Effects of porcine epidemic diarrhea virus on porcine monocyte-derived dendritic cells and intestinal dendritic cells

- We report the interaction of PEDV (CV777) with Mo-DCs in vivo and in vitro.
- There is enhancement in the ability of Mo-DCs infected with CV777 in vitro.
- There is enhancement in the ability of intestinal DCs infected with CV777 in vivo.

Infection with porcine epidemic diarrhea virus (PEDV) causes damage to intestinal epithelial cells and results in acute diarrhea and dehydration with high mortality rates in swine. Dendritic cells (DCs) are highly effective antigen-presenting cells widely distributed beneath the intestinal epithelium, thus making them an early target for virus contact. DCs uptake and present viral antigens to T cells, which then initiate a distinct immune response. In this study, we investigated how attenuated PEDV (CV777) affects the function of porcine monocyte-derived dendritic cells (Mo-DCs). Our results show that the expression of Mo-DC surface markers such as SWC3a+CD1a+, SWC3a+CD80/86+ and SWC3a+SLA-II-DR+ is increased after infection with CV777 for 24 h. Mo-DCs infected with CV777 produce higher levels of IL-12 and INF-γ compared to mock-infected Mo-DCs but the expression profile for IL-10 does not change. Interactions between Mo-DCs and CV777 significantly influence the stimulation of the T cell response in vitro. Consistent with these results, after 48 h of CV777 infection, there is enhancement in the ability of porcine intestinal DCs to sample the antigen and activate T-cell proliferation in vivo. The enhancement of sampling and presentation is most pronounced for immature Mo-DCs. These results suggest that CV777 stimulates the ability of Mo-DCs to sample and present antigen. We conclude that CV777 may be a useful vaccine to trigger adaptive immunity.