Many viruses, including MV, have developed strategies to alter antigen presentation or costimulatory properties of DCs in order to evade host immune responses, thereby causing immunosuppression and an increased susceptibility to opportunistic infections. Based on the present data, a similar mechanism is suggested for CDV-infection of dogs. The observed CDV-induced DC modulation might represent a mechanism to suppress protective immunity, which favors persistent infection in infected dogs. In agreement with this idea, it was reported that CDV-infected DC-like cells within lymphoid organs occur in advanced stages of canine distemper. Furthermore, the virtual lack of detectable cytopathogenic or lytic effects as determined by phase contrast microscopy, electron microscopy, and LDH assay might contribute to virus spread within the organism via circulating DCs as described for MV. Similarly, restricted viral infection of CNS cells together with prevention of cytolysis causes limited recognition by the immune surveillance, which favors viral persistence and transmission within the brain in canine distemper. In vitro experiments have demonstrated that virulent CDV strains exhibit conformational properties of the F protein, which limit cell-to-cell fusion activity and prevent cytopathogenicity, Thus, persistent infection with delayed production of infectious virus might be a consequence of reduced spread of less fusogenic viruses compared to cytolytic CDV strains. In addition, human cytomegalovirus, murine cytomegalovirus, and Epstein-Barr virus infect and manipulate DCs to circumvent cell death, which causes persistent infection. Besides this, disturbed function and prolonged survival of DC in canine distemper might compromise T cell maturation and selection, promoting the release of immature, potentially autoreactive cells as discussed for canine distemper. The present study shows, that CDV-infection down-regulates MHC class II and co-stimulatory molecules of DCs which could have the ability to impair T cell activation in affected dogs. Previous studies revealed an inhibition of antigen presenting cells in canine distemper as a consequence of reduced IL-1 production and increased prostaglandin E2 release. Thus, results of the present study further support the hypothesis that disturbed antigen presenting function contributes to reduced mitogen-induced lymphocyte proliferation observed in CDVinfected dogs. Moreover, diminished T helper cell function as a consequence of impaired antigen presentation in persistently infected dogs might lead to disturbed germinal center and plasma cell formation and reduced class switch from IgM to IgG in canine distemper. Dysregulation of antigen presenting properties is supposed to account for immunosuppression in human measles, by down-regulation of IL-12 by DCs, which leads to a failure to activate T cells. However, the precise role of DC infection in the pathogenesis of natural MVinfection.