Hepatitis C virus and antiviral innate immunity: Who wins at tug-of-war?

Figure 1 Immune sensing of hepatitis C virus by pattern recognition receptors. During hepatitis C virus (HCV) infection, PKR and RIG-I recognize dsRNA constructed in the HCV IRES and HCV PAMP with 5’-triphosphate plus 3’poly-U/UC region, respectively. In the late period of infection, HCV dsRNA from viral replication intermediates or extracellular dying cells is detected by TLR3. Activation of pattern recognition receptors (PRRs) leads to the transduction of signaling through adaptor protein MAVS or TRIF, and subsequent phosphorylation and dimerization of IRF3 to induce the production of IFN-β, IFN-λ, ISGs and proinflammatory cytokines. MT: Mitochondria; ER: Endoplasmic reticulum; ES: Endosome; PX: Peroxisome; MAVS: Mitochondrial antiviral signaling; PAMP: Pathogen-associated molecular pattern; IFN: Interferon; TRIF: TIR-domain-containing adaptor-inducing interferon-β.