A previous study has found infection of the S-INDEL strains could induce pro-inflammatory cytokines through the non-canonical NF-κB signaling pathway by activating RIG-I; however, infection of the non-S-INDEL strains suppresses the induction of pro-inflammatory cytokines and type-I interferon production by down-regulation of TLRs and downstream signaling molecules (Temeeyasen et al., 2018). Here, RIGI is linked to infection.