IRF6 controls Epstein-Barr virus (EBV) lytic reactivation and differentiation in EBV-infected epithelial cells.

ABSTRACT: Latent Epstein-Barr virus (EBV) infection promotes undifferentiated nasopharyngeal carcinoma (NPC) and gastric carcinoma (GC), while EBV infection of normal differentiated oropharyngeal epithelial cells is lytic and kills the cell. Establishment of viral latency within epithelial cells is likely essential for the development of EBV-induced NPCs and GCs, but the mechanism(s) by which EBV latency is maintained in epithelial cells are not fully understood. Here we demonstrate that the cellular tumor suppressor protein IRF6, a master regulator of squamous cell epithelial cell differentiation, plays a critical role in promoting TPA-induced lytic EBV reactivation in vitro in both EBV-infected NPC cells and EBV-infected GC cells. Using a telomerase-immortalized normal oral keratinocyte cell line

SUBMITTER: Fogarty SA 

PROVIDER: S-EPMC12200665 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature