FIG 6.

LXRs supported efficient HCV replication. (A and B) Huh7.5.1 cells transfected with the HCV replicon RNA were treated with or without 0.4% DMSO, 20 μM NeoB, and its derivatives (A) and with various concentrations of an LXR antagonist, 5CPPSS-50 (20, 30, and 40 μM). Luciferase activities were quantified as described in the legend of Fig. 2B. Cell viability was also measured as described in the legend of Fig. 1E. (C) HCV-infected Huh7.5.1 cells were transfected with randomized siRNAs [si-Ctr (1) and si-Ctr (2)] or siRNAs against LXRα (si-LXRα) and LXRβ (si-LXRβ) and subjected to immunoblotting to detect LXR, actin, HCV core, and HCV NS5A proteins in the cells. (D) Huh7.5.1 cells were transfected with an RNA Pol I-driven HCV replicon plasmid (see Materials and Methods) together with or without expression plasmids for both LXRβ and RXRα. The cells transfected with LXRβ/RXRα were also treated with 5 μM TO-901317 to activate LXR signaling. As a positive control, cyclosporine was added at 24 h after transfection. At 5 days posttransfection, the replication activity was determined by reporter assay. *, P < 0.05; **, P < 0.01.