title: Triploid atlantic salmon (Salmo salar L.) post-smolts accumulate prevalence more slowly than diploid salmon following bath challenge with salmonid alphavirus subtype 3.
abstract: Triploid Atlantic salmon (Salmo salar L.) may play an important role in the sustainable expansion of the Norwegian aquaculture industry. Therefore, the susceptibility of triploid salmon to common infections such as salmonid alphavirus (SAV), the causative agent of pancreas disease (PD), requires investigation. In this study, shortly after seawater transfer, diploid and triploid post-smolts were exposed to SAV type 3 (SAV3) using a bath challenge model where the infectious dose was 48 TCID50 ml-1 of tank water. Copy number analysis of SAV3 RNA in heart tissue showed that there was no difference in viral loads between the diploids and triploids. Prevalence reached 100% by the end of the 35-day experimental period in both infected groups. However, prevalence accumulated more slowly in the triploid group reaching 19% and 56% at 14 and 21 days post exposure (dpe) respectively. Whereas prevalence in the diploid group was 82% and 100% at the same time points indicating some differences between diploid and triploid fish. Both heart and pancreas from infected groups at 14 dpe showed typical histopathological changes associated with pancreas disease. Observation of this slower accumulation of prevalence following a natural infection route was possible due to the early sampling points and the exposure to a relatively low dose of virus. The triploid salmon in this study were not more susceptible to SAV3 than diploid salmon indicating that they could be used commercially to reduce the environmental impact of escaped farmed fish interbreeding with wild salmon. This is important information regarding the future use of triploid fish in large scale aquaculture where SAV3 is a financial threat to increased production.
authors.affiliation: Institute of Marine Research, Bergen, Norway.
authors.forename: Lindsey J
authors.initials: LJ
authors.lastname: Moore
authors.affiliation: Uni Research Environment, Bergen, Norway.
authors.forename: Tom Ole
authors.initials: TO
authors.lastname: Nilsen
authors.affiliation: Institute of Marine Research, Bergen, Norway.|Department of Biology, University of Bergen, Bergen, Norway.
authors.forename: Jiraporn
authors.initials: J
authors.lastname: Jarungsriapisit
authors.affiliation: Institute of Marine Research, Matre, Norway.
authors.forename: Per Gunnar
authors.initials: PG
authors.lastname: Fjelldal
authors.affiliation: Department of Biology, University of Bergen, Bergen, Norway.
authors.forename: Sigurd O
authors.initials: SO
authors.lastname: Stefansson
authors.affiliation: Institute of Marine Research, Bergen, Norway.
authors.forename: Geir Lasse
authors.initials: GL
authors.lastname: Taranger
authors.affiliation: Institute of Marine Research, Bergen, Norway.
authors.forename: Sonal
authors.initials: S
authors.lastname: Patel
mesh_terms: D000524:Alphavirus / Q000502:physiology*; D018354:Alphavirus Infections / Q000235:genetics / Q000662:veterinary* / Q000821:virology; D000818:Animals; D004171:Diploidy; D005260:Female; D005393:Fish Diseases / Q000235:genetics / Q000821:virology*; D020022:Genetic Predisposition to Disease; D008297:Male; D010179:Pancreas / Q000821:virology; D020317:Salmo salar / Q000235:genetics* / Q000821:virology; D057885:Triploidy