pDCs were initially identified in humans and mice based on the unique ability of these cells to secrete enormous amounts of IFN-a/b early in response to viral challenge [12] . pDCs respond in this way as a consequence of their ability to recognize molecular signatures of viruses in a manner that is independent of pDC infection [12, 13] . Early during the course of murine cytomegalovirus (MCMV) infection, pDCs are the major producers of interferons a and b (IFN-a/b) [13, 14] , which are critical for host survival [15, 16] . IFN-a/b have direct antiviral effects because they can inhibit viral replication in infected cells as well as convey to noninfected cells defense mechanisms that protect them from viral infection. IFN-a/b also mediate a variety of immunoregulatory functions, either activating or inhibitory [17, 18] . They contribute to the proliferation of NK cells and induce them to express functional cytotoxic granules, promote cDC phenotypic and functional maturation, and can help to activate antiviral CD8 T cells. In contrast, depending on the context, IFN-a/b can also compromise the immune response of the host by inhibiting DC differentiation [19] or by directly leading to the attrition of CD8 T cells [20, 21] . Indeed, different viruses have recently been suggested to induce a profound immunosuppression in the host by inducing overwhelming levels of IFN-a/b [19] . The importance of the host genotypes in the efficiency of IFN-a/b antiviral functions in the context of the infection with specific viruses are well documented [22, 23] . In contrast, it is not known whether naturally occurring differences in the interactions between a virus and its hosts exist that may shape IFN-a/b responses by specifically dampening the immunosuppressive functions of these cytokines that are detrimental to the host and beneficial to the pathogen. The identification of such conditions will help to better understand the physiopathology of viral infection and may lead to the development of innovative treatments to fight these infections.