Gallic acid inhibits Kaposi's Sarcoma-associated herpesvirus lytic reactivation by suppressing RTA transcriptional activities

Kaposi's sarcoma-associated herpesvirus (KSHV), an oncogenic virus, has two life cycle modes: the latent and lytic phases. KSHV lytic reactivation is known to be important both for viral propagation and for KSHV-induced tumorigenesis. The KSHV replication and transcription activator (RTA) protein is essential for lytic reactivation. Gallic acid (GA), one of the most abundant phenolic acids in the plant kingdom, has been shown potential chemotherapeutic efficacy against microbial and cancer. However, the effects of GA on KSHV replication and KSHV-induced tumorigenesis have not yet been reported. Here, we report that GA induces apoptotic cell death in BCBL-1 cells in a dose-dependent manner. GA inhibits KSHV reactivation and reduces the production of progeny virus from KSHV-harboring cells. GA inhibits RTA transcriptional activities by suppressing its binding to target gene promoters. These results suggest that GA may represent a novel strategy for the treatment of KSHV infection and KSHV-associated lymphomas.

Automated summary

Gallic acid (GA) induces apoptotic cell death in BCBL-1 cells in a dose-dependent manner, inhibits KSHV reactivation, reduces the production of progeny virus from KSHV-harboring cells, and suppresses the transcriptional activities of KSHV replication and transcription activator (RTA) protein by inhibiting its binding to target gene promoters. These results suggest that GA may represent a novel strategy for the treatment of KSHV infection and KSHV-associated lymphomas.