Comparative Genomic Analysis of Classical and Variant Virulent Parental/Attenuated Strains of Porcine Epidemic Diarrhea Virus.
Comparative Genomic Analysis of Classical and Variant Virulent Parental/Attenuated Strains of Porcine Epidemic Diarrhea Virus.
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猪流行性腹泻病毒经典毒株和变异毒力亲本/减毒株的比较基因组分析
DOI：
10.3390/v7102891
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发表时间：
2015-10-23
期刊：
影响因子：
--
通讯作者：
He Q
中科院分区：
文献类型：
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作者：
Chen F;Zhu Y;Wu M;Ku X;Ye S;Li Z;Guo X;He Q
自2010年以来，猪流行性腹泻变异病毒(PEDV)一直是全球猪流行性腹泻(PED)暴发的病原体。在本研究中，分离到了一株PEDV变异株YN1，并在Vero细胞上连续繁殖，并鉴定了200代。为了更好地阐明PEDV变异株Vero细胞适应的分子基础，我们对亲本YN1和第15、30、60、90、144和200代的全基因组序列进行了测序、比较和分析。结果表明，随着病毒传代时间的延长，变异程度增大。非结构蛋白(NSP)2、NSP4-7、NSP10、NSP12和NSP13基因的核苷酸序列在Vero细胞适应过程中没有变化。通过比较经典毒株和变异强毒/弱毒株的变异特征，发现PEDV的弱毒与开放阅读框(ORF1a/b)和S蛋白的9个−26氨基酸变化、ORF3的提前终止、E、M和N蛋白的1~3个氨基酸变化以及部分核苷酸序列的同义突变有关。S蛋白第144位氨基酸缺失可能是PEDV的致弱标志。PIG研究表明，ORF3中的早期终止对病毒细胞适应比病毒减毒更重要。
Since 2010, the variant porcine epidemic diarrhea virus (PEDV) has been the etiological agent responsible for the outbreak of porcine epidemic diarrhea (PED) worldwide. In this study, a variant PEDV strain YN1 was isolated, serially propagated on the Vero cells and was characterized for 200 passages. To better elucidate the molecular basis of Vero cell adaptation of variant PEDV strains, we sequenced, compared, and analyzed the full-genome sequences of parental YN1 and passages 15, 30, 60, 90, 144, and 200. The results showed that the variations increased with the viral passage. The nucleotides sequences of non-structural protein (NSP)2, NSP4-7, NSP10, NSP12 and NSP13 genes did not change during the Vero cell adaptation process. After comparison of the variation characteristic of classical, variant virulent/attenuated strains, it was found that attenuation of PEDV virus was associated with 9−26 amino acid (aa) changes in open reading frames (ORF) 1a/b and S protein, early termination in ORF3, 1–3 aa changes in E, M and N protein and some nucleotide sequences’ synonymous mutations. The aa deletion at about 144 aa of S protein could be the attenuation marker for the PEDV. The pig study showed that the early termination in ORF3 was more important for virus cell adaptation than virus attenuation.