[Interferon : antiviral mechanisms and viral escape]

Bull Cancer. 2003 Feb;90(2):131-41.
[Article in French]

Abstract

15 % of human cancers have virus origin, meaning that viruses are the second cause of cancers after tabagism. The knowledge of antiviral mechanisms is essential for treatment and prevention of infection evolution towards cancers. Interferons (IFNs) are a large family of multifunctional cytokines. They are involved in regulation of cell growth and modulation of immune response. But, all these functions seem to converge toward the most important of them : the antiviral activity. IFN secretion is the first event induced by viral infection, and will act on specific receptors on neighbour cells and prevent their infection by inducing numbers of antiviral genes. Although few of them are well known like the PKR, the 2-5OAS/RNase L pathway and the Mx proteins, many others need extensive studies to understand the wide range of IFN effect. Viruses have evolved to circumvent the IFN antiviral activity, and are able not only to divert the cellular machinery but also to lure the antiviral mechanisms of the host cell. The purpose of this review is to describe the many antiviral pathways and proteins induced by IFNs and to summarize the strategies of viral escape.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Animals
  • Endoribonucleases / metabolism
  • GTP-Binding Proteins / metabolism
  • Humans
  • Interferon Type I / physiology
  • Interferons / physiology*
  • Mice
  • Myxovirus Resistance Proteins
  • Neoplasms / virology
  • Signal Transduction / physiology
  • Virus Diseases / metabolism
  • Virus Diseases / virology*
  • eIF-2 Kinase / metabolism

Substances

  • Interferon Type I
  • Mx1 protein, mouse
  • Myxovirus Resistance Proteins
  • Interferons
  • eIF-2 Kinase
  • Endoribonucleases
  • 2-5A-dependent ribonuclease
  • GTP-Binding Proteins