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通过存活和病毒载量数据揭示虹鳟对传染性胰腺坏死病毒抗性的遗传学

The genetics of resistance to infectious pancreatic necrosis virus in rainbow trout unveiled through survival and virus load data.

作者信息

Ahmad Aqeel, Aslam Muhammad Luqman, Evensen Øystein, Gamil Amr A A, Berge Andreas, Solberg Thoralf, Schmitt Armin Otto, Gjerde Bjarne

机构信息

Department of Breeding and Genetics, Nofima, Ås, Norway.

Department of Animal and Aquacultural Sciences, Norwegian University of Life Sciences, Ås, Norway.

出版信息

Front Genet. 2024 Nov 19;15:1484287. doi: 10.3389/fgene.2024.1484287. eCollection 2024.

DOI:10.3389/fgene.2024.1484287
PMID:39628812
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11611855/
Abstract

Infectious Pancreatic Necrosis virus (IPNV) is one of the major threats to the animal welfare and economy of the rainbow trout farming industry. Previous research has demonstrated significant genetic variation for resistance against IPNV. The main objective of the study was to investigate the genetic architecture of resistance against IPNV in rainbow trout fry. To achieve this, 610 rainbow trout fry, from a full factorial mating between 5 sires and 5 dams, were bath challenged with the IPNV isolate (IPNV-AS) from Atlantic salmon reared at a commercial farm. The resistance against IPNV was accessed using three different phenotypes; binary survival (BS), total days survived (TDS) and virus load (VL) recorded on the fish throughout the 40-day challenge test. All fish were genotyped using a 57K Affymetrix SNP array. The IPNV-AS isolate resulted in an overall mortality of 62.1%. The heritability estimates for survival (BS h = 0.21 ± 0.06, TDS h = 0.25 ± 0.07) and VL traits (h = 0.23 ± 0.08) were moderate and indicative of potential use of selection for increased resistance to IPNV in rainbow trout selective breeding programs. The unity estimated genetic correlation between the two survival traits (BS and TDS) indicates that the traits can be considered the same trait. In contrast, a moderate favourable negative genetic correlation was found between VL and the two survival traits (-0.61 ± 0.22 to -0.70 ± 0.19). The GWAS of the traits with many QTLs crossing the chromosome-wide Bonferroni corrected threshold indicates the polygenic nature of the studied traits. Most of the 10 possible identified genes were found to be linked with immunity or viral pathogenesis, which could be potentially responsible for the significant genetic variation in survival against the IPNV-AS. The QTL validation analysis revealed no significant difference in the mortalities and VL among the three genotypes of the detected QTL. The VL trait showed larger variation among the dead fry and with a concordant pattern with the two survival phenotypes, but with no significant difference in the proportion of IPNV VL positive samples in the dead and the survived fry. Overall, the results indicate the polygenic nature of the studied traits and support the use of genomic selection to improve resistance against IPNV in rainbow trout breeding companies.

摘要

传染性胰腺坏死病毒(IPNV)是虹鳟鱼养殖业动物福利和经济的主要威胁之一。先前的研究表明,虹鳟鱼对IPNV的抗性存在显著的遗传变异。本研究的主要目的是调查虹鳟鱼苗对IPNV抗性的遗传结构。为实现这一目标,对来自5个父本和5个母本完全双列杂交的610尾虹鳟鱼苗,用商业养殖场养殖的大西洋鲑的IPNV分离株(IPNV-AS)进行浸浴攻毒。在为期40天的攻毒试验中,利用三种不同的表型评估虹鳟鱼苗对IPNV的抗性:二元存活(BS)、存活总天数(TDS)和病毒载量(VL)。所有鱼苗均使用57K Affymetrix SNP芯片进行基因分型。IPNV-AS分离株导致的总体死亡率为62.1%。存活(BS h = 0.21±0.06,TDS h = 0.25±0.07)和VL性状(h = 0.23±0.08)的遗传力估计值适中,表明在虹鳟鱼选育计划中,通过选择有可能提高对IPNV的抗性。两个存活性状(BS和TDS)之间的遗传相关估计值为1,表明这两个性状可视为同一性状。相比之下,VL与两个存活性状之间存在中等程度的有利负遗传相关(-0.61±0.22至-0.70±0.19)。对多个QTL超过全基因组Bonferroni校正阈值的性状进行全基因组关联研究(GWAS),表明所研究性状具有多基因性质。在10个可能鉴定出的基因中,大多数被发现与免疫或病毒发病机制有关,这可能是虹鳟鱼对IPNV-AS抗性存在显著遗传变异的潜在原因。QTL验证分析显示,检测到的QTL的三种基因型在死亡率和VL方面没有显著差异。VL性状在死亡鱼苗中表现出更大的变异性,并且与两种存活表型具有一致的模式,但在死亡鱼苗和存活鱼苗中,IPNV VL阳性样本的比例没有显著差异。总体而言,结果表明所研究性状具有多基因性质,并支持在虹鳟鱼育种公司中使用基因组选择来提高对IPNV的抗性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/9e57fbf06df3/fgene-15-1484287-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/ad2e50845c95/fgene-15-1484287-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/9e57fbf06df3/fgene-15-1484287-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/ad2e50845c95/fgene-15-1484287-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/eff39dba1f18/fgene-15-1484287-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/78c8c8f87ed0/fgene-15-1484287-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1a9/11611855/9e57fbf06df3/fgene-15-1484287-g004.jpg

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