Canine distemper is a highly contagious and immunosuppressive viral disease caused by canine distemper virus (CDV), an enveloped RNA virus of the family Paramyxoviridae. The susceptible host spectrum of CDV is broad and includes all families of the order Carnivora. To accomplish the infection, CDV requires an expression of signaling lymphocyte activation molecule (SLAM) functioning as a cellular receptor which generally presents in a variety of different lymphoid cell subpopulations, including immature thymocytes, primary B cells, activated T cells, memory T cells, macrophages and mature dendritic cells. The distribution of SLAM-presenting cells is in accordance with the lymphotropism and immunosuppression following morbillivirus infection. In the present study, the C57BL/6 mice engrafted with dog-specific SLAM sequence (DogSLAM) were used. The weanling (3-week-old) transgenic offspring C57BL/6 mice were infected with CDV Snyder Hill (CDV-SH) strain via the intranasal (n=6), intracerebral (n=6) and intraperitoneal (n=5) routes. Clinical signs, hematology, histopathology, immunohistochemistry, virus isolation and RT-PCR were observed for two weeks post infection. Results showed that CDV-SH-inoculated transgenic mice displayed mild-to-moderate congestion of various organs (brain, lung, spleen, kidney, lymph node, and adrenal gland). By means of immunohistochemistry, virus isolation and RT-PCR, CDV could not be detected. The evidence of CDV infection in this study could not be demonstrated in acute phase. Even though the transgenic mouse is not a suitable animal model for CDV, or a longer incubation period is prerequisite, it needs to be clarified in a future study.
