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. 2016 Mar 1;97(Pt 3):756–766. doi: 10.1099/jgv.0.000379

Fig. 5.

Fig. 5.

Overexpression of SGIV VP51 inhibits SGIV-induced apoptosis in FHM cells. (a) Overexpression of VP51 increases cell viability after SGIV infection. Cell viability was evaluated using a trypan blue exclusion assay. n = 3; error bars represent the mean ± sd; *P < 0.05 compared with the FHM-VP51. (b) Nuclear morphology after SGIV infection in WT cells (FHM), vector control cells (FHM-Vector), VP51-expressing cells (FHM-VP51) and the mutant-expressing cells (FHM-ΔCRD1, FHM-ΔCRD2 and FHM-ΔCRD3). Cells were infected with SGIV at an m.o.i. of 2 and stained with Hoechst 33342 at 18 h p.i. Bar, 25 μm. (c) Flow cytometric analysis of apoptosis in FHM-Vector cells, FHM-VP51 cells and the mutant-expressing cells infected with SGIV at 48 h p.i. (d) The percentage of subG0/G1 phase cells was calculated and indicated on the histogram. n = 3; error bars represent the mean ± sd; *P < 0.05 compared with the FHM-VP51. (e) Overexpression of VP51 inhibited caspase-3 activation induced by SGIV in FHM cells. n = 3; error bars represent the mean ± sd; *P < 0.05 compared with the control.