Hepatitis B virus replication is cell cycle independent during liver regeneration in transgenic mice.
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.
Guidotti
L G
LG
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. guidotti@scripps.edu
Matzke
B
B
Chisari
F V
FV
D000818:Animals; D002453:Cell Cycle; D002467:Cell Nucleus / Q000378:metabolism; D016207:Cytokines / Q000502:physiology; D003593:Cytoplasm / Q000378:metabolism; D006512:Hepatitis B Core Antigens / Q000378:metabolism; D006515:Hepatitis B virus / Q000254:growth & development*; D008099:Liver / Q000166:cytology / Q000382:microbiology*; D008115:Liver Regeneration; D051379:Mice; D008822:Mice, Transgenic; D014779:Virus Replication
D016207:Cytokines; D006512:Hepatitis B Core Antigens