Mechanisms of evasion of the type I interferon antiviral response by flaviviruses

J Interferon Cytokine Res. 2009 Sep;29(9):521-30. doi: 10.1089/jir.2009.0069.

Abstract

Virus survival and the ability to cause disease in mammalian hosts depend on their ability to avoid recognition and control by the interferon signal transduction and effector pathways. Flaviviruses comprise a large family of nonsegmented positive sense enveloped cytoplasmic RNA viruses, many of which are globally important human pathogens. Although the mechanistic details are still being dissected, new insight has emerged as to how a flavivirus minimizes the antiviral activity of type I interferon (IFN) to establish productive and potentially lethal infection. This review will summarize our current understanding of how mammalian cells recognize flaviviruses to induce an inhibitory IFN response and the countermeasures this group of viruses has evolved to antagonize this response.

Publication types

  • Review

MeSH terms

  • Animals
  • Flavivirus / immunology*
  • Flavivirus / pathogenicity
  • Flavivirus Infections / genetics
  • Flavivirus Infections / immunology*
  • Flavivirus Infections / transmission
  • Flavivirus Infections / virology*
  • Gene Expression Regulation
  • Humans
  • Immunity, Innate
  • Interferon Regulatory Factors / metabolism
  • Interferon Type I / genetics
  • Interferon Type I / immunology
  • Interferon Type I / metabolism*
  • Membrane Proteins / metabolism
  • Nerve Tissue Proteins / metabolism
  • Receptors, Cell Surface
  • STAT Transcription Factors / metabolism
  • Signal Transduction
  • Toll-Like Receptors / metabolism
  • Viral Nonstructural Proteins / immunology
  • Viral Nonstructural Proteins / metabolism*
  • Virulence

Substances

  • Interferon Regulatory Factors
  • Interferon Type I
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Receptors, Cell Surface
  • Robo3 protein, mouse
  • STAT Transcription Factors
  • Toll-Like Receptors
  • Viral Nonstructural Proteins