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

Luca G. Guidotti, Brent Matzke, Francis V. Chisari

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)4804-4808
Number of pages5
JournalJournal of Virology
Volume71
Issue number6
Publication statusPublished - Jun 1997

ASJC Scopus subject areas

  • Immunology

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