We can suggest a mechanism explaining our cytokine models for dengue fever (Figure 3) . MIP-1β would be associated with a protective pathway for its chemoattractive and activating effect on NK cells, which in turn are efficient cells in early virus clearance, by their antiviral cytokine production and cytotoxic activity against infected target cells. IFN-γ has a deleterious effect for the host regarding its action in activating T cells for virus anti-genic cross-reactive response and monocyte/dendritic cell activation. Mononuclear monocytes are activated by IFNγ and GM-CSF among other cytokines and in turn produce several factors such as IL-1β and MCP-1 that may act on vascular permeability leading to plasma leakage and haemoconcentration. As suggested by other authors, it is likely that viral replication in antigen presenting cells, cytokine liberation and circulation, and T cell activation may not be a linear process [55] , but in fact a complex interaction network, with positive and negative feedbacks, where viral clearance and pathologic events take place, such as increased vascular permeability and circulatory collapse, and their balance may determine the disease outcome.