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Beyond Double-Stranded RNA-Type I IFN Induction by 3pRNA and Other Viral Nucleic Acids

  • M. Schlee
  • W. Barchet
  • V. Hornung
  • G. Hartmann
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 316)

Abstract

Production of type I IFN is the key response to viral infection. Since the discovery of type I IFNs in 1957, long double-stranded RNA formed during replication of many viruses was thought to be responsible for type I IFN induction, and for decades double-stranded RNA-activated protein kinase (PKR) was thought to be the receptor. Recently, this picture has dramatically changed. It now became evident that not PKR but two members of the Toll-like receptor (TLR) family, TLR7 and TLR9, and two cytosolic helicases, RIG-I and MDA-5, are responsible for the majority of type I IFNs induced upon recognition of viral nucleic acids. In this review, we focus on the molecular mechanisms by which those innate immune receptors detect viral infection. Based on the recent progress in the field, we now know that TLR7, TLR9, and RIG-I do not require long double-stranded RNA for type I IFN induction.

Keywords

Plasmacytoid Dendritic Cell Viral Nucleic Acid Modify Nucleoside Short dsRNA Nucleoside Modification 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 2007

Authors and Affiliations

  • M. Schlee
    • 1
  • W. Barchet
    • 1
  • V. Hornung
    • 2
  • G. Hartmann
    • 1
  1. 1.Abteilung für Klinische PharmakologieUniversitätsklinikum BonnBonnGermany
  2. 2.Division of Clinical Pharmacology, Department of Internal MedicineUniversity of MunichMunichGermany

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