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Hepatitis B virus core protein inhibits TRAIL-induced apoptosis of hepatocytes by blocking DR5 expression

J Du1, X Liang, Y Liu

  • 1Department of Immunology, School of Medicine, Shandong University, Jinan, China.

Cell Death and Differentiation
|October 18, 2008
PubMed

Insights

Hepatitis B virus core protein (HBc) prevents liver cell death by inhibiting TRAIL-induced apoptosis, a key factor in chronic hepatitis and liver cancer development.

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Hepatitis B virus (HBV) infection leads to chronic hepatitis and hepatocellular carcinoma (HCC) in millions globally.
  • The molecular basis of HBV persistence and associated liver damage remains incompletely understood.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been identified as a factor in hepatocyte death during HBV infection.

Purpose of the Study:

  • To investigate the role of HBV core protein (HBc) in TRAIL-mediated apoptosis of hepatocytes.
  • To elucidate the molecular mechanisms by which HBc influences hepatocyte survival during HBV infection.
  • To assess the clinical relevance of HBc's effect on apoptosis in chronic hepatitis and HCC.

Main Methods:

  • Overexpression and knockdown of HBc in human hepatoma cells.
  • Assessment of TRAIL-induced apoptosis and death receptor 5 (DR5) expression.
  • Analysis of DR5 gene promoter activity.
  • HBc gene transfer in a mouse model of HBV-induced hepatitis.
  • Analysis of liver DR5 expression in patients with chronic hepatitis.

Main Results:

  • HBc significantly inhibited TRAIL-induced apoptosis in human hepatoma cells.
  • HBc overexpression reduced, while HBc knockdown enhanced, apoptosis.
  • HBc expression correlated with decreased DR5 expression and repressed DR5 promoter activity.
  • HBc gene transfer reduced hepatocyte death in vivo, and DR5 expression was reduced in patients with chronic hepatitis.

Conclusions:

  • HBc inhibits TRAIL-induced apoptosis by suppressing DR5 expression, contributing to chronic hepatitis and HCC.
  • HBc's mechanism of action may involve blocking hepatocyte death pathways.
  • These findings have implications for understanding HBV pathogenesis and potentially for HBc-based vaccine strategies.

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