Therefore, cellular factor, such as genetic alteration occurred during the establishment, might have conferred resistance to apoptosis and permissiveness for HCV persistent infection. It was noteworthy that prominent steatosis has sustained in HPI cells for long-term, from passage 8 to 166 as long as we observed. The core proteins were almost localized with the LDs, while the NS5A proteins were widely MI-2 distributed in the cytoplasm but partly surrounding the LDs. The distributions were similar to those of lytic infection, but the amount of LD was much more. Actually, quantification of cellular lipid contents showed that major components of LDs, free cholesterol, cholesterol esters, and triacylglycerol, increased significantly in the HPI cells, whereas minor components, phospholipids, did not increase so much. These result indicated HPI cell displayed prominent steatosis microscopically and biochemically. Then we analyzed the glycolysis pathway because it is at a center of metabolisms followed by the tricarboxylic acid cycle. As a first step, extracellular glucose is taken up into a cell and is converted to glucose-6-phosphate, whose level did not increase much in HPI cells. Nor, glucokinase, a rate-limiting enzyme for this step, was not up-regulated at least in the protein level. Nonetheless, three immediate intermediates of G6P increased remarkably: glucose-1-phosphate, 6-phosphogluconic acid, and fructose 6-phosphate, which lead to glycogenesis, pentose phosphate pathway, and glycolysis, respectively. Level of most metabolites in glycolysis did not change or even decreased except for increase in pyruvate, a final product. Although cell culture systems for HCV-persistent-infection have been reported, the period of persistency is months. Therefore, HPI cell is a bona fide Naftopidil HCV-persistently-infected cell line because it has supported HCV for more than two years. Clinically, genotype 1b HCV is more susceptible to chronic hepatitis leading to liver cirrhosis and carcinoma, and thus an infectious strain of genotype 1b has been more required and actually established. However, its infectivity is not so robust as the JFH-1.