人工感染禽腺病毒血清4型对鹅天然免疫反应的影响

将50只30日龄的健康鹅随机分为攻毒组、观察组和对照组,观察并采集样品,检测抗体水平、病毒血症、病毒载量,应用real-time PCR(RT-PCR)方法检测肝、心脏组织中β-防御素(Av BDs)、Toll样受体(TLRs)、细胞因子(cytokines)等基因表达量。初探人工感染鸡源禽腺病毒血清4型(FAdV-4)对鹅的致病性及机体对该病毒形成的天然免疫反应机制。结果显示,感染该FAdV-4毒株后,鹅均没有明显病症和死亡发生。宿主产生特异性抗体,并且肝、心脏组织出现病理学变化,宿主排毒率和病毒载量呈上升趋势。感染早期(36 h和72 h),Av BD1、2、5、9、16,TLR2、3、7、15,IL-1β、2、6、8、18以及髓样分化因子(My D88)在肝中的基因表达量显著上调(P<0.05)或有上调趋势。证实,鸡源FAdV-4对鹅的致病性较弱,可能与实验动物品种、日龄差异或感染途径等条件有关。宿主可通过TLRs-My D88途径引起机体产生大量的免疫因子,参与机体抗病毒免疫反应。本试验结果为深入研究FAdV-4与宿主早期天然免疫间的相互作用提供了新的参考。

Effects of artificially infected fowl adenovirus serotype 4 on natural immune response of geese

Fifty 30-day-old healthy geese were randomly divided into the infection group,the observation group after infection and the control group.The infected geese were observed twice daily to calculate the morbidity and the mortality.Tissue and blood sample were collected to detect the antibody level,viremia,and viral load.To understand the pathogenicity of fowl adenovirus serotype 4(FAd V-4)to geese after artificial infection and the innate immune response mechanism,real-time(RT-PCR)method was used to detect the expression level of genes includingβ-defensins(Av BDs),Toll-like receptors(TLRs)and cytokines in liver and heart.The results showed that all infected geese didn’t show clinical signs and death after infecting the FAd V-4 artificially.The antibody against FAd V-4 was detected positive in the infected geese and there was pathological lesions in the liver and the heart although no clinical signs were observed.Viral shedding from the swabs and viral load in the tissues were detected increase as the time duration of the infection.In the early stage of infection(36 h and 72 h),gene expression levels of Av BD1,2,5,9,16,TLR2,3,7,15,IL-1β,2,6,8,18 and myeloid differentiation factor 88(MyD88)in the liver were up-regulated or even significantly up-regulated(P<0.05)in some tissues.It was confirmed that there was very weak pathogenicity of FAd V-4 to geese,which may be influenced by the species of animal and the age of animal or the infection route.The host may produce a large number of immune factors through the TLRs-My D88 pathway to participate the antiviral immune response.This study provides a new reference for further study on the interaction between FAd V-4 and natural immunity in the early stage of infection.