Therefore, we generated chimeric HCV, TNS2J1, and have used it for transient infection experiments. We started with both JFH-1 and TNS2J1 for a persistent infection system. However, JFH-1-infected cells vanished completely after 3 months, the reason why was unknown. It was noteworthy that HPI cell has sustained steatosis as observed in chronic hepatitis C for long term. HCV modulates lipid metabolism to promote HCV replication and induces steatosis in its transgenic mice. HCV core protein associates with LDs. Moreover, LDs are shown to function in the assembly and Nebivolol release of HCV particles dependent on apolipoprotein B expression and VLDL secretion. Thus, we speculate the core protein plays a pivotal role in the development of steatosis as ��a viral factor�� in HPI cells. Since HMGCR is known to increase cholesterol and inhibitors of HMGCR, statins, inhibit HCV replication, it may be involved also in the persistence of HCV in HPI cells. Recent reports Triamcinolone demonstrated that miroRNA-122 regulates cholesterol metabolism by the down-regulation of HMGCR and HCV replication, Moreover, deletion of miR-122 results in hepatosteatosis and tumorigenesis in mice. Therefore, investigation of miroRNA including miR122 will be required for HPI cell. In relation to cholesterol, desmosterol was increased remarkably in HPI cell. Desmosterol is an immediate precursor of cholesterol. This conversion is catalyzed by 24-dehydrocholesterol reductase. A number of recent researches have shed light on unexpected and new roles of desmosterol and DHCR24 in metabolic diseases including hepatitis C. Another metabolite profiling study also showed increase of desmosterol in the HCV infected cells and demonstrated that activity of DHCR7, which catalyzes the reaction of desmosterol precursor to desmosterol, was important for HCV replication. We speculate that rather upregulation of HMGCH, rate-limiting enzyme for cholesterol, and SC5DL might enhance cholesterol synthesis pathway in the HPI cell and that down-regulation of DHCR24 might reduce the reaction of desmosterol to cholesterol resulting in the accumulation of desmosterol.