Extracellular vesicles derived EBV tegument protein BRRF2 suppresses cGAS phase separation to promote anti-viral innate immune evasion.

ABSTRACT: Viral strategies to antagonize the robust host innate immune response have a major function in the pathogenicity of viral infection and virus-associated cancers. Epstein-Barr virus (EBV) infection causes infectious mononucleosis (IM) and several human cancers. While latent EBV can reactivate in some nasopharyngeal carcinoma (NPC) cells, the impact of EBV reactivation on the anti-viral innate immune and immunotherapy response of NPC patients remains incompletely understood. Here, we reveal the function of the EBV-encoded BRRF2 protein as a pivotal regulator of the host immune system. We show that BRRF2, which is secreted via extracellular vesicles (EVs) from NPC cells undergoing EBV reactivation, specifically targets macrophages. It disrupts the cyclic GMP-AMP synthase (cGAS)-stimulator of

SUBMITTER: Hu ZL 

PROVIDER: S-EPMC12514055 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature