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
Copyright policy )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.
- Cleveland Clinic United States
- Aarhus University Denmark
- Osaka University Japan
- Cleveland Clinic Lerner Research Institute United States
- The University of Texas Southwestern Medical Center United States
Fibroblasts, DEAD-box RNA Helicases, Mice, Toll-Like Receptor 9, Endoribonucleases, Interferon Type I, Animals, DEAD Box Protein 58, Simplexvirus, Cells, Cultured
Fibroblasts, DEAD-box RNA Helicases, Mice, Toll-Like Receptor 9, Endoribonucleases, Interferon Type I, Animals, DEAD Box Protein 58, Simplexvirus, Cells, Cultured
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