Cardiomyopathy syndrome is a severe, viral disease of Atlantic salmon that mostly affects farmed animals during their late production stage at sea. Caused by piscine myocarditis virus (PMCV), over the past few years outbreaks due to this disease have resulted in significant losses to the aquaculture industry. However, there is currently no vaccine that has proven effective against this virus. In this study, using a challenge model, we investigated the genetic variation for resistance to PMCV, by screening a large number of animals using a 55 K SNP array. In particular, we aimed to identify genetic markers that are tightly linked to higher disease resistance and can potentially be used in breeding programs. Using genomic information, we estimated a heritability of 0.51 ± 0.06, suggesting that resistance against this virus, to a great extent, is controlled by genetic factors. Through association analysis, we identified a significant quantitative trait locus (QTL) on chromosome 27, explaining approximately 57% of the total additive genetic variation. The region harboring this QTL contains various immune-related candidate genes, many of which have previously been shown to have a different expression profile between the naïve and infected animals. We also identified a suggestive association on chromosome 12, with the QTL linked markers located in 2 putatively immune-related genes. These results are of particular interest, as they can readily be implemented into breeding programs, can further assist in fine-mapping the causative mutations, and help in better understanding the biology of the disease and the immunological mechanisms underlying resistance against PMCV.
Keywords: Atlantic salmon; cardiomyopathy syndrome (CMS); genome-wide association study (GWAS); piscine myocarditis virus (PMCV); single nucleotide polymorphism (SNP).
© The American Genetic Association. 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.