Autophagy is a self-eating process, in which the damaged or excessed cell 
organelles and misfolded protein aggregates are removed from the cellular 
microenvironment. Autophagy is generally thought of as a pro-survival mechanism 
which is not only important for balancing energy supply at times of nutrient 
deprivation but also in the removal of various stress stimuli to ensure 
homeostasis. In addition to the target materials of "self" origin, autophagy can 
also eliminate intracellular pathogens and acts as a defense mechanism to curb 
infections. In addition, autophagy is linked to the host cell's innate immune 
response. However, viruses have evolved various strategies to manipulate and 
overtake host cell machinery to establish productive replication and maintain 
infectious process. In fact, replication of many viruses has been found to be 
autophagy-dependent and suppression of autophagy can potentially affect the 
viral replication. Thus, autophagy can either serve as an anti-viral defense 
mechanism or a pro-viral process that supports viral replication. Hepatitis B 
virus (HBV) and hepatitis C virus (HCV) are known to co-opt cellular autophagy 
process as a pro-viral tool. Both viruses also induce mitophagy, which 
contributes to the establishment of chronic hepatitis. This review focuses on 
the roles of autophagy and mitophagy in the chronic liver disease pathogenesis 
associated with HBV and HCV infections.