Abstract
The hepatic microRNA (miRNA), miR-122, is the most abundant miRNA within the liver, where it accounts for 70% of the total miRNA pool. It is known that miR-122, as an unusual host factor, increases the abundance of hepatitis C virus (HCV) RNA in HCV infection by binding directly to the 5'-UTR of the viral genome. Therefore, it has been suggested as a potential target for the treatment of hepatitis C. However, recent evidence shows that miR-122 decreases HBV replication through the inhibitory effect of p53 on HBV transcription, and consequently it acts as a tumor-suppressor through both a decrease in HBV replication and by directly targeting cyclin G1, as well as Wnt/beta-catenin, and NDRG3 pathways. This paper will briefly discuss the underlying mechanisms for the dual role of miR-122 in viral hepatitis, and explains why therapeutic applications of miR-122 may differ based on the underlying disease.