The present study demonstrates that risk G1 and G2 variants of APOL1 enhances HIV-1 accumulation and persistence in human podocytes, and also contributes to spread infection to neighbor CD4pos T cells.This process is amplified by IL-1β, whose priming of human podocytes increases viral entry and, together with HIV-1 itself, up-regulates the APOL1 gene expression (Fig. 5). This evidence concerns the gene IL1B and infection.