The initial target cells during dengue infection are believed to be Langerhans cells [4] . Through means not yet fully understood, Langerhans cells spread the virus, via the lymphatic system, to other tissues such as liver, spleen, kidney and blood, whereas monocytes, macrophages and endothelial cells are the major cell types in which the virus replicates [5] . In the majority of symptomatic dengue infections, a fever of 5-7 days duration develops together with bone and joint pain, retro-orbital pain, nausea and fatigue, this is called dengue fever (DF). While the majority of DF patients recover without intervention, 2-5% develop a more severe form of the disease, called dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), characterized by thrombocytopenia and vascular leakage, causing hypervolemic shock and death if not promptly treated [6] . The cause of DHF/DSS is not clear. Antibody dependent enhancement (ADE) is the most widely supported theory explaining the higher risk of DHF/DSS associated with a heterologous secondary infection [7] . The phenomenon of T cell ''original antigenic sin'' has also been described [8] . Like many viruses, dengue inhibits IFNa and IFNb signaling by suppressing Jak-Stat activation, resulting in reduced host antiviral response [9] . The combination of a reduced host defense, increased uptake of the virus and delayed viral clearance likely synergizes to produce higher viremia resulting in a more severe outcome.