HCV and Oxidative Stress: Implications for HCV Life Cycle and HCV-Associated Pathogenesis

Figure 1

Hypothetical model summarizing the interplay between Nrf2, phosphor-p62, ROS, and autophagy. As described by Carvajal-Yepes et al. [58], Nrf2/ARE-signaling in HCV positive cells is impaired by translocation of sMaf from the nucleus to NS3 in the replicon complexes on the cytoplasmic face of the ER. This leads to the sequestration of Nrf2 to the replicon complex-bound sMaf and prevents the phospho-p62-dependent released Nrf2 from the entry in the nucleus and thereby inhibits the induction of Nrf2/ARE-dependent genes. This would contribute to an impaired elimination of ROS that contribute to the induction of autophagy that is crucial for the HCV life cycle.