ITIH4 and HIV infectious disease: Collectively, these findings support the hypothesis that virus-bound or shed gp120 [125] can function as a viral superantigen activating HMMCs and basophils to release proinflammatory mediators (histamine, LTC4), cytokines (IL-4 and IL-13), and angiogenic/lymphangiogenic factors (VEGF-A and VEGF-C), thus contributing to the dysregulation of immune system in HIV infection.