[miR-122 participates in the cell tropism of hepatitis C virus].

Hepatitis C virus (HCV) exhibits a narrow host range and a specific tissue tropism. Studies on HCV life cycle have been progressed by the developments of in vitro replication and infection systems and an HCV laboratory strain (HCVcc) capable of propagating in human hepatoma cell line, Huh7 cells. Mice expressing four human entry receptor candidates for HCV permit entry of HCVcc, therefore tissue tropism of HCV was believed to be rely on the expression of the entry receptors. However, HCV infection is often associated with extra-hepatic manifestations and the determinants for cell tropism of HCV remain elusive. Recently, we have shown that several nonhepatic cell lines permit HCV-RNA replication through an expression of a liver-specific microRNA, miR-122, upon infection with HCVcc, while no infectious particle was produced. In the nonhepatic cells, only small numbers of lipid droplets and low levels of VLDL-associated proteins were observed in compared with Huh7 cells, suggesting that expression of miR-122 and functional lipid metabolism participates in the replication and assembly of HCVcc, respectively In this review, we would like to discuss about involvement of miR-122 and functional lipid metabolism in the determination of HCV cell tropism.