Salmonid alphavirus infection results in pancreas disease causing severe economic losses for Atlantic salmon aquaculture. Knowledge about genes and pathways contributing to resistance is limited. A 54 K SNP panel was used to genotype 10 full-sibling families each consisting of ~ 110 offspring challenged with salmonid alphavirus subtype 3. Relative heart viral load was assessed at 4-and 10-weeks post-infection using quantitative PCR. A moderate genomic heritability of viral load at 4 weeks (0.15-0.21) and a high positive correlation with survival (0.91-0.98) were detected. Positions of QTL detected on chromosome 3 matched those for survival detected by other studies. The SNP of highest significance occurred in the 3′ untranslated region of gig1, a fish-specific antiviral effector. Locus B of immunoglobulin heavy chain mapped to an area containing multiple SNPs with genome-wide association. Heart mRNA-seq comparing parr from families with high-versus lowgenomic breeding value, and matching sample genotypes for SNPs, identified two eQTL for salmonid alphavirus load. Immune genes associated with trans-eQTL were numerous and spread throughout the genome. QtL regions contained several genes with known or predicted immune functions, some differentially expressed. The putative functional genes and variants identified could help improve marker-based selection for pancreas disease resistance. Infectious diseases are a major threat to the sustainability of Atlantic salmon farming, causing production and economic losses, and having a negative impact on fish welfare and the environment. One of the major disease problems in Atlantic salmon aquaculture is pancreas disease (PD), which affects mainly first year Atlantic salmon smolts 1-8. Mortality due to natural outbreaks of PD is variable, ranging from negligible up to 63% 7,9-12. A Norwegian cohort study (2006-2008) reported an average PD-associated mortality of ~ 6.9% (range 0.7-26.9%) 13. However, economic losses due to morbidity can be high due to prolonged loss of appetite, growth retardation, and reduced filet quality 7,11. There have been several reports describing after-effects of PD outbreaks including the development of runts, and significantly lower growth in PD affected fish 11,14-16. PD is caused by Salmonid alphavirus (SAV), an infectious single-stranded positive-sense RNA virus 17,18. The mode of the spread of infection of salmonid diseases between co-habitants in water, and the ability to perform controlled disease challenge tests on large families of Atlantic salmon, provides us with a convenient model to use for investigating genes affecting resistance to this alphavirus, and the knowledge generated using such models might provide leads for the treatment or prevention of alphavirus disease in other species. Globally, six subtypes of SAV virus have been identified 19 , each distributed over a specific geographic range 8,20 .