Increased iron in HCV infection: Collateral damage or antiviral defense?

Iron accumulation of an HCV-infected hepatocyte as an antiviral strategy? Among other sources, ROS are generated by NADPH-dependent oxidases of innate immune cells (NOX1) and hepatocytes (NOX4) in HCV infected livers. This oxidative stress eventually leads to intracellular iron accumulation via suppressed hepcidin or activation of IRP1 or TfR1. This iron can clear the hepatocyte from the virus since iron is a potent inhibitor of viral replication. In contrast, infection with the hepatitis C virus leads to an iron-depleted hepatocyte phenotype via still unknown mechanisms. IRP1, iron regulatory protein 1, TfR1, transferrin receptor 1.