Site-Specific Mutation Of The Hepatitis B Virus Enhancer Iib1 Element: Effect On Virus Transcription And Replication

The hepatitis B virus (HBV) enhancer II (E-11) is highly liver-specific and plays an important role in regulating the transcription of all HBV genes. In this report, mutational analysis on the Rip-binding site in the major functional unit of HBV E-11 is described. The activity of HBV E-11 in E-11-CAT reporter plasmids was significantly decreased when the sequence of the B1F-binding site in E-11 was mutated. Furthermore, a single point mutation in the B1 element that aborted the binding of B1F caused a dramatic decrease in viral gene transcription initiated from the HBV core promoter, which resulted in a reduction of the production of the HBV e antigen and pregenomic RNA, the template for viral DNA replication. In conclusion, the interaction of B1F with its target binding sequence in the E-11 region is crucial for liver-specific transcription and DNA replication of the virus.