Alphaviruses such as Chikungunya virus (CHIKV) are small enveloped viruses with a message-sense RNA genome, which are known to be strong inducers of type-I IFN in vivo [8, 9] , a key response for the host to control the infection [10, 11, 12] . In vitro, however, response to RNA viruses is heterogeneous, since Sindbis virus (SINV), do not elicit detectable IFN-a/b production in infected of murine embryonic fibroblasts (MEFs) [13] . The specific points of blockage of type-I IFN production during infection are still not well delineated, but SINV and other alphaviruses could antagonize IFN production by shut-off of host macromolecular synthesis in infected cells [14, 15, 16] . Recently, human fibroblasts infection by CHIKV was shown to trigger abundant IFN-a/b mRNA transcription, while preventing mRNA translation and secretion of these antiviral cytokines [13, 15] . Contrasting with these reports, other groups using different CHIKV strains have observed abundant type-I IFNs release in the culture supernatants of CHIKV-infected human monocytes [17] , human lung cells , human foreskin fibroblasts and MEFs [10] . Type-I IFN stimulation of non-hematopoietic cells has also been shown to be essential to clear infection upon CHIKV inoculation in mouse, but CHIKV was found to be a poor inducer of IFN secretion by human plasmacytoïd dendritic cells [10] . Thus, great disparities regarding alphavirus-triggered IFN responses exist between viral strains and the nature of host cells or animal models.