FIGURE 1.

General overview of intracellular innate immune signaling and some representative viral immune escape mechanisms. Sensing virus by PRRs initiates innate immune signaling through the hierarchical activation of PRRs family-specific adaptor proteins (TRIF, MAVS, STING, MYD88, and so forth) to activate transcriptional factors, such as IRF3/5/7, NF-kB, and others. Activated transcriptional factors translocate into nucleus and induce robust expression of IFNs. Secreted IFNs bind to their respective receptors and activate JAK-STAT signaling and form a transcriptional factor called ISGF3. ISGF3, then, translocates into nucleus to induce expression of numerous antiviral effectors (ISGs) to impede viral infection. Although antiviral innate immunity consists of well-equipped arsenals to impede viral infection and invasion, viruses circumvent or escape from these antiviral arsenals to establish successful infection through several mechanisms. Of these escape mechanisms, viral components inhibit innate immune signaling by diversified tactics, such as interacting directly or indirectly with crucial innate elements, targeting and cleaving adaptor proteins involved in innate immune signaling or interference of IFN signaling, degradation of JAK/STAT components, and so forth. Some representative viral immune escape tactics are shown in the Figure 1.