Inducible expression of human hepatitis B virus (HBV) in stably transfected hepatoblastoma cells: A novel system for screening potential inhibitors of HBV replication

Stephanie K. Ladner, Michael J. Otto, Christopher S. Barker, Katie Zaifert, Guang Hua Wang, J. U.Tao Guo, Christoph Seeger, Robert W. King

Research output: Contribution to journalArticlepeer-review

529 Scopus citations

Abstract

We report the development and isolation of a cell line, termed HepAD38, that replicates human hepatitis B virus (HBV) under conditions that can be regulated with tetracycline. In the presence of the antibiotic, this cell line is free of virus due to the repression of pregenomic (pg) RNA synthesis, Upon removal of tetracycline from the culture medium, the cells express viral pg RNA, accumulate subviral particles in the cytoplasm that contain DNA intermediates characteristic of viral replication, and secrete virus-like particles Into the supernatant. Since the HepAD38 cell line can produce high levels of HBV DNA, it should be useful for analyses of the viral replication cycle that depend upon viral DNA synthesis in a synchronized fashion, In addition, this cell line has been formatted into a high-throughput, cell-based assay that permits the large-scale screening of diverse compound libraries for new classes of inhibitors of HBV replication.
Original languageEnglish
Pages (from-to)1715-1720
Number of pages6
JournalAntimicrobial Agents and Chemotherapy
Volume41
Issue number8
DOIs
StatePublished - Aug 1997

Keywords

  • Cell Line
  • DNA, Viral/analysis
  • Hepatitis B virus/drug effects
  • Hepatoblastoma/pathology
  • Humans
  • Liver Neoplasms/pathology
  • Protein Synthesis Inhibitors/pharmacology
  • RNA, Viral/analysis
  • Tetracycline/pharmacology
  • Transfection
  • Tumor Cells, Cultured/pathology
  • Virus Replication/drug effects

Fingerprint

Dive into the research topics of 'Inducible expression of human hepatitis B virus (HBV) in stably transfected hepatoblastoma cells: A novel system for screening potential inhibitors of HBV replication'. Together they form a unique fingerprint.

Cite this