Using interferon-alpha to block expression of cellular ribosome subunit S24 variant 2 in human fibroblasts inhibits translation of the poliovirus genome

Viral Immunol. 2007 Spring;20(1):142-9. doi: 10.1089/vim.2006.0058.

Abstract

Studies about the proteins induced by interferon (IFN-)-alpha stimulation have provided some data on their mechanism of antiviral effect. These proteins were confirmed to contribute to antiviral functions. In this study, IFN-alpha stimulation of human fibroblasts was shown to induce the inhibition of S24 variant 2 (a structural component of the ribosomal small subunit) at the mRNA and protein levels, implying a possible antiviral mechanism for IFN-alpha in human fibroblasts. The delay of poliovirus replication by IFN-alpha was partially compensated for by S24 variant 2 expressed in pcDNA vector-transfected cells, and the interference RNA of S24 variant 2 was able to induce mimetically, to some extent, this poliovirus replication delay. These observations revealed that S24 variant 2 could be involved in the antiviral effects of IFN-alpha in human fibroblasts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / pharmacology*
  • Cell Line
  • Fibroblasts / virology
  • Genome, Viral
  • Humans
  • Interferon-alpha / pharmacology*
  • Poliovirus / genetics*
  • Protein Biosynthesis / drug effects*
  • RNA Interference
  • Ribosomal Proteins / antagonists & inhibitors*
  • Ribosomal Proteins / genetics

Substances

  • Antiviral Agents
  • Interferon-alpha
  • RPS24 protein, human
  • Ribosomal Proteins