Immune Evasion of Enteroviruses Under Innate Immune Monitoring

FIGURE 1. The main mechanism of innate immunity evasion by enteroviruses in host cells. Host cells identify external pathogens through their PRRs, including TLRs, RIG-I, and NLRs. The PRRs initiate conformational changes and recruit adaptor molecules in their signaling pathways. Then, the downstream signals are propagated through the activation of core components, such as TRAF6 and the IKK complex, culminating in the activation of transcription factors, which regulate the production of genes associated with the innate immune response. In addition, during binding of IFNs to the IFN receptors, multiple signaling pathways are activated. Then, activation of the kinases and downstream formation of various STAT complexes mediates IFN-dependent gene transcription of IFN-stimulated genes. The adapter proteins and key kinases that mediate these signaling pathways are targeted by viral proteins (such as 2A, 2C, and 3C) or microRNAs (miR-146a). TLRs, toll-like receptors; RIG-I, RIG-I-like receptors; NLRs, NOD-like receptors; NOD2, nucleotide binding oligomerization domain 2; MDA5, melanoma differentiation gene 5; MAVS, mitochondrial antiviral signaling protein; NLRP3, NOD-like receptor 3; TIRAP,…