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. 2018 Jun 18;156:92–101. doi: 10.1016/j.antiviral.2018.06.011

Fig. 6.

Fig. 6

The effects of the combination of 6-TG with IFNα, or ribavirin on rotavirus replication. (A) Treatment with IFNα (48 h) significantly inhibited viral genomic RNA in SA11 rotavirus infected Caco2 cells in a dose-dependent manner (n = 4, means ± SEM, **P < 0.01, Mann-Whitney test). (B) Treatment with IFNα (48 h) remarkably inhibited viral VP4 protein in SA11 rotavirus infected Caco2 cells in a dose-dependent manner (The ratio of VP4/β-actin was expressed in arbitrary units). (C) Effect of the combination of various concentrations of 6-TG and IFNα on rotavirus replication in Caco2 cells. (D) Synergy plot representing the percentage of antiviral activity above/below the expected activity for the 6-TG-IFNα combination based on the data shown in C. (E) Treatment with ribavirin (48 h) significantly inhibited viral genomic RNA in SA11 rotavirus infected Caco2 cells in a dose-dependent manner (n = 4–7, means ± SEM, *P < 0.05, **P < 0.01, Mann-Whitney test). (F) Treatment with ribavirin (48 h) remarkably inhibited viral VP4 protein in SA11 rotavirus infected Caco2 cells in a dose-dependent manner (The ratio of VP4/β-actin was expressed in arbitrary units). (G) Effect of the combination of various concentrations of 6-TG and ribavirin on rotavirus replication in Caco2 cells. (H) Synergy plot representing the percentage of antiviral activity above/below the expected activity for the 6-TG-ribavirin combination based on the data shown in G.