“…The N-terminal protease and C-terminal helicase domains of HCV NS3 are interdependent, and both enzymatic activities are essential for HCV replication, assembly, and pathogenesis [ 5 ]. Although current treatment therapy, comprising of directly acting antiviral agents (DAAA), is highly effective [ 6 ], still virus in 4-5% of the individuals do not respond to the therapy [ 7 ]. Furthermore, numerous reports have identified the emergence of drug resistance mutations, which can affect the activity of DAAAs [ 8 ].…”