p73beta inhibits transcriptional activities of enhancer I and X promoter in hepatitis B virus more efficiently than p73alpha.

AIM: p73, as a novel member of a family of p53-related transcription factors, shares redundant functions with p53, such as the abilities of inducing apoptosis and suppressing growth. It is well known that p53 can repress HBV expression and transcription efficiently. The aim of this paper is to investigate the transcriptional effect of p73alpha and p73beta on hepatitis B virus (HBV) and to understand the correlation between HBV and p73.
METHODS: To construct an x-gene inactivated HBV plasmid which was cotransfected with p73alpha or p73beta expression vectors into HepG2 cells. After transiently transfection, HBV surface antigen (HBsAg) and HBV e antigen (HBeAg) were detected by ELISA. Viral transcripts synthesized by HBV were evaluated by Northern blotting analysis. The activities of HBV regulatory elements, including enhancer I/X promoter (ENI/Xp) and enhancer II/core promoter (ENII/Cp) were monitored by luciferase assays.
RESULTS: Both p73alpha and p73beta could repress HBsAg and HBeAg expression by downregulating the ENI/Xp and ENII/Cp activities. But p73beta exerted stronger inhibition on the activity of ENI/Xp than p73alpha, resulting in much lower level of viral transcripts and the antigens expression.
CONCLUSION: p73beta as a novel member of p53 family can efficiently inhibit HBV transcription mainly through downregulating the activities of the HBV ENI/Xp regulatory elements.