Murine cytomegalovirus (MCMV) is a betaherpesvirus that can establish acute infection in multiple organs including the liver. Acute MCMV infection induces an early systemic proinflammatory cytokine response including high levels of type I IFNs, IFN-c, IL-12 and TNF-a [15] [16] [17] [18] [19] . Infection in the liver induces early production of IFN-a, predominantly by plasmacytoid dendritic cells (pDCs), by 40 h post-infection [20, 21] . Type I IFN production mediates downstream responses including chemokine and cytokine production as well as monocyte/macrophage, natural killer (NK) cell and T cell recruitment [20] [21] [22] [23] . Early type I IFN signaling is necessary for NK cell recruitment to the liver, where they deliver the antiviral cytokine IFN-c within the first 48 h post-MCMV infection [23] . The NK cell IFN-c response is an important early step in the control of liver infection [24, 25] . This response induces IFN-c-dependent chemokines, which contribute to the recruitment of CD8+ T cells to the liver [26] . Liver CD8+ T cell responses occur by days 5 and 7 post-MCMV infection and are an important source of cytokines late in acute infection that contribute to resistance against MCMV [26] [27] [28] [29] [30] .