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Interleukin-2 down-regulates hepatitis-B virus gene-expression in transgenic mice by a posttranscriptional mechanism

Academic Article
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Overview

authors

  • Guilhot, S.
  • Guidotti, Luca
  • Chisari, Francis

publication date

  • December 1993

journal

  • Journal of Virology  Journal

abstract

  • We have recently demonstrated that tumor necrosis factor alpha (TNF-alpha) and interleukin-2 (IL-2) downregulate the hepatic steady-state content of hepatitis B virus (HBV) mRNA in vivo in HBV-transgenic mice and that the IL-2 effect is mediated by TNF-alpha. In the current study, we demonstrate that IL-2-induced downregulation of hepatic HBV 2.1-kb mRNA is not due to changes in the transcription rate or the intranuclear maturation or export of this transcript but that it is selectively and profoundly depleted from the cytoplasm of the liver cells in vivo following IL-2 administration. Collectively, these results suggest that IL-2 alters the steady-state content of hepatic HBV mRNA by a posttranscriptional mechanism in vivo, that this effect is mediated by TNF-alpha, and that it probably reflects increased cytoplasmic degradation of the viral transcript.

subject areas

  • Animals
  • Base Sequence
  • Cell Compartmentation
  • Cell Nucleus
  • Cytoplasm
  • Down-Regulation
  • Gene Expression Regulation, Viral
  • Hepatitis B virus
  • Interleukin-2
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Nucleic Acid Hybridization
  • Promoter Regions, Genetic
  • RNA Probes
  • RNA Processing, Post-Transcriptional
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Identity

PubMed Central ID

  • PMC238210

International Standard Serial Number (ISSN)

  • 0022-538X

PubMed ID

  • 8230465
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Additional Document Info

start page

  • 7444

end page

  • 7449

volume

  • 67

issue

  • 12

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