BST2 and HIV infectious disease: In addition to the reported mechanisms involved in IFN-λ-mediated HIV inhibition (17, 18, 50): the induction of extracellular factors, e.g., CC chemokines that block HIV entry into macrophages, and the activation of intracellular innate immunity, e.g., the induction of type I IFNs and APOBEC3G/F, we demonstrated that IFN-λ treatment of macrophages induced the expression of tetherin, a cellular factor that can block HIV infection by preventing virus release from infected cells (Figure 4).