Abstract
BackgroundPancreas disease (PD) is a contagious disease caused by salmonid alphavirus (SAV) with significant economic and welfare impacts on salmon farming. Previous work has shown that higher resistance against PD has underlying additive genetic components and can potentially be improved through selective breeding. To better understand the genetic basis of PD resistance in Atlantic salmon, we challenged 4506 smolts from 296 families of the SalmoBreed strain. Fish were challenged through intraperitoneal injection with the most virulent form of the virus found in Norway (i.e., SAV3). Mortalities were recorded, and more than 900 fish were further genotyped on a 55 K SNP array.ResultsThe estimated heritability for PD resistance was 0.41 ± 0.017. The genetic markers on two chromosomes, ssa03 and ssa07, showed significant associations with higher disease resistance. Collectively, markers on these two QTL regions explained about 60% of the additive genetic variance. We also sequenced and compared the cardiac transcriptomics of moribund fish and animals that survived the challenge with a focus on candidate genes within the chromosomal segments harbouring QTL. Approximately 200 genes, within the QTL regions, were found to be differentially expressed. Of particular interest, we identified various components of immunoglobulin-heavy-chain locus B (IGH-B) on ssa03 and immunoglobulin-light-chain on ssa07 with markedly higher levels of transcription in the resistant animals. These genes are closely linked to the most strongly QTL associated SNPs, making them likely candidates for further investigation.ConclusionsThe findings presented here provide supporting evidence that breeding is an efficient tool for increasing PD resistance in Atlantic salmon populations. The estimated heritability is one of the largest reported for any disease resistance in this species, where the majority of the genetic variation is explained by two major QTL. The transcriptomic analysis has revealed the activation of essential components of the innate and the adaptive immune responses following infection with SAV3. Furthermore, the complementation of the genomic with the transcriptomic data has highlighted the possible critical role of the immunoglobulin loci in combating PD virus.
Highlights
Pancreas disease (PD) is a contagious disease caused by salmonid alphavirus (SAV) with significant economic and welfare impacts on salmon farming
The findings reported in this study provide knowledge, necessary for helping us better understand the genetic basis of resistance against PD
Our data confirm that PD resistance has a high heritable, additive genetic component
Summary
Pancreas disease (PD) is a contagious disease caused by salmonid alphavirus (SAV) with significant economic and welfare impacts on salmon farming. To better understand the genetic basis of PD resistance in Atlantic salmon, we challenged 4506 smolts from 296 families of the SalmoBreed strain. Fish were challenged through intraperitoneal injection with the most virulent form of the virus found in Norway (i.e., SAV3). Pancreas disease (PD) is a severe contagious disease of farmed Atlantic salmon (Salmo salar) and rainbow trout (Oncorhynchus mykiss), affecting fish during the seawater phase of the production. The aetiological agent, salmonid alphavirus (SAV), is a single-stranded RNA virus belonging to the Togaviridae family [1], and it has become a pathogen of high economic concern in the salmon farming countries such as Norway, Scotland and Ireland. The number of PD cases throughout Norway, due to SAV3 infection, has remained relatively constant with about 100 outbreaks per year [9]
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