From viral load to survival: Unveiling new genetic links for resistance against PMCV in Atlantic Salmon (Salmo salar).

Abstract

The infectious agent piscine myocarditis virus (PMCV) causes cardiomyopathy syndrome (CMS) and is responsible for substantial mortality and economic losses in the Atlantic salmon (Salmo salar) farming industry. Previous research has demonstrated that breeding for resistance against PMCV is an effective approach to mitigate the disease's impact. In this study, a new quantitative trait locus (QTL) is described on chromosome 23, together with previously described QTLs on chromosomes 12 and 27. The findings are based on two genome-wide association studies conducted on two different year-classes of Atlantic salmon of the Rauma strain. In this study, we utilized data from an experimental challenge trial with the viral load as the phenotype and a field outbreak of CMS with survival data as the phenotype. The estimated SNP-based heritability was 0.55 and 0.44 in the two studies, respectively. In the infection trial, the top associated SNP on chromosome 23 accounted for approximately 46% of the genetic and 25.53% of the phenotypic variations in the viral load. In the field outbreak, we identified a QTL on the same genomic region of chromosome 23. The most significantly associated marker on this chromosome explained 13.57% and 5.97% of the genetic and phenotypic variations. The QTL on chromosome 23 is in proximity to delta-5 fatty acyl desaturase and fatty acid desaturase 2 genes, both of which play a role in the production of polyunsaturated fatty acids. This proximity is particularly interesting as it offers valuable insights into enhancing our understanding of resistance against PMCV.