High systemic levels of IFN-a/b production have been shown to lead to the ablation of cDCs [19] and to the attrition of both antigen-specific and bystander CD8 T cell populations during infection with lymphocytic choriomeningitis virus (LCMV) [20, 21] . We therefore hypothesized that the high systemic levels of IFN-a/b induced during MCMV infection in the context of inefficient NK cell activity could lead to the ablation of cDCs and may impinge on the development of antiviral CD8 T cell responses. Indeed, it has been previously reported that MCMV infection leads to a severe ablation of CD8a cDCs in BALB/c mice that is prevented by efficient antiviral NK cell functions in C57BL/ 6 animals [36] . However, the cause for this ablation of cDCs in BALB/c animals has not been identified, and the effect of this ablation on the development of antiviral CD8 T cells has not been evaluated. Thus, we next compared the numbers of DC subsets and the activation of antiviral CD8 T cells at different time points after infection between Klra8 and BALB/c mice.