HIV-1 induces CXCL8 production via at least two mechanisms, directly via its viral components such as gp120, Nef, Vpr and Tat (for review see ref. 25) and also indirectly via IL-1β and TNF-α32, two proinflammatory cytokines also produced by HIV-1 infection. This evidence concerns the gene IL1B and HIV-1 infection.