A Minireview: Molecular Understanding of HCV Infection Mechanism

Hepatitis C (HCV) is a positive polarity single-stranded (ss) RNA virus belongs to Flaviviridae family. It infects about 2% people annually throughout the world (WHO, 2012) and causes both acute and chronic hepatitis consequences permanent liver damage, hepatocellular carcinoma (HCC) and eventually death. The absence of effective means of treatment makes HCV infection a global health hazard. Due to lack of pin point of molecular mechanism, precise drug target and efficient preventive measure is still unclear. Therefore, identifying and understanding mechanistic underpinnings of viral entry, replication, assembly, and budding are crucial in owing to the development of antiviral therapy. Current host-pathogen interactions data and the infection model suggest that RNA dependent RNA polymerase activity of NS5B, along with NS5A and NS3 play central role in HCV infection mechanisms. It has been shown in numerous studies that the interactions between 5' and 3' UTRs (Un-translated regions) and the interactions UTRs verses host proteins play fundamental role in regulating replication and translation processes as well as their successive switching.