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亚洲和欧洲研发的减毒活鹅细小病毒疫苗株序列变化的鉴定

Identification of sequence changes in live attenuated goose parvovirus vaccine strains developed in Asia and Europe.

作者信息

Shien J-H, Wang Y-S, Chen C-H, Shieh H K, Hu C-C, Chang P-C

机构信息

Department of Veterinary Medicine, National Chung Hsing University, Taichung, Taiwan.

出版信息

Avian Pathol. 2008 Oct;37(5):499-505. doi: 10.1080/03079450802356979.

Abstract

Live attenuated vaccines have been used for control of the disease caused by goose parvovirus (GPV), but the mechanism involved in attenuation of GPV remains elusive. This report presents the complete nucleotide sequences of two live attenuated strains of GPV (82-0321V and VG32/1) that were independently developed in Taiwan and Europe, together with the parental strain of 82-0321V and a field strain isolated in Taiwan in 2006. Sequence comparisons showed that 82-0321V and VG32/1 had multiple deletions and substitutions in the inverted terminal repeats region when compared with their parental strain or the field virus, but these changes did not affect the formation of the hairpin structure essential for viral replication. Moreover, 82-0321V and VG32/1 had five amino acid changes in the non-structural protein, but these changes were located at positions distant from known functional motifs in the non-structural protein. In contrast, 82-0321V had nine changes and VG32/1 had 11 changes in their capsid proteins (VP1), and the majority of these changes occurred at positions close to the putative receptor binding sites of VP1, as predicted using the structure of adeno-associated virus 2 as the model system. Taken together, the results suggest that changes in sequence near the receptor binding sites of VP1 might be responsible for attenuation of GPV. This is the first report of complete nucleotide sequences of GPV other than the virulent B strain, and suggests a possible mechanism for attenuation of GPV.

摘要

减毒活疫苗已被用于控制由鹅细小病毒(GPV)引起的疾病,但GPV减毒所涉及的机制仍不清楚。本报告展示了在台湾和欧洲独立研发的两种GPV减毒株(82 - 0321V和VG32/1)的完整核苷酸序列,以及82 - 0321V的亲本毒株和2006年在台湾分离的一株野毒株。序列比较显示,与它们的亲本毒株或野毒株相比,82 - 0321V和VG32/1在反向末端重复区域有多个缺失和替换,但这些变化不影响病毒复制所必需的发夹结构的形成。此外,82 - 0321V和VG32/1在非结构蛋白中有五个氨基酸变化,但这些变化位于远离非结构蛋白中已知功能基序的位置。相比之下,82 - 0321V在其衣壳蛋白(VP1)中有九个变化,VG32/1有11个变化,并且这些变化大多发生在靠近预测的VP1受体结合位点的位置,预测时以腺相关病毒2的结构作为模型系统。综上所述,结果表明VP1受体结合位点附近的序列变化可能是GPV减毒的原因。这是除强毒株B之外的GPV完整核苷酸序列的首次报告,并提出了一种可能的GPV减毒机制。

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