As we learned in class, Hepatitis C virus (HCV) conducts microRNA-122 (miRNA-122)-dependent replication in the liver. More specifically, the HCV viral particle must actually physically bind to miRNA-122 in order to initiate replication. A heretofore unrealized consequence of this attraction is the "sequestration" of miRNA-122, or the "pulling away" of this molecule from its normal day job, which is to regulate genes. The consequences of this effect may be far-reaching and may underlie HCV pathology.
An article in the March 2015 issue of Cell, "Hepatitis C Virus RNA Functionally Sequesters miR-122," by Luna et al. establishes this phenomenon. The researchers, who conducted their work at Rockefeller University, posit that their conclusions suggest strongly that miRNA-122 should be a target molecule in drug development.
microRNA is an RNA subtype specifically equipped to dampen gene expression by recruiting "silencing proteins" to an mRNA transcript before it can be translated. miRNA-122 in particular governs the gene expression of factors involved in crucial functions like iron and cholesterol metabolism and circadian rhythms.
Source: Luna, J M et al. "Hepatitis C Virus RNA Functionally Sequesters miR-122." Cell. 2015: vol. 160, no. 6. http://www.sciencedirect.com/science/article/pii/S0092867415001919.