Herpesviruses are well controlled by immunocompetent hosts, since most humans are infected by HCMV, EBV, or HSV, and yet do not develop any clinical symptoms. All three of these viruses appear particularly efficient at activating pDCs. Therefore, it seems reasonable to consider that pDCs may contribute to the induction of the strong, protective, adaptive immune responses observed to occur naturally in most infected individuals. Interestingly, the ability to trigger a variety of TLRs and to activate multiple DC subsets, including pDCs, is part of the explanation that has been proposed for the high efficacy of the attenuated yellow fever virus vaccine [166] . In the case of herpesviruses, other factors are also likely to contribute to the induction of long-lasting protective adaptive immunity. In particular, this is the case of the inflation over time of the memory CD8 T cells directed against the products of immediate early genes [167] . This inflation occurs due to the natural boosts provided by expression of these antigens during partial reactivation of virus from latently infected cells over the lifetime of the infected individuals [168] . Therefore, it would be worth considering the exploitation of herpesviruses as potent vectors for vaccination against other intracellular pathogens or tumors. Indeed, this has been already done rather successfully in mouse models of vaccination against influenza or LCMV, where the target antigens had been introduced under the control of the promoter of the gene encoding the immediate early antigen-2 [169] as well as very recently in rhesus macaques for vaccination against SIV although expression of the vaccine antigens had been driven by the promoter of a structural gene which should not induce CD8 T cell memory inflation [170] . The role of pDCs in the success of these vaccination protocols would be interesting to evaluate.