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dc.contributor.authorJarungsriapisit, J.
dc.contributor.authorMoore, L. J
dc.contributor.authorTaranger, G. L
dc.contributor.authorNilsen, T. O
dc.contributor.authorMorton, H. C
dc.contributor.authorFiksdal, I. U
dc.contributor.authorStefansson, S.
dc.contributor.authorFjelldal, P. G
dc.contributor.authorEvensen, Ø.
dc.contributor.authorPatel, S.
dc.date.accessioned2016-05-11T10:56:19Z
dc.date.available2016-05-11T10:56:19Z
dc.date.issued2016-04-11
dc.PublishedVirology Journal. 2016 Apr 11;13(1):66eng
dc.identifier.urihttp://hdl.handle.net/1956/11987
dc.description.abstractBackground Pancreas disease (PD), caused by salmonid alphavirus (SAV), is an important disease affecting salmonid aquaculture. It has been speculated that Atlantic salmon post-smolts are more prone to infections in the first few weeks following seawater- transfer. After this period of seawater acclimatization, the post-smolts are more robust and better able to resist infection by pathogens. Here we describe how we established a bath immersion (BI) model for SAV subtype 3 (SAV3) in seawater. We also report how this challenge model was used to study the susceptibility of post-smolts to SAV3 infection in two groups of post-smolts two weeks or nine weeks after seawater - transfer. Methods Post-smolts, two weeks (Phase-A) or nine weeks (Phase-B) after seawater- transfer, were infected with SAV3 by BI or intramuscular injection (IM) to evaluate their susceptibility to infection. A RT-qPCR assay targeting the non-structural protein (nsP1) gene was performed to detect SAV3-RNA in blood, heart tissue and electropositive-filtered tank-water. Histopathological changes were examined by light microscope, and the presence of SAV3 antigen in pancreas tissue was confirmed using immuno-histochemistry. Results Virus shedding from the Phase-B fish injected with SAV3 (IM Phase-B) was markedly lower than that from IM Phase-A fish. A lower percentage of viraemia in Phase-B fish compared with Phase-A fish was also observed. Viral RNA in hearts from IM Phase-A fish was higher than in IM Phase-B fish at all sampling points (p < 0.05) and a similar trend was also seen in the BI groups. Necrosis of exocrine pancreatic cells was observed in all infected groups. Extensive histopathological changes were found in Phase-A fish whereas milder PD-related histopathological lesions were seen in Phase-B fish. The presence of SAV3 in pancreas tissue from all infected groups was also confirmed by immuno-histochemical staining. Conclusion Our results suggest that post-smolts are more susceptible to SAV3 infection two weeks after seawater-transfer than nine weeks after transfer. In addition, the BI challenge model described here offers an alternative SAV3 infection model when better control of the time-of-infection is essential for studying basic immunological mechanisms and disease progression.en_US
dc.language.isoengeng
dc.publisherBioMed Centralen_US
dc.rightsAttribution CC BY 4.0eng
dc.rights.urihttp://creativecommons.org/licenses/by/4.0eng
dc.subjectBath challengeeng
dc.subjectBath immersioneng
dc.subjectViral sheddingeng
dc.subjectSalmon pancreas disease viruseng
dc.subjectSPDVeng
dc.subjectPancreas diseaseeng
dc.subjectPlasma cortisoleng
dc.subjectATPase activityeng
dc.subjectCondition factoreng
dc.titleAtlantic salmon (Salmo salar L.) post-smolts challenged two or nine weeks after seawater-transfer show differences in their susceptibility to salmonid alphavirus subtype 3 (SAV3)en_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2016-04-11T16:02:26Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright Jarungsriapisit et al. 2016en_US
dc.identifier.doihttps://doi.org/10.1186/s12985-016-0520-8
dc.subject.nsiVDP::Medisinske Fag: 700en_US


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Attribution CC BY 4.0
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