Guiping Yuan, Anchun Cheng, Mingshu Wang, Xiaoying Han, Yi Zhou, Fei Liu
Avian Disease Research Center, College of Animal Science and Veterinary Medicine, Sichuan Agricultural University, Yaan, Sichuan 625014, China.
Avian Dis. 2007 Jun;51(2):546-9. doi: 10.1637/0005-2086(2007)51[546:PSODEV]2.0.CO;2.
We studied apoptosis induced by duck enteritis virus (DEV) in vivo, focusing on the lymphoid organs that constitute the main targets for infection: thymus, bursa of Fabricius (BF), and spleen. Fifty Pekin ducks were inoculated subcutaneously with a virulent strain of DEV. The morphology of lymphoid organs of these infected ducks was observed by light microscopy and transmission electron microscopy. Cell death by classical necrosis was observed in lymphocytes of the DEV-infected thymus, BF, and spleen. Lymphocyte apoptosis also was observed at the same time, and it was further confirmed by in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling and agarose gel electrophoresis. We conclude that apoptosis and necrosis of lymphocytes induced by DEV infection resulted in the depletion of lymphocytes and that apoptosis of lymphocytes may play an important role in the pathogenesis of duck viral enteritis.
我们研究了鸭肠炎病毒(DEV)在体内诱导的细胞凋亡,重点关注构成主要感染靶器官的淋巴器官:胸腺、法氏囊(BF)和脾脏。50只北京鸭皮下接种了一株DEV强毒株。通过光学显微镜和透射电子显微镜观察这些感染鸭的淋巴器官形态。在DEV感染的胸腺、BF和脾脏的淋巴细胞中观察到经典坏死引起的细胞死亡。同时也观察到淋巴细胞凋亡,并通过原位末端脱氧核苷酸转移酶dUTP缺口末端标记和琼脂糖凝胶电泳进一步证实。我们得出结论,DEV感染诱导的淋巴细胞凋亡和坏死导致淋巴细胞耗竭,并且淋巴细胞凋亡可能在鸭病毒性肠炎的发病机制中起重要作用。