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. 2011 Jan 5;85(6):2818–2827. doi: 10.1128/JVI.01969-10

FIG. 2.

FIG. 2.

RTKIs AG879 and A9 effectively block influenza A virus replication in cell culture. (A) AG879 and A9 block the multiplication of influenza A/WSN virus in both MDCK and A549 cells. Cells were infected with A/WSN at an MOI of 0.1 for 18 h in the presence of DMSO, AG879 (10 μM), tyrphostin A9 (4 μM), or AG494 (10 μM). Virus titer was determined by plaque assay. (B) AG879 and A9 inhibit influenza A/PR8 virus replication. A similar virus yield inhibition assay was performed with A549 cells infected with A/PR8 strain at an MOI of 0.1 for 18 h in the presence of DMSO or various inhibitors. (C) AG879 and A9 block single-round replication of influenza A virus. Virus titers were determined at various time points after A/WSN infection of A549 cells at a high MOI (MOI of 2) in the presence of DMSO or various inhibitors. (D) Western blot analysis of viral NP proteins at 8 hpi in cells mock infected (mock) or infected with A/WSN virus (MOI of 1) and treated with DMSO or AG879. (E) RTKIs AG879 (10 μM) and A9 (4 μM) inhibited influenza virus replication much more strongly than MEK inhibitor U0126 (50 μM) and NF-κB inhibitor Bay11-7082 (Bay11) (10 μM). Pairwise statistical comparisons to the DMSO control group were performed using Student's t test (**, P < 0.01; ***, P < 0.001; ****, P < 0.0001). Error bars indicate SD (n = 3).