Fig. 3.

RCMV-mediated rat Clr-11 downregulation and RCTL immunoevasin induction are prevented by UV-inactivation and inhibition of early viral and host protein synthesis. a Characterization of rClr-11 expression on RCMV-E-infected REFs upon treatment with UV-inactivated RCMV WT or ΔRCTL-mutant virus. Treated cells were analyzed by flow cytometry for rClr-11/RCTL (R3A8 mAb) expression (numbers indicate MFI values). b Quantitation of R3A8 MFI levels shown in a relative to mock-treated controls. c Characterization of rClr-11/RCTL (R3A8 mAb) expression upon RCMV WT or ΔRCTL-mutant virus infections in the presence of various chemical inhibitors. REFs were pretreated with DMSO (controls), ActD (10 nM), CHX (10 μg/ml), PAA (400 μg/ml) or AraC (50 μg/ml), and then infected with RCMV WT or ΔRCTL-mutant virus and analyzed by flow cytometry at 24 h.p.i. for R3A8 expression. R3A8 rClr-11/RCTL mAb (shaded histogram); secondary reagent alone (black line); reference for mock-treated control MFI level (dotted vertical line). Numbers indicate MFI values. d Quantitation of rClr-11/RCTL (R3A8 mAb) MFI levels in c normalized to DMSO-treated mock control MFI levels. Graphs show mean ± SEM. Experiments were analyzed using ANOVA with Bonferroni's post hoc analysis. * p < 0.05, ** p < 0.01, *** p < 0.001. All data are representative of at least 3 independent experiments.