Abstract
BackgroundInfectious Salmonid Anaemia Virus (ISAV) causes a notifiable disease that poses a large threat for Atlantic salmon (Salmo salar) aquaculture worldwide. There is no fully effective treatment or vaccine, and therefore selective breeding to increase resistance to ISAV is a promising avenue for disease prevention. Genomic selection and potentially genome editing can be applied to enhance host resistance, and these approaches benefit from improved knowledge of the genetic and functional basis of the target trait. The aim of this study was to characterise the genetic architecture of resistance to ISAV in a commercial Atlantic salmon population and study its underlying functional genomic basis using RNA Sequencing.ResultsA total of 2833 Atlantic salmon parr belonging to 194 families were exposed to ISAV in a cohabitation challenge in which cumulative mortality reached 63% over 55 days. A total of 1353 animals were genotyped using a 55 K SNP array, and the estimate of heritability for the trait of binary survival was 0.13–0.33 (pedigree-genomic). A genome-wide association analysis confirmed that resistance to ISAV was a polygenic trait, albeit a genomic region in chromosome Ssa13 was significantly associated with resistance and explained 3% of the genetic variance. RNA sequencing of the heart of 16 infected (7 and 14 days post infection) and 8 control fish highlighted 4927 and 2437 differentially expressed genes at 7 and 14 days post infection respectively. The complement and coagulation pathway was down-regulated in infected fish, while several metabolic pathways were up-regulated. The interferon pathway showed little evidence of up-regulation at 7 days post infection but was mildly activated at 14 days, suggesting a potential crosstalk between host and virus. Comparison of the transcriptomic response of fish with high and low breeding values for resistance highlighted TRIM25 as being up-regulated in resistant fish.ConclusionsISAV resistance shows moderate heritability with a polygenic architecture, but a significant QTL was detected on chromosome 13. A mild up-regulation of the interferon pathway characterises the response to the virus in heart samples from this population of Atlantic salmon, and candidate genes showing differential expression between samples with high and low breeding values for resistance were identified.
Highlights
Infectious Salmonid Anaemia Virus (ISAV) causes a notifiable disease that poses a large threat for Atlantic salmon (Salmo salar) aquaculture worldwide
infectious salmon anaemia (ISA) is classified as a list II disease by the EU fish health directive and as a notifiable disease by the World Organisation for Animal Health [11], which means that entire stocks have to be culled upon detection of the virus to avoid the spread to nearby farms
Disease challenge and genetic parameters of ISAV resistance The ISAV cohabitation challenge on 2833 fish belonging to 194 families (15.9 ± 4.5 fish per family) from Benchmark Genetics commercial breeding programme showed substantial variation in mortality rate between families (Fig. 1a), with values ranging from 7 to 100%, suggesting the presence of a genetic component underlying resistance to ISAV in this population
Summary
Infectious Salmonid Anaemia Virus (ISAV) causes a notifiable disease that poses a large threat for Atlantic salmon (Salmo salar) aquaculture worldwide. While aquaculture production has risen steadily in the recent decades [6], it can be high-risk, in part due to infectious diseases, which pose major threats to entire production systems, with downstream impacts on efficiency and sustainability. One such disease threat for farmed Atlantic salmon (Salmo salar) is infectious salmon anaemia (ISA), caused by an aquatic orthomyxovirus of the same name (ISAV). There are no effective treatments against ISAV, and available vaccines are typically only partially protective [21]
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