Innate immunity establishes the first line of defense against
pathogenic microorganisms. The host senses pathogenic microorganisms
invasion by recognition of pathogen-associated molecular
patterns (PAMP) with pattern recognition receptors (PRR),
including Toll-like receptor (TLR), RIG-I-like receptors (RLRs) and
NOD-like receptors (NLRs) [1]. RLRs mainly sense cytoplasmic viral
RNA and play a key role in regulating the inflammatory response
against infectious viruses [2]. The RLRs family contains three
members: RIG-I, MDA5 (Melanoma differentiation associated gene
5), and LGP2. All three RLRs contain a DExD/H-box helicase domain
and a C-terminal domain. RIG-I and MDA5 further contain N-terminal
tandem caspase activation and recruitment domain (CARD)
which LGP2 lacks [3]. The CARD within these RLRs are mainly
responsible for downstream signaling by interacting with its
adaptor protein MAVS (Mitochondrial antiviral signaling protein) to
activate the transcription factors NF-kB and IRFs, and then induce
production of type I IFNs and pro-inflammatory cytokines.