HCV-induced autophagy and innate immunity. Hepatitis C virus (HCV) induces autophagy, a cellular process that removes damaged organelles and protein aggregates, and uses it to enhance its replication. Autophagy also functions as an innate immune response to trap pathogens. However, HCV manipulates autophagy to evade host immune responses. Mitophagy, a form of autophagy targeting mitochondria, alters mitochondrial dynamics and metabolism, which are important for host antiviral responses. HCV promotes mitophagy to prevent premature cell death and reduce interferon (IFN) responses. Additionally, HCV disrupts inflammasome signaling, leading to IFN resistance and immune tolerance. These immune evasion strategies allow HCV to persist in host cells. The article discusses HCV-induced autophagy and its associated immune responses, highlighting the role of autophagy in HCV replication and immune evasion. HCV proteins such as NS3/4A and NS4B inhibit IFN signaling by cleaving key signaling proteins. HCV also exploits autophagy membranes for RNA replication and infectious particle production. Autophagy suppresses IFN responses by degrading IFN receptors and signaling proteins. HCV-induced autophagy also regulates the inflammasome and innate immune responses. The interplay between HCV-induced autophagy and innate immunity is complex, with HCV using autophagy to enhance replication while evading immune responses. The article also discusses the role of Nrf2 in HCV-induced oxidative stress and the impact of mitochondrial dynamics on innate immunity. Overall, HCV has developed strategies to manipulate autophagy and innate immunity to establish chronic infection and evade immune responses.HCV-induced autophagy and innate immunity. Hepatitis C virus (HCV) induces autophagy, a cellular process that removes damaged organelles and protein aggregates, and uses it to enhance its replication. Autophagy also functions as an innate immune response to trap pathogens. However, HCV manipulates autophagy to evade host immune responses. Mitophagy, a form of autophagy targeting mitochondria, alters mitochondrial dynamics and metabolism, which are important for host antiviral responses. HCV promotes mitophagy to prevent premature cell death and reduce interferon (IFN) responses. Additionally, HCV disrupts inflammasome signaling, leading to IFN resistance and immune tolerance. These immune evasion strategies allow HCV to persist in host cells. The article discusses HCV-induced autophagy and its associated immune responses, highlighting the role of autophagy in HCV replication and immune evasion. HCV proteins such as NS3/4A and NS4B inhibit IFN signaling by cleaving key signaling proteins. HCV also exploits autophagy membranes for RNA replication and infectious particle production. Autophagy suppresses IFN responses by degrading IFN receptors and signaling proteins. HCV-induced autophagy also regulates the inflammasome and innate immune responses. The interplay between HCV-induced autophagy and innate immunity is complex, with HCV using autophagy to enhance replication while evading immune responses. The article also discusses the role of Nrf2 in HCV-induced oxidative stress and the impact of mitochondrial dynamics on innate immunity. Overall, HCV has developed strategies to manipulate autophagy and innate immunity to establish chronic infection and evade immune responses.