To fight viral infections, vertebrates have developed a battery of innate and adaptive immune responses aimed at inhibiting viral replication or at killing infected cells. These responses include the early production of innate antiviral cytokines, especially interferons a and b (IFN-a/b), and the activation of cytotoxic lymphocytes such as the innate natural killer (NK) cells and the adaptive CD8 T cells. While critical for antiviral defense, cytokine or CD8 T cell responses can be detrimental or even fatal to the host when deregulated. Therefore, we need to better understand how the different arms of antiviral immunity are regulated. In particular, NK cells are proposed to play a protective role in a variety of viral infection in humans, but the underlying mechanisms remain poorly understood. Here, in a mouse model of cytomegalovirus infection, we demonstrate that NK cells prevent an excessive production of IFN-a/b and promote more efficient antiviral CD8 T cell responses. We thus show that NK cells can help promote health over disease during viral infections by regulating both innate and adaptive immune responses. It will be important to examine in humans whether NK cells control innate cytokine production to prevent immunopathology and to promote adaptive immunity against herpesviruses, HIV-1, influenza, or SARS.