College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, Hubei, China.
Poult Sci. 2012 Mar;91(3):583-91. doi: 10.3382/ps.2011-01743.
Duck hepatitis virus type 1 (DHV-1) causes a highly contagious disease in ducklings and is often associated with liver necrosis, hemorrhages, and high mortality. In the current study, the expression levels of gene transcripts encoding proinflammatory cytokines and the virus were measured by quantitative reverse-transcription PCR in duck livers after infection with a DHV-1 JX isolate obtained from natural cases in Hubei Province, China. In addition, sera IL-1β, IL-6, and alanine aminotransferase levels were quantified. Liver histopathology was examined following DHV-1 infection. The ducklings died within 1 to 2 d postinfection (d.p.i.) because of typical liver degeneration, hemorrhage, necrosis, and bile-duct epithelial cell proliferation. Transcripts of the cytokines IFN-α, IL-6, TNF-α, and IL-10 decreased by 0.5 d.p.i. and then gradually increased at 1 d.p.i. Similarly, DHV-1 JX 3D gene levels in the liver sharply increased at 1 d.p.i. and then maintained a high level. In contrast, liver TNF-α and IL-1β transcripts showed no increased expression of the cytokine gene postinfection and significantly decreased compared with the expression at 0.25 d.p.i., only the expression of IFN-α transcripts increased 128-fold by 1 d.p.i. Changes in the serum IL-6 level remained relatively stable postinfection and not significantly different compared with that of the control (P > 0.05), whereas serum levels of IL-1β significantly decreased at 0.5 d.p.i. and increased from 1 d.p.i. onwards (P < 0.05). Serum alanine aminotransferase levels significantly increased 2 d.p.i. compared with that of the control group (P < 0.01), which seemed to keep with the number of dead ducks. The cytokines exhibited a biphasic pattern following DHV-1 JX infection. Taken together, the data indicated that duckling liver inflammatory responses were produced following experimental DHV-1 JX infection involving multiple cytokines.
鸭肝炎病毒 1 型（DHV-1）可引起雏鸭高度传染性疾病，常伴有肝坏死、出血和高死亡率。在本研究中，通过定量逆转录 PCR 测量了中国湖北省自然病例获得的 DHV-1 JX 分离株感染鸭肝脏后编码促炎细胞因子和病毒的基因转录本的表达水平。此外，还定量了血清中 IL-1β、IL-6 和丙氨酸氨基转移酶的水平。DHV-1 感染后检查了肝组织病理学。雏鸭在感染后 1 至 2 天（d.p.i.）内死亡，因为典型的肝退化、出血、坏死和胆管上皮细胞增生。细胞因子 IFN-α、IL-6、TNF-α和 IL-10 的转录物在 0.5 d.p.i.时下降，然后在 1 d.p.i.时逐渐增加。同样，肝中 DHV-1 JX 3D 基因水平在 1 d.p.i.时急剧增加，然后维持高水平。相比之下，肝 TNF-α和 IL-1β转录物在感染后没有增加细胞因子基因的表达，与 0.25 d.p.i.相比显著降低，只有 IFN-α转录物在 1 d.p.i.时增加 128 倍。感染后血清 IL-6 水平的变化相对稳定，与对照组相比没有显著差异（P>0.05），而血清 IL-1β水平在 0.5 d.p.i.时显著降低，并从 1 d.p.i.开始增加（P<0.05）。血清丙氨酸氨基转移酶水平在 2 d.p.i.时与对照组相比显著增加（P<0.01），这似乎与死亡鸭的数量相符。细胞因子在 DHV-1 JX 感染后呈双峰模式。总之，数据表明，雏鸭肝脏炎症反应是由实验性 DHV-1 JX 感染引起的，涉及多种细胞因子。
