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Related Experiment Videos

Interferon-regulated pathways that control hepatitis B virus replication in transgenic mice.

Luca G Guidotti1, Amber Morris, Heike Mendez

  • 1Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. guidotti@scripps.edu

Journal of Virology
|February 28, 2002
PubMed
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Interferon regulatory factor 1 (IRF-1) and protein kinase R (PKR) modulate hepatitis B virus (HBV) replication. RNase L does not appear to play a role in HBV replication in this mouse model.

Area of Science:

  • Virology
  • Immunology
  • Hepatology

Background:

  • Interferons (IFNs) inhibit hepatitis B virus (HBV) replication noncytopathically in mouse livers.
  • The intracellular mechanisms mediating this IFN-induced antiviral effect remain largely unknown.

Purpose of the Study:

  • To identify interferon (IFN)-inducible intracellular genes involved in controlling HBV replication.
  • To investigate the roles of IFN regulatory factor 1 (IRF-1), protein kinase R (PKR), and RNase L in HBV replication.

Main Methods:

  • Crossed HBV transgenic mice with mice deficient in IRF-1, PKR, or RNase L.
  • Assessed HBV replication levels in unmanipulated and IFN-stimulated knockout mice.
  • Evaluated responses to poly(I-C) and recombinant murine IFN-gamma.

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Main Results:

  • IRF-1(-/-) and PKR(-/-) mice showed slightly increased HBV replication under basal conditions.
  • IRF-1(-/-) and PKR(-/-) mice retained responsiveness to IFN-alpha/beta and IFN-gamma.
  • RNase L(-/-) mice exhibited no significant differences compared to controls in HBV replication.

Conclusions:

  • IRF-1 and PKR individually modulate HBV replication under basal conditions.
  • Either IRF-1 or PKR, or other IFN-inducible genes, can mediate IFN-induced antiviral activity against HBV.
  • RNase L is not implicated in modulating HBV replication in this model.