IFN-γ is produced during a T-lymphocyte helper response type 1 and may reflect CD8+ T cell activation with production of inflammatory cytokines. High levels of IFN-γ were observed in patients with dengue from Asian and Latin America and were associated with severity [9] . IFN-γ produced by T cells may also activate mononuclear phagocytes (monocytes and dendritic cells), which would produce factors such as TNF-α, tissue factor, and plateletactivating factor, among other mediators. These factors may all participate in platelet and endothelial cell activation, leading to platelet consumption, increase in endothelial permeability, hypotension and ultimately to shock. IFN-γ has also been associated with secondary heterologous Dengue virus infections [47, 48] inducing a strong antigenically cross-reactive inflammatory response, probably inefficient in terms of antibody and T-cell specific response. Indeed, we observed earlier in several patients a CD8+T cell activation with HLA-DR+ subset increase that was associated with severity [9] .