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Hepatitis B virus replication is cell cycle independent during liver regeneration in transgenic mice

Academic Article
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Overview

authors

  • Guidotti, Luca
  • Matzke, B.
  • Chisari, Francis

publication date

  • June 1997

journal

  • Journal of Virology  Journal

abstract

  • The content of hepatitis B virus (HBV) replicative forms and HBV core protein in the liver of HBV transgenic mice is transiently reduced during massive liver regeneration following partial hepatectomy while the steady-state content of viral RNA is unchanged. This antiviral effect is triggered by interferon and tumor necrosis factor that are induced in the liver following hepatectomy and either prevent the formation or accelerate the degradation of viral nucleocapsids in the cytoplasm of the hepatocyte. Despite massive hepatocellular turnover, this effect is independent of liver cell division, indicating that HBV replicates efficiently in resting and dividing hepatocytes.

subject areas

  • Animals
  • Cell Cycle
  • Cell Nucleus
  • Cytokines
  • Cytoplasm
  • Hepatitis B Core Antigens
  • Hepatitis B virus
  • Liver
  • Liver Regeneration
  • Mice
  • Mice, Transgenic
  • Virus Replication
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Identity

PubMed Central ID

  • PMC191703

International Standard Serial Number (ISSN)

  • 0022-538X

PubMed ID

  • 9151875
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Additional Document Info

start page

  • 4804

end page

  • 4808

volume

  • 71

issue

  • 6

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