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The mechanism of apoliprotein A1 down-regulated by Hepatitis B virus

Yuanyuan Wang1, Junli Hao1, Xiaohong Liu1

  • 1School of Biomedical Sciences, Chengdu Medical College, Sichuan, 610500, China.

Lipids in Health and Disease
|March 27, 2016
PubMed

Insights

Hepatitis B virus (HBV) downregulates Apolipoprotein A1 (ApoA1) via DNA hypermethylation, contributing to chronic hepatitis B (CHB) pathogenesis. Restoring ApoA1 may impact HBV progression.

Area of Science:

  • Hepatology and Virology
  • Molecular Biology
  • Epigenetics

Background:

  • Hepatitis B virus (HBV) infection is a major global health concern, linked to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
  • The precise mechanisms driving chronic hepatitis B (CHB) pathogenesis remain incompletely understood.
  • Apolipoprotein A1 (ApoA1), a key component of high-density lipoprotein primarily secreted by hepatocytes, may be negatively affected by HBV infection.

Purpose of the Study:

  • To investigate the molecular mechanisms by which HBV downregulates ApoA1 expression.
  • To elucidate the role of ApoA1 dysregulation in the pathogenesis of CHB.
  • To explore potential therapeutic targets related to ApoA1 and HBV interaction.

Main Methods:

  • Quantitative assessment of ApoA1 mRNA and protein levels in CHB patients and HBV-infected cell lines (HepG2.2.15) using RT-PCR and Western blot.
  • Analysis of ApoA1 promoter DNA methylation status in CpG islands using methylation-specific PCR (MSP).
  • Investigating the effect of DNA methyltransferase inhibitor (5-aza-dC) and ApoA1 siRNA on ApoA1 and HBV expression, including HBsAg and HBeAg secretion via ELISA.

Main Results:

  • ApoA1 mRNA, protein, and serum levels were significantly decreased in CHB patients and HBV-infected cells compared to controls.
  • HBV infection led to hypermethylation of specific CpG islands in the ApoA1 promoter.
  • Inhibition of DNA methylation or ApoA1 overexpression increased HBV expression, while ApoA1 knockdown reversed these effects.

Conclusions:

  • HBV induces epigenetic silencing of the ApoA1 gene through CpG island hypermethylation, contributing to CHB pathogenesis.
  • ApoA1 downregulation by HBV is a key factor in the disease's progression.
  • Targeting epigenetic modifications of ApoA1 presents a potential therapeutic strategy for CHB.
Abstract

Keywords:
5-aza-dCApolipoprotein A1Hepatitis B virusHypermethylation

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