EHEC O157:H7 clade 6 strains harboring stx2a and/or stx2c and clade 8 strains harboring stx2a or stx2a/stx2c were frequently associated with childhood HUS cases in Japan. Rapid and specific detection of such lineages are required for infection control measures.

Because appropriate cell-culture systems or small-animal models have been lacking, the early steps in the HCV life cycle have been difficult to study. A cell culture system was developed recently that allows production of infectious HCV. In this study, infectious HCV particles produced in cultured cells were used. To clarify the role of CD81 in HCV attachment and entry, the effect of anti-CD81 antibody was examined. The antibody blocked HCV virion entry but not particle attachment. Only the fraction bound to a heparin affinity column and eluted with 0.3 M NaCl productively infected Huh7 cells, indicating that infectious HCV particles bind to heparin. Both heparin treatment of the virus particles and heparinase treatment of the Huh7 cells reduced virus-cell binding without substantially inhibiting HCV infectivity. Finally, to confirm the role of both heparin sulfate proteoglycan (HSPG) and CD81 in HCV entry, the effects of heparinase I and anti-CD81 antibody were analyzed. No productive RNA replication was detected in the Huh7 cells in the presence of both heparinase I and anti-CD81 antibody. In conclusion, these data suggested that both HSPG and CD81 are important for HCV entry. HSPG may play a role in the initial cell surface binding of infectious HCV particles and CD81 is conceivably correlated with HCV entry after viral attachment.

Summary Type I interferons (IFNs), IFN‐α and IFN‐β, are widely used for treating chronic hepatitis C. Although retrospective studies have suggested that type I IFNs have direct antifibrotic effects, little is known about these mechanisms. The present study was designed to clarify the preventive mechanisms of type I IFNs in the progression of fibrosis for the establishment of a more effective therapy. A murine fibrosis model comprising immunological reactions was induced by the administration of concanavalin A (0·3 mg/body) into mice once a week for 4 weeks. Liver injury and the degree of fibrosis were determined by measuring the serum alanine aminotransferase activities and liver hydroxyproline contents with or without IFN‐β pretreatment. IFN‐β suppressed the hepatocellular injury and increased the hydroxyproline content induced by repeated concanavalin A injections, but had no effect on established fibrosis. Furthermore, IFN‐β reduced the expressions of transforming growth factor‐β, basic fibroblast growth factor, collagen type I A2 and tissue inhibitor of metalloproteinase 1 messenger RNAs, which are related to the progression of liver fibrosis. The IFN‐β reduced the liver injury and fibrosis induced by immunological reactions. These data suggest that type I IFNs suppress the progression of cirrhosis through inhibition of repeated hepatocellular injury and/or factors that promote the liver fibrosis induced by hepatitis virus infection.

Selectable infection was established using HCV replicon containing full-length genotype 2a JFH-1 cDNA. This system might be useful for HCV research.