E2F1 suppresses Epstein-Barr virus lytic reactivation through cellular and viral transcriptional networks.

ABSTRACT: Epstein-Barr virus (EBV) establishes life-long persistence infection displaying a biphasic viral life cycle - latent phase and lytic replication. While latent EBV infection is linked to several B- and epithelial cell malignancies, periodic lytic-cycle reactivation is crucial for maintaining viral progeny and transmission. Targeting lytic reactivation offers a promising therapeutic avenue for EBV-associated cancers. Our genome-wide transcriptomic analysis reveals that E2F1 is transcriptionally activated during EBV latency but significantly suppressed during lytic reactivation. While ectopic E2F1 expression suppresses lytic replication, E2F1 depletion markedly accelerates this process. Mechanistically, we establish that E2F1 and the lytic transactivator BZLF1 form a negative transcriptional

SUBMITTER: Biswas J 

PROVIDER: S-EPMC12349880 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature