Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

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

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Guidotti, Luca
  • Morris, A.
  • Mendez, H.
  • Koch, R.
  • Silverman, R. H.
  • Williams, B. R. G.
  • Chisari, Francis

publication date

  • March 2002

journal

  • Journal of Virology  Journal

abstract

  • We previously showed that the intrahepatic induction of cytokines such as alpha/beta interferon (IFN-alpha/beta) and gamma interferon (IFN-gamma) inhibits hepatitis B virus (HBV) replication noncytopathically in the livers of transgenic mice. The intracellular pathway(s) responsible for this effect is still poorly understood. To identify interferon (IFN)-inducible intracellular genes that could play a role in our system, we crossed HBV transgenic mice with mice deficient in IFN regulatory factor 1 (IRF-1), the double-stranded RNA-activated protein kinase (PKR), or RNase L (RNase L) (IRF-1(-/-), PKR(-/-), or RNase L(-/-) mice, respectively), three well-characterized IFN-inducible genes that mediate antiviral activity. We showed that unmanipulated IRF-1(-/-) or PKR(-/-) transgenic mice replicate HBV in the liver at slightly higher levels than the respective controls, suggesting that both IRF-1 and PKR individually appear to mediate signals that modulate HBV replication under basal conditions. These same animals were responsive to the antiviral effects of the IFN-alpha/beta inducer poly(I-C) or recombinant murine IFN-gamma, suggesting that under these conditions, either the IRF-1 or the PKR genes can mediate the antiviral activity of the IFNs or other IFN-inducible genes mediate the antiviral effects. Finally, RNase L(-/-) transgenic mice were undistinguishable from controls under basal conditions and after poly(I-C) or IFN-gamma administration, suggesting that RNase L does not modulate HBV replication in this model.

subject areas

  • Animals
  • DNA-Binding Proteins
  • Endoribonucleases
  • Gene Expression Regulation, Viral
  • Hepatitis B
  • Hepatitis B virus
  • Interferon Regulatory Factor-1
  • Interferon-gamma
  • Liver
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Phosphoproteins
  • Poly I-C
  • Recombinant Proteins
  • Virus Replication
  • eIF-2 Kinase
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0022-538X

Digital Object Identifier (DOI)

  • 10.1128/jvi.76.6.2617-2621.2002

PubMed ID

  • 11861827
scroll to property group menus

Additional Document Info

start page

  • 2617

end page

  • 2621

volume

  • 76

issue

  • 6

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support