Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem to the aquaculture of Atlantic salmon (Salmon salar), during both the freshwater and seawater stages of production. Genetic variation in resistance to IPN has previously been demonstrated and the purpose of this study was to determine whether this variation includes loci of major effect. The initial QTL detection methodology utilized the limited recombination seen in male salmon to detect QTL in ten large full-sib families, using a genome-wide scan of two to three markers per linkage group. QTL were then positioned by adding additional markers to the significant linkage groups in a female-based analysis. The most significant QTL was mapped to LG 21, and further confirmation of the LG 21 QTL is provided in an analysis of the QTL flanking markers in an additional nine full-sib families from the same population. The size of QTL effect is such that the QTL flanking markers can be immediately applied in marker-assisted selection programmes to improve the resistance of salmon populations to IPN, thus reducing mortality due to the disease.