Cytokine synthesis shift to the Th1 (microbicidal action of pro-inflammatory IFN-γ) from Th2 (anti-inflammatory IL-4, -10 and -13) in severe infection, when accompanied by the increased pro-inflammatory cytokine levels arising from chronic diseases, both can lead to endothelial dysfunction and a subsequent range of complications, including allergy, vascular leakage, ascites and pericardial effusion as observed in DENV [19, 141, 149–151]. The gene discussed is IFNG; the disease is infection.