Hep3B human hepatoma cells support replication of the wild-type and a 5'-end deletion mutant GB virus B replicon

J Virol. 2003 Nov;77(22):11875-81. doi: 10.1128/jvi.77.22.11875-11881.2003.

Abstract

Hepatitis C virus (HCV) and GB virus B (GBV-B) replicons have been reported to replicate only in Huh7 cells. Here we demonstrate that subpopulations of another human hepatoma cell line, Hep3B, are permissive for the GBV-B replicon, showing different levels of enhancement of replication from those of the unselected parental cell population. Adaptive mutations are not required for replication of the GBV-B replicon in these cells, as already demonstrated for Huh7 cells. Nonetheless, we identified a mutant replicon in one of the selected cell lines, which, although lacking the 5' end proximal stem-loop, is able to replicate in Hep3B cells as well as in Huh7 cells. This mutant indeed shows a higher replication efficiency than does wild-type replicon, especially in the Hep3B cell clone from which it was originally recovered. This indicates that the stem-loop Ia is not necessary for replication of the GBV-B replicon in human cells, unlike what occurs with HCV, and that its absence can even provide a selective advantage.

MeSH terms

  • 5' Untranslated Regions / chemistry
  • Carcinoma, Hepatocellular / virology*
  • Cell Line, Tumor
  • GB virus B / genetics
  • GB virus B / physiology*
  • Humans
  • Liver Neoplasms / virology*
  • Mutation
  • Protein Biosynthesis
  • RNA, Viral / chemistry
  • Replicon*
  • Virus Replication*

Substances

  • 5' Untranslated Regions
  • RNA, Viral