The results indicated that RIG-1 (rs3739674 and rs9695310) polymorphisms are associated with an increased risk of enterovirus 71-induced hand foot and mouth disease in Chinese children whereas RIG-1 rs3739674 and TLR3 rs5743305 polymorphisms are associated with disease severity. These findings support an important role of innate immune mechanism in enterovirus 71 infection.
DDX58_rs10813831 T-allele may be associated with a reduced risk of nodular sclerosis EBV-related cHL which suggests a role for RIG-I (retinoic acid-inducible gene I) encoded by DDX58 in these cases.
mutations in the genes encoding for RIG-I and MDA5 have been identified to cause rare diseases including Aicardi-Goutieres syndrome Systemic Lupus Erythematosus in certain individuals as well as classic and atypical Singleton-Merten syndrome. Patients carrying mono-allelic mutations in MDA5 and RIG-I show constitutive activation of the RIG-I receptors and downstream signalling
DDX58 mutations cause atypical Singleton-Merten syndrome manifesting with variable expression of glaucoma aortic calcification and skeletal abnormalities without dental anomalies.
genetic associations between common single nucleotide polymorphisms in RIG-I-like receptor and IL-4 signaling genes and severe respiratory syncytial virus infection in children
RIG-I has a functional role in plasmacytoid DCs which respond to cytosolic delivery of synthetic (non-self) dsRNA in a RIG-I-dependent manner explaining RSV-induced type I IFN production independent of endosomal toll-like receptors and protein kinase R.
DDX58 is expressed in skin and lymph node of a patient with Sweet's syndrome Kikuchi's disease and hemophagocytic syndrome and may suggest association with RIG-I-related innate immunity.
IL28B and DDX58 single nucleotide polymorphisms that are favorable when present in the non-transplant setting or in the recipient are unfavorable when present in a donor liver graft.
influenza A(H1N1)pdm09 virus suppresses anti-viral immune responses in infected human lung through inhibition of viral-mediated induction of the pattern recognition receptor RIG-I though proinflammatory cytokine induction was unaltered.
These results suggested that West Nile virus evades the host response by sequestering RIG-I-specific pathogen associated molecular patterns within the complete genome and antigenome at early times post-infection.
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