Innate immune responses are the first line of defense against microbial infection, and they play a major role in restricting infection by viruses. These responses, which are well documented in organisms ranging from simple invertebrates to mammals, classically involve recognition of pathogen-associated molecular patterns on the invading infectious agent by host pattern recognition receptors (PRRs) such as retinoic-acid-inducible gene-l (RIG-l)-like receptors (RLRs), nucleotide-oligomerization-domain-like receptors, and Toll-like receptors (TLRs) [1]. The interaction between pathogen-associated molecular patterns and PRRs triggers a cascade of events that leads to the production of pro-inflammatory cytokines and three classes of interferons (IFNs): type I (IFN-alpha and IFN-beta), type II (IFN-gamma), and type III (IFN-A1, IFN-A2, and IFN-A3). Key steps in the induction of IFNs and pro-inflammatory cytokines include activation and nuclear translocation of NF-kB, iFN-regulatory factor 3 (IRF3), and IFN-regulatory factor 7 (IRF7).
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