Fig. 1

Inhibition of RhoA promotes PRV infection. A PK-15 cells were treated with Rhosin (0–2 µmol/L) for 24 h. CCK-8 assays were then used to determine the cell viability (%). B PK-15 cells were pretreated with various concentrations of Rhosin for 4 h and infected with PRV-QXX (MOI = 0.1) for 24 h, expression analysis of PRV gB and TK mRNA levels using RT-qPCR. GAPDH served as a loading control. C Immunoblotting analysis of PK-15 cells treated as in B and infected with PRV-QXX (MOI = 1) with the indicated antibodies. D Gray value analysis of C using Image J software. E PK-15 cells treated as in B and infected with PRV-GFP (MOI = 0.01) for 24 h, then cells were observed under fluorescence microscope and the GFP-positive cells were measured by flow cytometry. Scale bar, 100 μm. F PK-15 cells treated as in B and infected with PRV-QXX (MOI = 0.1), viruses were harvested with three freeze–thaw cycles, and the viral titer was determined by PFU assay. G PK-15 cells treated as in B and infected with PRV-QXX (MOI = 0.1), determination of the PRV genome copy number based on PRV-gH. All the data are shown as mean ± SD based on three independent experiments