.

Other names

EBV lytic induction therapyEpstein-Barr virus reactivationLytic induction of EBVEBV lytic cycle switch

Induction of viral immediate-early genes (BZLF1 and BRLF1) through epigenetic modification (HDAC inhibition) or cellular stress pathways, followed by viral kinase-mediated activation of antiviral prodrugs (e.g., ganciclovir) to induce selective cell death.