HCMV encoded UL84 hijacks FHL2 to suppress type I interferon production and enhance viral replication.

ABSTRACT: Virus infection activates the host's innate immune responses, which is a very precise and complex biological process and will lead to the immediate transcription of type I interferon. The general transcriptional activator proteins such as IRF3, ATF2/c-Jun, and NF-κB can be induced to form a stable enhanceosome in the transcriptional regulatory region of IFN-β promoter. Several cellular factors have recently been reported to be involved in the transcriptional regulation of IFN-β under certain physiological conditions. Here, we identified four and a half LIM domains protein 2 (FHL2) as an interacting protein of the Human Cytomegalovirus (HCMV) replication-related protein UL84 and determined that FHL2 plays an architectural role in enhancing the transcription of IFN-β induced by HCMV infectio

SUBMITTER: Li R 

PROVIDER: S-EPMC12863675 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature