Session topic


Title: Overcoming the barrier of the respiratory epithelium in the early phase of the infection by canine distemper virus (CDV)
ID: PS 19
Type: Poster session
Talk time: 3 + 2 min
Session: Poster session 1
Receptors and entry

Speaker: Dai-Lun Shin (Hannover/DE)

Abstract - Text

Abstract text (incl. references and figure legends)

The canine distemper virus (CDV), a member of the genus Morbillivirus within the Paramyxoviridae family, is an important infectious agent in veterinary medicine. It is known to enter the respiratory tract and spread to various organs and tissues. The prototype of a morbillivirus, measles virus (MV), binds to two specialized cellular receptors, SLAM and Nectin-4 to initiate the infection process, either via vehicle transmission within immunocytes or by binding to the adherence junctions located at the basolateral side of epithelial cells, respectively. It is believed that CDV uses similar receptors as MV to induce infection, however, the lack of a well-described in vitro model limits the further investigation of how CDV infects and disseminates to other tissues. Our goal is to explore how CDV overcomes the epithelial barrier and then spreads to the immune cells. We established the well-differentiated air-liquid interface (ALI) cell culture model from the primary dog trachea airway epithelial cells. These polarized cells contain specialized functions including cilia beating and mucus-production. The ALI cell culture model provides an excellent tool to study how CDV enters the airway epithelial cells and how it is released from them. A GFP-conjugated CDV vaccine strain has been used to visualize the course of infection. After CDV infection, we observed that airway epithelial cells from the dogs appear to be directly infected by CDV via the apical surface, which is different from what had been known from MV infection studies. Mechanical scratching and EGTA pretreatment of the well-differentiated cell membranes resulted in increased efficiency of infection by CDV, but only after basolateral administration of the inoculum, not after apical infection.
The prevalent view of MV pathogenesis indicates that the initiation of morbillivirus infection cannot occur via epithelial cells, since the nectin-4 receptor is located below the tight junctions. Our findings, however, show that CDV can overcome the epithelial barrier through different strategies including a direct infection and maybe also via paracellular routes. Further studies including a co-culture system of dog immunocyte together with the ALI culture may provide a better description of the dissemination of CDV.