IFNG and infection: However, the death of high-affinity DENV-specific T-cells induces the predominance of low-affinity, bystander-activated T-cells (or serotype cross-reactive T-cells in the case of DENV secondary infections), that produce proinflammatory cytokines and have low IFN-γ production, inducing endothelial dysfunction, vascular leakage, and organ damage (Figure 4).