As Klra8 and BALB/c mice differ for the whole NK cell locus, which includes genes expressed in several leukocyte subsets, we sought to ensure that the differences observed in the activation kinetics of CD8 T cells between these two mouse strains i) were not due to intrinsic differences in the reactivity of CD8 T cells and ii) were dependent on Ly49Hmediated NK cell activation. This was achieved by showing that no accelerated expansion of CD8 T cells occurs in Klra8 animals i) when the antibacterial responses of Klra8 and BALB/c mice are compared during Listeria monocytogenes infection ( Figure S4 ), or ii) in response to MCMV infection when Klra8 mice are depleted of NK cells ( Figure 5A ), or when the CD8 T cell responses of Klra8 and BALB/c mice are compared during infection with a Dm157 virus as opposed to infection with wild-type or revertant viruses ( Figure 5B ). Moreover, the impact of efficient NK cell activity on the development of antiviral CD8 T cell responses was confirmed in mice of another genetic background, as a delay in antiviral CD8 T cell activation was observed in B10.D2 animals deficient for Ly49H-mediated NK cell activation due to the inactivation of the associated adaptor molecule DAP12 (B10.D2.DAP128), as compared to wild-type controls ( Figure  5C ). Altogether, these data show that efficient NK cell responses to a viral infection accelerate the development of effector antiviral CD8 T cell responses.