We tested the importance of PKR during CHIKV infection by infecting WT and PKR 2/2 MEFs with CHIKV-GFP, at a multiplicity of infection (MOI) of 10 and 50. Productive infection was estimated by GFP expression (Fig. 5A, left panel) , while culture supernatants were monitored for the presence of IFN-b (5A, right panel). PKR was found to be necessary to control CHIKV infection in vitro, since at least 60% of PKR-inactivated cells were infected after 24 of viral exposure, compared to only 15% in the control fibroblasts population. WT MEFs produced efficiently IFN-b, while the hypersensitivity to infection of the PKR 2/2 MEFs was correlated to a reduced type-I IFN production capacity after infection. Thus, during CHIKV infection, PKR is required for normal IFN production by MEFs. We also monitored protein synthesis in infected WT and PKR 2/2 fibroblasts using puromycin labeling followed by immunofluorescence confocal microscopy (Fig. 5B) . CHIKV-GFP positive PKR 2/2 MEFs were found to incorporate efficiently puromycin, while in their infected WT counterpart protein synthesis was efficiently inhibited. Thus CHIKV, in this experimental model, induces a PKR-dependent protein synthesis inhibition and is therefore particularly relevant to further confirm our observations on the role of GADD34 in controlling type-I IFN production during response to viral RNAs.