For the infections with HIV-1 or simian immunodeficiency virus (SIV), there has recently been a striking paradigm shift regarding the role of pDCs in the natural history of the disease. HIV-infected individuals show decreased number of pDCs and their PBMCs are impaired for IFN-I production upon in vitro restimulation. Therefore, it was first hypothesized that a lack of pDC responses contributed to the failure to control viral replication early on after primary infection [63] . However, recently, evidences have been obtained of a massive IFN-I response during HIV-1 infection, starting early on during acute infection [136] and sustained thereafter [137, 138] . This chronic production of IFN-I has been proposed to contribute to CD8 T cell disarming and uninfected CD4 T cell killing [139] . The cellular source of the IFN-I produced during chronic infection is debated [59], but pDCs could contribute [140, 141] . More generally, pDCs have been reported to be hyperactivated during HIV infection and to likely contribute to immune deregulation and disease by a number of mechanisms [139, 141] . Strikingly, comparisons between pDC responses of non human primate models with contrasting susceptibilities to SIV-induced disease have demonstrated much higher pDC activation in the susceptible rhesus macaques as compared to the resistant African green monkeys [142] or sooty mangabeys [138] , associated with a polymorphism in the Irf7 gene between rhesus macaques and sooty mangabeys [138] . In summary, recent investigations strongly suggest that pDCs play a deleterious role for the host during infections with HIV-1 or SIV. This possibility has not yet been extensively examined during herpesvirus infections, but will be worth considering under specific conditions based on the data discussed below. Direct antiviral effects [15] Development of autoimmunity or immunopathology [15, 143] Promotion of cDC maturation [13, 23] Induction of DC apoptosis [144] promotion of cDC cross-presentation [24] Prevention of DC renewal [145] promotion of NK cell activation [19, 22] General inhibition of hematopoiesis [146, 147] Help to CD8 T lymphocytes [17, 18, 20] Anti-proliferative or pro-apoptotic effects on CD8 T cells [15, 148, 149] Help to B lymphocytes [150, 151] Susceptibility to bacterial surinfections [152, 153] 