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. Author manuscript; available in PMC: 2012 May 25.
Published in final edited form as: Virology. 2011 Apr 22;414(1):10–18. doi: 10.1016/j.virol.2011.03.026

Fig. 1. BMS-790052 blocks HCV genome replication.

Fig. 1

Fig. 1

(a) Structure of BMS-790052

(b) Effect of BMS-790052 on stable replication of a HCV replicon derived from genotype 1b. Huh7 cells harboring replicating subgenomic replicons derived from genotype 1b were treated with 0, 0.1, 1, 10, 100, or 1000 pM of BMS-790052 for 3 days. A total cell lysate from cells was prepared and an equal amount of each cell lysate was separated by SDS-PAGE. Levels of NS5A and β-actin protein expression were examined by western blot analysis using monoclonal anti-NS5A and anti-β-actin antibodies.

(c) Huh7.5 cells were infected with a vaccinia virus expressing a T7 RNA polymerase and then transfected with either Bart79I or Bartman (Con1) plasmid construct containing the NS viral proteins downstream of a T7 promoter. Transfected cells were incubated with 0.1 % of DMSO or 0.01, 0.1, 1, 10, or 100 nM of BMS-790052 for 9 hours. A total cell lysate was prepared and an equal amount of each cell lysate was separated by SDS-PAGE. Levels of NS5A protein expression were examined by western blot analysis using a monoclonal anti-NS5A antibody.

(d) All procedures were performed as in Fig. 1(c) except that levels of NS3 protein expression were examined by western blot analysis using a monoclonal anti-NS3 antibody.