FIG. 1.

PI3K inhibition enhances apoptosis of cells infected with Sendai virus or hPIV3. (A) HT1080 cells were pretreated with the PI3 kinase inhibitor LY294002 (LY; 20 μM) or vehicle control for 30 min. Cells were then mock infected or infected with Sendai virus (80 hemagglutinating units/ml) as indicated. Six hours after virus addition, cells were fixed, permeabilized, and stained for DNA fragmentation using a TUNEL protocol. The same field of cells was imaged for phase contrast and TUNEL staining. (B) HT1080 cells were treated as described for panel A. After 6 hours, whole-cell extracts were prepared, and proteins (30 μg) were separated by SDS-PAGE and transferred to PVDF. A Western blot assay was performed with an antibody specific for the cleaved PARP protein (C-PARP). A Western blot assay against actin controlled for protein loading. (C) Cells were pretreated with the LY inhibitor and infected with the Sendai virus as described for panel A. Extracts were prepared at the indicated times, and Western blot assays for cleaved PARP and actin were performed as described for panel B. (D and E) A549 (D) and BEAS-2B (E) cells were pretreated with the PI3K inhibitor LY, infected with SeV, and stained as described for panel A. (F) A549 cells were pretreated with LY and stained as described for panel A. Cells were mock infected or infected with hPIV3 (multiplicity of infection, 2) as indicated.