We next aimed at further understanding the link between NK cell functions, IFN-a/b production, and downstream effects on DCs and CD8 T cells. As BALB/c mice have a much higher viral burden after infection with MCMV, it seemed plausible that the difference in viral load between Klra8 and BALB/c mice could have an impact on the intensity of the DC and CD8 T cell responses. In order to test the impact of the extent of viral replication in vivo on pDC cytokine production and on antiviral CD8 T cell activation, independently of the function of NK cells, we sought a strategy to control viral replication efficiently in BALB/c mice with a tightly controlled timing and magnitude. To achieve this, we utilized an MCMV (DN-SCP-MCMV) that is genetically engineered so that its in vivo replication can be effectively arrested by the administration of doxycycline [44] .