Aricibasi Merve, Jung Arne, Heller E Dan, Rautenschlein Silke
Clinic for Poultry, University of Veterinary Medicine Hannover, Hannover, Germany.
The Hebrew University, Robert H. Smith Faculty of Agriculture, Food and Environment, Rehovot, Israel.
Vet Immunol Immunopathol. 2010 May 15;135(1-2):79-92. doi: 10.1016/j.vetimm.2009.11.005. Epub 2009 Nov 18.
Previous studies and field observations have suggested that genetic background influences infectious bursal disease virus (IBDV) pathogenesis. However, the influence of the virulence of the infecting IBDV strain and the mechanisms underlying the differences in susceptibility are not known. In the present study IBDV pathogenesis was compared between specific-pathogen-free layer-type (LT) chickens, which are the most susceptible chicken for IBDV and have been used as the model for pathogenesis studies, and broiler-type (BT) chickens, which are known to be less susceptible to clinical infectious bursal disease (IBD). The innate and acquired immune responses were investigated after inoculation of an intermediate (i), virulent (v) or very virulent (vv) strain of IBDV. IBDV pathogenesis was comparable among genetic backgrounds after infection with iIBDV. After infection with vIBDV and vvIBDV, LT birds showed severe clinical disease and mortality, higher bursal lesion scores and IBDV-antigen load relative to BT birds. Circulating cytokine induction varied significantly in both timing and quantity between LT and BT birds and among virus strains (P<0.05). Evaluation of different immune cell populations by flow-cytometric analysis in the bursa of Fabricius provided circumstantial evidence of a stronger local T cell response in BT birds vs. LT birds after infection with the virulent strain. On the other hand, LT birds showed a more significant increase in circulating macrophage-derived immune mediators such as total interferon (IFN) and serum nitrite than BT birds on days 2 and 3 post-vIBDV infection (P<0.05). Stronger stimulation of innate immune reactions especially after vIBDV infection in the early phase may lead to faster and more severe lesion development accompanied by clinical disease and death in LT chickens relative to BT chickens. Interestingly, no significant differences were seen between genetic backgrounds in induction of the IBDV-specific humoral response: timing of IBDV-antibody induction and antibody levels were comparable between BT and LT birds. This study clearly demonstrates a significant influence of chickens' genetic background on disease outcome. The difference between backgrounds in IBDV susceptibility is further influenced by the virulence of the infecting virus strain.
以往的研究和现场观察表明，遗传背景会影响传染性法氏囊病病毒（IBDV）的发病机制。然而，感染的IBDV毒株毒力的影响以及易感性差异背后的机制尚不清楚。在本研究中，对无特定病原体的蛋鸡型（LT）鸡和肉鸡型（BT）鸡的IBDV发病机制进行了比较。蛋鸡型鸡是对IBDV最易感的鸡种，一直被用作发病机制研究的模型；肉鸡型鸡已知对临床传染性法氏囊病（IBD）的易感性较低。接种中等毒力（i）、强毒力（v）或超强毒力（vv）的IBDV毒株后，对先天免疫和后天免疫反应进行了研究。感染iIBDV后，不同遗传背景的IBDV发病机制具有可比性。感染vIBDV和vvIBDV后，相对于BT鸡，LT鸡表现出严重的临床疾病和死亡率、更高的法氏囊病变评分和IBDV抗原载量。LT鸡和BT鸡之间以及不同病毒毒株之间，循环细胞因子的诱导在时间和数量上均有显著差异（P<0.05）。通过流式细胞术分析法氏囊中不同免疫细胞群体，为感染强毒株后BT鸡相对于LT鸡更强的局部T细胞反应提供了间接证据。另一方面，在感染vIBDV后的第2天和第3天，LT鸡循环中巨噬细胞衍生的免疫介质如总干扰素（IFN）和血清亚硝酸盐的增加比BT鸡更显著（P<0.05）。与BT鸡相比，先天免疫反应的更强刺激，尤其是在早期感染vIBDV后，可能导致LT鸡更快、更严重的病变发展，并伴有临床疾病和死亡。有趣的是，在IBDV特异性体液反应的诱导方面，不同遗传背景之间没有显著差异：BT鸡和LT鸡之间IBDV抗体诱导的时间和抗体水平相当。本研究清楚地证明了鸡的遗传背景对疾病结局有显著影响。IBDV易感性的遗传背景差异进一步受到感染病毒毒株毒力的影响。
