In a microglial model of the human immunodeficiency virus (HIV), TLR3 activation mediated by poly(I:C) effectively and dose-dependently inhibited HIV infection by triggering the IFN signaling pathway, inducing the expression of ISGs (IFN-stimulated genes; restriction factors involved in anti-HIV activities), and the production of chemokines (RANTES, MIP-1α and MIP-1β) [137]. The gene discussed is IFNA1; the disease is HIV infectious disease.