RIG-I-like receptor regulation in virus infection and immunity

Curr Opin Virol. 2015 Jun;12:7-14. doi: 10.1016/j.coviro.2015.01.004. Epub 2015 Jan 30.

Abstract

Mammalian cells have the intrinsic capacity to detect viral pathogens and to initiate an antiviral response that is characterized by the induction of interferons (IFNs) and proinflammatory cytokines. A delicate regulation of the signaling pathways that lead to cytokine production is needed to ensure effective clearance of the virus, while preventing tissue damage caused by excessive cytokine release. Here, we focus on the mechanisms that modulate the signal transduction triggered by RIG-I-like receptors (RLRs) and their adaptor protein MAVS, key components of the host machinery for sensing foreign RNA. Specifically, we summarize recent advances in understanding how RLR signaling is regulated by posttranslational and posttranscriptional mechanisms, microRNAs (miRNAs) and autophagy. We further discuss how viruses target these regulatory mechanisms for immune evasion.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Animals
  • Autophagy
  • Cytokines / immunology
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases / genetics
  • DEAD-box RNA Helicases / metabolism*
  • Gene Expression Regulation
  • Humans
  • Immune Evasion
  • Immunity, Innate
  • Interferons / immunology
  • MicroRNAs / genetics
  • Signal Transduction*
  • Virus Diseases / immunology*
  • Virus Diseases / virology*
  • Viruses / immunology*
  • Viruses / pathogenicity*

Substances

  • Adaptor Proteins, Signal Transducing
  • Cytokines
  • MAVS protein, human
  • MicroRNAs
  • Interferons
  • DDX58 protein, human
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases