Evidence map›Paper›PMID 40646468›Full record

ArticleBMC genomics2025

Dissecting the genetic basis of response to salmonid alphavirus in Atlantic salmon.

Domniki Manousi, Dorota Monika Jaskula, Fabian Grammes, Tim Martin Knutsen, Shahmir Naseer, Samuel Am Martin, Thomas Moen, Marie Saitou, Sigbjørn Lien

Abstract read
In one paragraph

Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Domniki ManousiCentre for Integrative Genetics, Department of Animal and Aquacultural Sciences, Faculty of Biosciences, Norwegian University of Life Sciences, Oluf Thesens vei 6, Ås, 1433, Norway. domniki.manousi@nmbu.no.
Dorota Monika JaskulaCentre for Integrative Genetics, Department of Animal and Aquacultural Sciences, Faculty of Biosciences, Norwegian University of Life Sciences, Oluf Thesens vei 6, Ås, 1433, Norway.
Fabian GrammesAquaGen AS, Havnegata 9, Trondheim, 7010, Norway.
Tim Martin KnutsenAquaGen AS, Havnegata 9, Trondheim, 7010, Norway.
Shahmir NaseerScottish Fish Immunology Research Centre, School of Biological Sciences, University of Aberdeen, Aberdeen, AB24 2TZ, UK.
Samuel Am MartinScottish Fish Immunology Research Centre, School of Biological Sciences, University of Aberdeen, Aberdeen, AB24 2TZ, UK.
Thomas MoenAquaGen AS, Havnegata 9, Trondheim, 7010, Norway.
Marie SaitouCentre for Integrative Genetics, Department of Animal and Aquacultural Sciences, Faculty of Biosciences, Norwegian University of Life Sciences, Oluf Thesens vei 6, Ås, 1433, Norway.
Sigbjørn LienCentre for Integrative Genetics, Department of Animal and Aquacultural Sciences, Faculty of Biosciences, Norwegian University of Life Sciences, Oluf Thesens vei 6, Ås, 1433, Norway.

Funding

Norges Forskningsråd 325874
6 · The paper itself

Abstract

backgroundThe development of effective disease management strategies is crucial for the assurance of welfare and sustainability of the aquaculture industries. Pancreas disease (PD) is a major challenge faced by Atlantic salmon aquaculture with viral outbreaks resulting in substantial production losses and raising significant welfare concerns for farmed salmon populations. Previous research has identified several quantitative trait loci (QTL) associated with PD resistance accounting for a substantial additive genetic component. However, pinpointing the underlying causal variation remains challenging, partly due to the location of the QTL within duplicated regions of the Atlantic salmon genome that share high sequence similarity. The present study leverages the latest advancements in Atlantic salmon genomics in order to uncover the genetic landscape underlying PD resistance and identify genomic variation with putative functional impact on disease response.

resultsAssociation mapping and haplotype analysis of fish challenged with salmonid alphavirus (SAV3), either through peritoneal injection or infectious cohabitation, confirmed the presence of a major QTL region on chromosome Ssa03. Additionally, another QTL on Ssa07 was detected, linked to infection-specific response. Transcriptomics analysis of the genes overlapping the Ssa03 QTL region revealed significant expression differences among three tandemly duplicated gig1-like genes, whereas allele-specific expression analysis detected several SNPs with putative functional impact on the particular genes. Use of long-read sequencing and construction of disease-associated haplotypes identified more complex variation in the region, offering a detailed exploration of the genetic architecture underlying PD resistance. Finally, integration of the regulatory landscape of Atlantic salmon during response to viral infection improved genomic resolution, providing novel insight into the potential causal variation underlying pancreas disease in Atlantic salmon.

conclusionsThis study provides a detailed investigation of the genetic architecture underlying PD resistance in farmed Atlantic salmon. Using advanced genomic resources, three copies of the gig1-like gene were identified as likely causal candidates for a major QTL associated with PD resistance. Additionally, genomic variations with potential functional impact on gig1-like expression were uncovered. These findings hold promise for application in developing effective disease management strategies in Atlantic salmon aquaculture.

Indexed as

AlphavirusAlphavirus InfectionsDisease ResistanceFish DiseasesSalmo salarAnimalsChromosome MappingHaplotypesPancreatic DiseasesPolymorphism, Single NucleotideQuantitative Trait LociAtlantic salmonPancreas diseaseSalmonid alphavirusStructural variationWhole genome duplication

Identifiers

PMID40646468
PMCPMC12247413

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.