In recent years, most of the studies on CHIKF have been addressed with the clinical description of the disease [4] [5] [6] [7] [8] [9] 11, 17, 18, 21] , the molecular nature of the virus [9, 10, 19] and diagnostics methods [8] [9] [10] 24] , and the interactions of the virus with its mosquito vector, Aedes [1] [2] [3] [11] [12] [13] [14] [15] . Here, we describe for the first time the comprehensive systemic production of cytokines, chemokines, and growth factors during acute CHIKV infection which may light the path ahead in understanding the innate response to the infection. We first showed that a wide range of cytokines such as IFN-a, IL-5, IL-6, IL-7, IL-10, IL-15 were produced in response to CHIKV infection. IFN-a is a potent antiviral cytokine and has been shown to strongly inhibit CHIKV in vitro [32] . The high levels of IFN-a that we detected provide a logical explanation for how the body rapidly brings CHIKV viremia under control [8, 11] . It has been shown that the main producers of IFN-a are plasmocytoid dendritic cells [33] and monocytes [34] . The profile of circulating cytokines revealed a predominance of Type 2 cytokines. Mainly IL-5, IL-6 and IL-10 levels were increased and those of IFN-c or TNF-a were unchanged as compared to noninfected controls. This suggests that acute CHIKV infection tilts the cytokine profile to anti-inflammatory response, which would argue against the common understanding of CHIKV infection which does not really support the common description of the CHIKV infection as an inflammatory disease [8] . Alternatively, it is possible that an inflammatory response might occur earlier when the virus is actively replicating, and then gets down-regulated by a counter-anti-inflammatory response when the virus is being eliminated from circulation. High levels of anti-inflammatory IL-10 and the presence of high levels of chemokines IP-10 and MIG (ligands of CXCR3 associated with Th1-type reactions) [35] , detected here would support this hypothesis. Further studies would be needed to clarify this issue. The Type 2 cytokines detected are also important mediators of B cell growth and maturation, and thus may allow the production of high levels of persisting anti-CHIKV IgG [5] .