By activating type Iα phosphatidylinositol-4-phosphate 5-kinase (PI4P5-K Iα) at virus-cell contact regions, HIV-1 is known to trigger the production of this PIP2-fusogenic lipid to promote fusion pore formation and viral infection [22], and the depletion of syntenin-1 allows a higher pool of free PIP2 to accumulate at the plasma membrane after HIV-1 attachment [10]. The gene discussed is SDCBP; the disease is viral infectious disease.