These studies implicated cervical tissue damage [50], induced recruitment of immune cell populations [50], and the production of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and IL-8 [51-53] as explanations for the general failure of an N-9-based microbicide, as well as increases in HIV-1 infection after high-frequency application [54]. This evidence concerns the gene IL1B and HIV-1 infection.