Zhao L, Yin HC, Li SQ, Niu YJ, Jiang XJ, Xu LJ, Lu TF, Han LX, Liu SW, Chen HY

J Gen Virol. 2016 Dec 23

Abstract

Duck enteritis virus (DEV) is an acute, septic, sexually transmitted disease that occurs in ducks, geese, and other poultry. Autophagy is an evolutionarily ancient pathway that is important in many viral infections. Despite extensive study, the interplay between DEV and autophagy of host cells is not clearly understood. In this study, we found that DEV infection triggers autophagy in duck embryo fibroblast (DEF) cells, as demonstrated by the appearance of autophagosome-like double or single-membrane vesicles in the cytoplasm of host cells and the numbers of GFP-LC3 dots. In addition, increased conversion of the autophagy marker protein LC3-I to LC3-II and decreased p62/SQSTM1 indicated complete autophagy flux. Heat-inactivated DEV infection did not induce autophagy, suggesting that the trigger of autophagy in DEF cells depended on DEV replication. When autophagy was pharmacologically inhibited by LY294002 or wortmannin, DEV replication decreased. The DEV offspring yield decreased when siRNA was used to interfere with autophagy related to the genes Beclin-1 and Atg5. In contrast, after treating DEF cells with rapamycin, an inducer of autophagy, DEV replication increased. These results indicated that DEV infection induced autophagy in DEF cells and autophagy facilitated DEV replication.