中文摘要：

为了追踪高致病性猪繁殖与呼吸综合征病毒（Highly pathogenic porcine reproductive and respiratory syn-drome virus,HP-PRRSV）毒力逐渐减弱的分子轨迹,我们以HP-PRRSV亲本毒HuN4株及其系列传代致弱毒株为研究对象,对HuN4株及其不同代次毒株其全基因序列进行了序列比较分析。结果显示由高致病性的亲本毒HuN4株到无致病性的F112代的疫苗毒,共有65个核苷酸发生突变,其中导致41个氨基酸发生突变,这些突变的氨基酸分散性的存在于不同基因区域。与已经报道的高致病性JXA1株及其致弱毒株JXA80株相比较,可以看到两个强毒株毒力致弱的演变轨迹并不完全相同,二者之间不仅氨基酸突变数量不一致,而且突变氨基酸的位置也不完全相同,但其共同特点是由强毒株到弱毒株的变化过程中,突变率较高的结构蛋白相一致,突变率较高的非结构蛋白基本一致。分析结果提示我们决定高HP-PRRSV毒力强弱的因素可能不是由单个氨基酸的突变来决定的,推测是由一个基因或多个基因或多种因素共同造成的,同时也使我们认识到PRRSV的非结构蛋白区在病毒毒力变化中可能发挥重要作用。

英文摘要：

To identify the possible sites of attenuation,genomic characterization of Highly pathogenic porcine reproductive and respiratory syndrome virus（PRRSV） strain HuN4 and its attenuated intermediates was described.The results showed that there are a total of 65 nucleotide mutations,which cause mutations in 41 amino acids,between HuN4 and its attenuated strain at passage 112th（HuN4-F112）.These mutations of amino acids present in different regions of the genome.The attenuation process of HuN4 is not exactly same as previous report about the attenuation of highly pathogenic JXA1 strain and its attenuated JXA80 strain.Not only the number of mutations of amino acids between the two strains is inconsistent,but the location of amino acid mutation is not exactly the same.However,during the attenuation of HuN4 and JXA1,structural proteins and non-structural proteins with higher mutation rate are same.The analysis result showed that the highly pathogenic PRRSV virulence factors might not be determined by a single amino acid mutation,and might be determined by one gene or multiple genes.The result also revealed that the non-structural protein might play an important role in the change of PRRSV virulence.