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Related Experiment Video

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Interferon lambda receptor-1 isoforms differentially influence gene expression and HBV replication in stem

Laura A Novotny1, J Grayson Evans1, Haitao Guo2

  • 1Division of Infectious Diseases, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA.

Antiviral Research
|December 9, 2023
PubMed
Summary

Altering interferon lambda receptor-1 (IFNLR1) isoforms in hepatocytes differentially impacts response to lambda IFNs (IFNLs) and hepatitis B virus (HBV) replication. Isoform 1 enhances antiviral activity, while isoforms 2 and 3 show limited efficacy.

Keywords:
HBV DNAIFNLR1Induced hepatocytescccDNAinterferon lambda

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Area of Science:

  • Hepatology
  • Immunology
  • Virology

Background:

  • Chronic hepatitis B virus (HBV) infection persists due to ineffective interferon signaling in the liver.
  • Interferon lambda (IFNL) signaling, mediated by interferon lambda receptor-1 (IFNLR1), is crucial for antiviral responses.
  • Hepatocytes express multiple IFNLR1 isoforms with unclear roles in IFNL signaling and HBV control.

Purpose of the Study:

  • To investigate the differential effects of IFNLR1 isoforms on hepatocellular response to IFNLs.
  • To determine how modulating IFNLR1 isoform expression impacts HBV replication.

Main Methods:

  • Hepatocytes derived from induced pluripotent stem cells (iHeps) were engineered with inducible IFNLR1 isoforms.
  • Engineered iHeps were infected with HBV and treated with IFNL3.
  • Assessed gene expression, HBV replication, and cell viability.

Main Results:

  • Overexpression of IFNLR1 isoform 1 significantly boosted interferon-stimulated gene (ISG) expression and HBV replication inhibition.
  • Isoform 1 also induced proinflammatory gene expression without affecting cell viability.
  • IFNLR1 isoforms 2 and 3 showed partial ISG induction but minimal impact on HBV replication or proinflammatory gene expression.

Conclusions:

  • IFNLR1 isoforms differentially regulate IFNL-induced gene expression and HBV replication in hepatocytes.
  • Targeting IFNLR1 expression could be a strategy to enhance antiviral responses against HBV.