Figure 1

TNF-α activates ISG transcription and exerts antiviral activity against HCV and HEV.
(A) In the Huh7 cell-based subgenomic HCV replicon, treatment with recombinant human TNF-α (100 ng/ml) inhibited HCV replication-related luciferase activity as measured at 3 different time points (n = 5). (B) Same as (A) for the Huh7 cell-based subgenomic HEV replicon model. (C) In the Huh7 cell-based ISRE luciferase reporter cells, treatment with IFN-α resulted in a dose-dependent induction of ISRE-related luciferase activity (n = 3 independent experiments with 2–3 replicates each). (D) Same as (C) for TNF-α . (E) Expression profile of 20 antiviral ISGs in Huh7 cells as measured by qRT-PCR. Most ISGs were highly up-regulated with TNF-α treatment (n = 5). Data presented as mean ± SD (*P < 0.05; **P < 0.01; ***P < 0.001).