FIG 2.

TCDC does not inhibit CMV replication by inducing cytotoxicity. (A) Primary mouse hepatocytes were incubated for 48 h with 25 μM and 50 μM TCDC. A potential impact on cell viability was assessed by performing a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT) assay. (B) To test the contribution of caspases to the antiviral activity of TCDC, primary mouse hepatocytes were conditioned with a 50 μM concentration of the pan-caspase inhibitor Z-VAD-FMK starting 30 min prior to the 3-h TCDC treatment (25 μM). The cells were infected with Δm157-MCMV-luciferase (0.1 PFU/cell) and lysed 24 h later for the determination of the luciferase activity. Functionality of the pan-caspase inhibitor was confirmed in parallel by coadministration with 100 μM cycloheximide (CHX) and 30 ng/ml TNF-α. Under this condition, Z-VAD-FMK effectively prevented caspase-dependent apoptosis (right panels).