Recently, the induction of IFN-β by TLR9 triggering on HCMV-infected fibroblasts has been reported to promote their survival and to increase their production of viral particles [154] . However, this proviral effect occurred only when fibroblasts were simulated with CpG shortly after infection. In contrast, a treatment concomitant to viral challenge almost completely abrogated fibroblast infection and virus production. Thus, it is unlikely that this mechanism plays a significant proviral role to the disadvantage of the host during infections with most herpesviruses in vivo, as systemic production of IFN-I by pDCs should lead to the induction of antiviral defenses in most cells before they encounter the virus. However, the possibility remains that this mechanism could have been exploited by herpesviruses which can productively infect pDCs such as HHV-6 and HHV-7 [9, 10] . Some data suggest that pDCs could participate to the local replication and to the dissemination of HHV-6 and HHV-7, as skin lesions induced by the infections with these viruses have been reported to be infiltrated by infected pDCs [10] , and infected pDCs can transmit the virus to stimulated T cells [9] .