FIG 6.

G₂/M arrest improves viral replication only when active type I IFN signaling inhibits viral replication. (A to E) Suit2 cells (A, C, and E), HPAF-II cells (B), or MIA PaCa-2 cells (D) were treated with medium or different concentrations of paclitaxel (Pac) at the indicated concentration ranges for 24 h and then infected (or mock infected) with VSV-ΔM51 (MOI of 0.1 for Suit2 or MOI of 10 for HPAF-II cells), WT VSV (MOI of 0.1), or Sendai virus recombinant SeV-GFP (MOI of 0.1). The MOI for each virus was calculated based on virus titration on BHK-21 cells. The level of GFP intensity was measured in cells over time. (F) BHK-21 cells were treated 26 h prior to or following VSV-ΔM51 infection at an MOI of 0.01 with medium, paclitaxel, colchicine (Col), or ruxolitinib (Ruxo) at the indicated concentration ranges. After infection, virus replication was measured at regular intervals by way of GFP fluorescence. The means and SD of the means are indicated.