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. 2014 Sep;88(17):10026–10038. doi: 10.1128/JVI.00725-14

FIG 1.

FIG 1

Silencing of integrin αvβ3, but not other integrins, reduces HSV plaque formation. (a) CaSki cells were transfected with siRNA targeting αv, α5, β1, β3, β6, or β8 alone or a combination of αvβ3 and were infected 72 h later with serial dilutions of HSV-2(G). Viral plaques were counted at 48 h p.i. Results are presented as PFU on siRNA-transfected cells as a percentage of PFU on nontransfected cells and are means (± standard deviations [SD]) from at least 3 independent experiments conducted in duplicate. Only wells in which the number of plaques ranged between 25 and 200 plaques were used to calculate the viral titer. (b) CaSki cells were transfected with siRNA targeting the indicated integrins, and gene expression was determined by RT-PCR at 72 h posttransfection. Results are presented as percent expression relative to that of nontransfected cells and are means (± SD) from at least 3 independent experiments. (c) CaSki cells were transfected with siControl (siCtrl) or siRNA targeting integrin αvβ3 (here termed siIntegrinαvβ3 or siInαvβ3), siIntegrin β3 (siIntβ3), siIntegrin β6 (siIntβ6), or siIntegrin β8 RNA (siIntβ8), and protein expression was evaluated by Western blotting at 72 h posttransfection; the blots are representative of at least 2 independent experiments. (d) Primary vaginal cells cultivated from CVL pellets were transfected with the indicated siRNA and were infected 72 h later with HSV-2(333)ZAG (MOI, 0.1 PFU/cell) and monitored for GFP expression; images are representative of 2 independent experiments. Asterisks indicate significant difference relative to the control (*, P < 0.05; **, P < 0.01; ***, P < 0.001).