The article discusses the interplay between hepatitis C virus (HCV) and the host's autophagy and innate immune responses. HCV impairs pattern-recognition receptor (PRR) signaling pathways that recognize pathogen-associated molecular patterns (PAMPs). Autophagy, a cellular catabolic process, is also an innate immune response that traps and degrades pathogens. However, HCV controls the autophagic pathway and uses autophagic membranes for its replication. Mitophagy, a selective autophagy targeting mitochondria, alters mitochondrial dynamics and metabolism, which are crucial for antiviral responses. HCV promotes mitophagy to prevent premature cell death and reduce interferon (IFN) response. Additionally, HCV dysregulates the inflammasomal response, leading to IFN resistance and immune tolerance. These immune evasion mechanisms allow HCV to replicate and persist in host cells. The article reviews the regulation of HCV-induced autophagy/mitophagy and its associated immunological responses, providing insights into how these processes are regulated in HCV-infected cells.The article discusses the interplay between hepatitis C virus (HCV) and the host's autophagy and innate immune responses. HCV impairs pattern-recognition receptor (PRR) signaling pathways that recognize pathogen-associated molecular patterns (PAMPs). Autophagy, a cellular catabolic process, is also an innate immune response that traps and degrades pathogens. However, HCV controls the autophagic pathway and uses autophagic membranes for its replication. Mitophagy, a selective autophagy targeting mitochondria, alters mitochondrial dynamics and metabolism, which are crucial for antiviral responses. HCV promotes mitophagy to prevent premature cell death and reduce interferon (IFN) response. Additionally, HCV dysregulates the inflammasomal response, leading to IFN resistance and immune tolerance. These immune evasion mechanisms allow HCV to replicate and persist in host cells. The article reviews the regulation of HCV-induced autophagy/mitophagy and its associated immunological responses, providing insights into how these processes are regulated in HCV-infected cells.