新城疫病毒人工感染鹅脾脏差异表达蛋白质组初步分析

Preliminary Analysis of Differentially Expressed Proteins in Spleen from Geese Experimentally Infected with Newcastle Disease Viruses

脾脏是新城疫病毒(Newcastle disease virus,NDV)感染的重要靶器官,本试验旨在从分子水平上分析NDV与宿主之间的相互作用,探寻早期基因Ⅳ型强毒Herts/33和晚期基因Ⅶ型强毒JS5/05造成鹅脾脏病变差异的相关蛋白。30日龄非免疫鹅分别人工感染NDV强毒株Herts/33和JS5/05,并于感染后36、72、108h采集2个感染组和对照组的鹅脾脏,提取脾脏蛋白,以17cm、pH5～8的IPG胶条进行二维电泳,运用PDQuest 8.0.1软件对凝胶图谱进行差异蛋白分析。结果显示:与对照组相比,Herts/33感染组和JS5/05感染组脾脏组织分别有154个和148个蛋白出现了显著的差异表达,其中有86个蛋白点是不同感染组共有的差异点,包括52个感染后上调表达蛋白点,34个下调表达蛋白点;另外,有130个差异蛋白点为NDV感染鹅后不同毒株之间产生的差异表达,包括71个感染后上调表达蛋白点,59个下调表达蛋白点。基因Ⅳ型NDV强毒和基因Ⅶd亚型NDV强毒分别感染鹅后,能引起宿主脾脏组织蛋白表达谱发生不同的改变,这为进一步研究Ⅶd亚型NDV对水禽致病性增强的机制提供了重要线索。

Spleen is the target organ of Newcastle disease virus（NDV）.To elucidate the interaction between NDV and its hosts,and to further evaluate the pathological differences of spleen from the geese infected by the early-genotype NDV strain Herts/33（IV） and recent-genotype NDV strain JS5/05（VIId）,the comparative proteomes of spleen from geese infected with these two NDVs were analyzed using two-dimensional gel electrophoresis（2-DE）.Thirty-six 30-day-old geese were divided into three groups.The spleens from the geese in different groups were collected at 36 hours,72 hours and 108 hours post infection.The soluble proteins were extracted and then separated with 17 cm IPG strips（pH 5-8）.Moreover,the 2-DE maps were comparatively analyzed by the software PDQuest 8.0.1.Compared with the control group,154 and 148 differentially expressed protein spots were found in Herts/33-and JS5/05-infected group,respectively.There were 86 spots shared by the two NDV-infected groups,with 52 proteins up-regulated and 34 proteins down-regulated.In addition,a total of 130 differentially expressed protein spots were identified between Herts/33-and JS5/05-infected groups,including 71 up-regulated proteins and 59 down-regulated proteins.The virulent genotype Ⅳ and genotype Ⅶd NDVs induced distinct splenic protein expression profiles after infection,which provided useful information to further elucidate the molecular mechanisms of increased pathogenicity of genotype Ⅶd NDV to waterfowl.