In this study, we showed that HIV-1-infection-induced activation of microglia in all primary cell culture models was triggered by cytoplasmic export of icRNA, since infection with HIV expressing a Rev mutant deficient for CRM1 interaction (M10) was unable to induce innate immune activation (Fig. 2), and CRM1 inhibitors suppressed HIV-induced activation in microglia (Fig. 2, 3, and 5). The gene discussed is XPO1; the disease is infection.