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. 2018 Jul 18;9:1611. doi: 10.3389/fmicb.2018.01611

FIGURE 3.

FIGURE 3

Classical interferon (IFN) and IFN-stimulated gene (ISG) induction in response to viral infection. In the cytoplasm, viral DNA is recognized by cGAS, DDX41, or IFI16, leading to the activation of STING, which further recruits TBK1 for IRF activation and translocates to the nucleus to initiate IFN production. Viral RNA is detected by RIG-I and MDA5, and recruits another adaptor protein: MAVS (IPS-1), resulting in TBK1 activation, IRF phosphorylation, and IFN induction. Then, IFNs are secreted from the cells and bind to IFNAR1/2, leading to JAK/STAT activation. The activated ISGF3 trimer or STAT1 dimer bind to the ISRE or GAS sequence and promote the expression of ISGs. ISGs inhibit HBV as shown in the black box. cGAS, cyclic GMP-AMP synthase; DDX41, DEAD-box protein 41; IFI16, γ-IFN-inducible protein 16; STING, stimulator of IFN genes; TBK1, TANK-binding kinase 1; IFNAR1, type I IFN receptor 1; JAK, Janus tyrosine kinase; STAT, signal transducer and activator of transcription.