Figure 2
HBx inhibits virus-triggered signaling at the level of VISA. HBx inhibits activation of the IFN-β promoter mediated by RIG-I-N (a), MDA5-N (b), VISA (c) and MITA (d), but not TBK1 (e). The 293 cells (1×105) were transfected with the IFN-β promoter plasmid (0.1 µg) and the indicated expression plasmids. Luciferase assays were performed 24 h after transfection. (f) HBx inhibits virus-triggered ISRE activation at a level upstream of TBK1. Experiments were performed as in (a)–(e), with the exception that an ISRE reporter was used. (g) The role of HBx in the cellular antiviral response. The 293 cells (1×105) were transfected with the indicated expression plasmids. Twenty-four hours after transfection, cells were infected with VSV (MOI=0.1) and supernatants were harvested at 12 hpi. Supernatants were analyzed for VSV production by standard plaque assay. HBx, HBV-encoded X protein; hpi, hours postinfection; IFN, interferon; ISRE, IFN-stimulated response element; MOI, multiplicity of infection; TBK1, TANK-binding kinase 1; VSV, vesicular stomatitis virus.
