Abstract
Chronic hepatitis B infection (HBV) is major cause of morbidity and mortality throughout the world. Currently there is limited understanding on the cellular proteins and related molecules involved in the critical steps of viral entry into the cytoplasm and persistent viral replication in cell culture. In order to address these fundamental questions, we designed and implemented a new model of hepatitis B: infectious transgenic hepatitis B virus composed of a complete virus plus a foreign gene. The foreign gene allows identification of cells that are infected by the transgenic virus. The transgenic virus was used in a functional assay to identify cellular proteins necessary for viral replication. This assay repeatedly identified the protein UQCR10. After restoring UQCR10 levels in HepG2 and Huh7 cells, they can be infected by intact virions of transgenic hepatitis B. These results demonstrate the usefulness of this new transgenic hepatitis B model.
Highlights
Chronic hepatitis B infection (HBV) is major cause of morbidity and mortality throughout the world
While seminal studies have identified the Hepatitis B virus (HBV) receptor as sodium taurocholate co-transporting polypeptide[2], encoded by SLC10A1, data is sparse on the other cellular proteins and related molecules that are critical to viral entry and sustained viral replication
The foreign gene contained by the transgenic hepatitis B virus allows selection for subgroups of cells that have become infected by the transgenic virus
Summary
Chronic hepatitis B infection (HBV) is major cause of morbidity and mortality throughout the world. After restoring UQCR10 levels in HepG2 and Huh[7] cells, they can be infected by intact virions of transgenic hepatitis B These results demonstrate the usefulness of this new transgenic hepatitis B model. New treatment approaches are most likely to succeed when they are firmly grounded in scientific understandings of viral biology In this regard, much of the details on the biology of HBV remains unknown. In order to study these key issues, we developed a new transgenic model of hepatitis B This tool allowed the use of a functional approach to identifying key viral entry factors/early replication factors, an approach that was solely based on viral entry and replication in cells and was not dependent on a prior knowledge of necessary viral entry or post-entry factors necessary for sustained infectivity
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