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Site-specific mutation of the hepatitis B virus enhancer II B1 element: effect on virus transcription and replication

Max-Planck-Institut für Biochemie¹ and ³Am Klopferspitz 18a and D-82152 Martinsried, Germany
Institute of Biochemistry and Cell Biology, Shanghai Institute for Biological Science, Shanghai, China²

Author for correspondence: Ludwig Weiss. Fax +49 89 7092 9559. e-mail Ludwig-Weiss{at}t-online.de

The hepatitis B virus (HBV) enhancer II (E_II) 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_II is described. The activity of HBV E_II in E_II–CAT reporter plasmids was significantly decreased when the sequence of the B1F-binding site in E_II 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_II region is crucial for liver-specific transcription and DNA replication of the virus.

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