Our analysis has indentified 2 cytokine profiles that followed disease onset and continued with disease progression/convalescence. We found CXCL9, CXCL10, CCL2 and IL-6 levels were high in the acute phase and decreased as patients convalesced. Conversely, the trend for TNF-a, IL-1b, IL-2, IL-5 and IL-12 were low initially and increased as patients began to recover from acute illness. High levels of CXCL9, CXCL10, CCL2, and IL-6 in the acute phase possibly indicated an inflammatory program initiating adaptive T-cell immunity [27] . CXCL9 and CXCL10 are both chemokines induced by IFN-c and are part of the chemokine program that regulates the migration of monocytes/ macrophages, memory T cells and NK cells and are associated with the polarization of T cells [27] . IL-6, a pleiotropic cytokine, has a destructive role in rheumatoid arthritis (RA), contributing to joint inflammation as well as joint pain [28, 29] . The increased IL-6 levels in the acute phase of our study may be the initiating factor of the severe joint pain symptoms reported in CHIKV patients which mimics RA. Furthermore, IL-6 is important during acute phases of the disease by acting as an important immune mediator of fever activating muscle metabolism to increase core body temperature [28] . Since fever is a common symptom of acute CHIKV disease, it is highly probable that the high IL-6 levels were contributing to the acute fever and the IL-6 decreasing trend followed patient core body temperature as it returned to resting temperature in the follow-up.