1887

Abstract

The hepatitis B virus (HBV) enhancer II (E) is highly liver-specific and plays an important role in regulating the transcription of all HBV genes. In this report, mutational analysis on the B1F-binding site in the major functional unit of HBV E is described. The activity of HBV E in E–CAT reporter plasmids was significantly decreased when the sequence of the B1F-binding site in E 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 region is crucial for liver-specific transcription and DNA replication of the virus.

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2001-03-01
2024-05-06
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