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Histone Deacetylase 3 Inhibitor Suppresses Hepatitis C Virus Replication by Regulating Apo-A1 and LEAP-1 Expression

Yuan Zhou1, Qian Wang2, Qi Yang1,3

  • 1State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.

Virologica Sinica
|October 18, 2018
PubMed

Insights

HDAC3 inhibitors suppressed hepatitis C virus (HCV) replication in liver cells and mice without toxicity. This epigenetic therapy approach shows promise for treating HCV-associated diseases like liver cancer.

Area of Science:

  • Hepatology
  • Virology
  • Epigenetics

Background:

  • Histone deacetylase (HDAC) inhibitors are investigated for cancer treatment, including hepatocellular carcinoma (HCC).
  • Hepatitis C virus (HCV) infection is a major cause of HCC, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the impact of HDAC inhibitor treatment on HCV replication.
  • To explore the underlying molecular mechanisms and therapeutic potential in preclinical models.

Main Methods:

  • Treatment of Huh7 human liver cells and a mouse model with an HDAC3 inhibitor.
  • Analysis of viral replication, cellular toxicity, gene expression (microarray, qRT-PCR), and protein-DNA interactions (promoter binding assays).

Main Results:

  • HDAC3 inhibition markedly suppressed HCV replication below 1 mmol/L without cellular toxicity.
  • Upregulation of liver-expressed antimicrobial peptide 1 (LEAP-1) and downregulation of apolipoprotein-A1 (Apo-A1) were observed.
  • HDAC3 modulated the binding of C/EBPα, HIF1α, and STAT3 to the LEAP-1 promoter, and HCV replication was blocked in vivo.

Conclusions:

  • HDAC3 inhibition effectively suppresses HCV replication through epigenetic modulation of LEAP-1.
  • Epigenetic therapy using HDAC3 inhibitors presents a potential treatment strategy for HCV-associated diseases, including HCC.
Keywords:
Apolipoprotein-A1(Apo-A1)HDAC3Hepatitis C virus (HCV)Hepatocellular carcinomaLEAP-1Viral replication

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