Porcine epidemic diarrhea virus inhibits dsRNA-induced interferon-ß production in porcine intestinal epithelial cells by blockade of the RIG-I-mediated pathway

Cao, Liyan; Ge, Xuying; Gao, Yu; Herrler, Georg; Ren, Yudong; Ren, Xiaofeng; Li, Guangxing

During viral infection and replication, the host innate immune response is the first line of defense; therefore, the ability of viruses to suppress or avoid this response is crucial for their pathogenic potential. IFN-α/β is an essential element of the host innate immune response against viral infections. Double-stranded RNA (dsRNA), the replicative intermediate of most viruses, is a potent inducer of IFN-β, which is recognized as a pathogen-associated molecular pattern (PAMP) by host pattern recognition receptors (PRRs). Two of major PRRs, retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) detect dsRNA in the cytoplasm [15] . Following dsRNA binding, RIG-I and MDA5 recruit corresponding adapter protein IFN-β promoter stimulator 1 (IPS-1) that, in turn, activate downstream signaling of TANK-binding kinase 1 (TBK1) and inhibitor of κB kinase-ε (IKKε) transduction, leading to the activation of transcription factor IFN regulatory factor 3 (IRF-3) and nuclear factor-kappaB (NF-κB). Activated IRF-3, and NF-κB bind to IFN-β enhancer and initiate IFN-β transcription [16] .