中文摘要：

为了进一步明确各编码蛋白基因在鹅细小病毒（gooseparvovirus）鹅胚化疫苗株毒力减弱中的作用，以先前构建的弱毒疫苗株感染性质粒pSYG61v和强毒株感染性质粒pLH为基础，通过重叠PCR方法，在pSYG61v和pLH质粒之间互换Rep1和VP1基因片段，获得了6个嵌舍质粒pSYG-vRepl、pSYG-vVPl、pSYG-vRC、pLH-aRepl、pLH-aVP1和pLH-aRC。将质粒以绒毛尿囊膜途径转染11日龄鹅胚分别拯救出嵌合病毒。嵌合病毒的雏鹅攻毒试验表明，携带强毒株VP1基因的psYGvRC、pSYG-vVP1和pLH—aRepl这3个嵌合病毒对雏鹅表现出明显致病性，死亡率在75．0％-82．5％。完全携带弱毒株rep-cap编码框的pLH-aRC嵌合病毒攻毒组雏鹅无一死亡。携带强毒株Repl基因的pLH—aVP1和psYpvRep1嵌合病毒攻毒组雏鹅也无一死亡，但在试验期内部分雏鹅明显生长迟缓。嵌合病毒攻毒试验结果表明，结构蛋白VP1基因的氨基酸点突变对GPV鹅胚化疫苗株的毒力减弱起着关键作用。

英文摘要：

To dissect the role of coding protein genes in the attenuation of the goose embryo-adap- ted vaccine strain of goose parvovirus,six chimeric plasmids were constructed by swapping the dif- ferent fragments between the infectious plasmid pLH and the plasmid pSYG61 ,which contain the genome of the virulent strain LH and the vaccine strain SYG61v, respectively. The six plasmids, designated as pSYG-vRepl, pSYG-vVP1, pSYG-vRC, pLH-aRepl, pLH-aVP1 and pLH-aRC, were transfected respectively in l 1-day-old embryonated goose eggs via the chorioallantoic membrane infiltration route, resulting in rescue of infectious viruses. The pathogenicity of six chimeric viruses were evaluated in susceptible goslings. Challenge experiments revealed that the rescued pSYG- vRepl, pSYG-vVP1, and pSYG-vRC viruses, which harbored the VP1 gene from the virulent strain, exhibited an obvious pathogenicity to goslings, with the mortality rates ranging from 75.0% to 87.5~. No death cases and other lesions were observed in goslings changed with the pLH-aRC virus that contained the whole rep-cap coding frame from the vaccine strain. In goslings challenged respectively with the pLH-aVP1 virus or pSYG-vRepl virus that carried the Rep gene from the virulent strain and the VP1 gene from the vaccine strain,all goslings survived,meanwhile, partial goslings showed obvious growth retardations in the experimental period. The overall challenge results demonstrate that the point mutations in the VP1 gene play the key role in the attenuation of the goose embryo-adapted vaccine strain.