Kaposi's sarcoma-associated herpesvirus (KSHV) is the most recently discovered human herpesvirus, first isolated and identified from a Kaposi's sarcoma lesion in 1994. It is the etiological agent of Kaposi's sarcoma, a vascular lesion that is the predominant cancer among AIDS patients. KSHV is also the primary etiological agent of two B-cell lymphomas, primary effusion lymphoma and multicentric Castleman's disease. KSHV can exist in either a lytic phase, in which the viral DNA is actively replicated and virions are assembled, or in a latent phase, in which the viral genome is tethered to the host chromosome via protein-protein interactions. The lytic cycle generally occurs following primary infection, and within 72-96 h in most cell types, the virus enters the latent state. Reactivation from latency also leads to the intiation of the lytic cycle, which is necessary for virus propagation and survival in the host. Several KSHV proteins have been implicated in modulation of the host immune response to viral infection. This article summarizes recent discoveries involving the innate immune response to KSHV infection.