Herpes simplex virus infection is sensed by both Toll-like receptors and retinoic acid-inducible gene- like receptors, which synergize to induce type I interferon production.
The innate antiviral response is initiated by pattern recognition receptors, which recognize viral pathogen-associated molecular patterns. Here we show that retinoic acid-inducible gene (RIG)-I-like receptors (RLRs) in cooperation with Toll-like receptor (TLR) 9 is required for expression of type I interferons (IFNs) after infection with herpes simplex virus (HSV). Our work also identified RNase L as a critical component in IFN induction. Moreover, we found that TLR9 and RLRs activate distinct, as well as overlapping, intracellular signalling pathways. Thus, RLRs are important for recognition of HSV infection, and cooperate with the Toll pathway to induce an antiviral response.
Rasmussen
Simon B
SB
Institute of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark.
Jensen
Søren B
SB
Nielsen
Christoffer
C
Quartin
Emanuel
E
Kato
Hiroki
H
Chen
Zhijian J
ZJ
Silverman
Robert H
RH
Akira
Shizuo
S
Paludan
Søren R
SR
D000818:Animals; D002478:Cells, Cultured; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000276:immunology*; D004722:Endoribonucleases / Q000276:immunology; D005347:Fibroblasts / Q000821:virology; D007370:Interferon Type I / Q000096:biosynthesis*; D051379:Mice; D018139:Simplexvirus / Q000276:immunology*; D051217:Toll-Like Receptor 9 / Q000276:immunology*
D007370:Interferon Type I; D051217:Toll-Like Receptor 9; D004722:Endoribonucleases; C031956:2-5A-dependent ribonuclease; C503356:Ddx58 protein, mouse; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases