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三十年来苏格兰水产养殖场感染性胰脏坏死病毒分离株的分子流行病学研究。

Molecular epidemiological study on Infectious Pancreatic Necrosis Virus isolates from aquafarms in Scotland over three decades.

机构信息

1​Institute of Aquaculture, University of Stirling, Stirling, UK.

2​Max Planck Institute of Psychiatry, Munich, Germany.

出版信息

J Gen Virol. 2018 Dec;99(12):1567-1581. doi: 10.1099/jgv.0.001155. Epub 2018 Oct 25.

DOI:10.1099/jgv.0.001155
PMID:30358526
Abstract

In order to obtain an insight into genomic changes and associated evolution and adaptation of Infectious Pancreatic Necrosis Virus (IPNV), the complete coding genomes of 57 IPNV isolates collected from Scottish aquafarms from 1982 to 2014 were sequenced and analysed. Phylogenetic analysis of the sequenced IPNV strains showed separate clustering of genogroups I, II, III and V. IPNV isolates with genetic reassortment of segment A/B of genogroup III/II were determined. About 59 % of the IPNV isolates belonged to the persistent type and 32 % to the low-virulent type, and only one highly pathogenic strain (1.79 %) was identified. Codon adaptation index calculations indicated that the IPNV major capsid protein VP2 has adapted to its salmonid host. Under-representation of CpG dinucleotides in the IPNV genome to minimize detection by the innate immunity receptors, and observed positive selection in the virulence determination sites of VP2 embedded in the variable region of the main antigenic region, suggest an immune escape mechanism driving virulence evolution. The prevalence of mostly persistent genotypes, together with the assumption of adaptation and immune escape, indicates that IPNV is evolving with the host.

摘要

为了深入了解传染性胰脏坏死病毒(IPNV)的基因组变化及其相关的进化和适应,我们对 1982 年至 2014 年期间从苏格兰水产养殖场采集的 57 株 IPNV 分离株的完整编码基因组进行了测序和分析。对测序的 IPNV 株系进行的系统发育分析显示,基因群 I、II、III 和 V 分别聚类。确定了具有基因群 III/II 节段 A/B 遗传重配的 IPNV 分离株。约 59%的 IPNV 分离株属于持续性类型,32%属于低毒力类型,仅鉴定出一株高致病性株(1.79%)。密码子适应指数计算表明,IPNV 的主要衣壳蛋白 VP2 已适应其鲑鱼宿主。为了最小化被先天免疫受体检测到的可能性,IPNV 基因组中 CpG 二核苷酸的表达不足,并且在主要抗原区的可变区中嵌入的 VP2 的毒力决定位点观察到阳性选择,这表明一种免疫逃避机制驱动着毒力的进化。主要持续性基因型的流行,加上适应和免疫逃避的假设,表明 IPNV 正在与宿主一起进化。

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