The same strain of Piscine orthoreovirus (PRV-1) is involved in the development of different, but related, diseases in Atlantic and Pacific Salmon in British Columbia

Piscine orthoreovirus Strain PRV-1 is the causative agent of heart and skeletal muscle inflammation (HSMI) in Atlantic salmon (Salmo salar Linnaeus, 1758). Given its high prevalence in net pen salmon, debate has arisen on whether PRV poses a risk to migratory salmon, especially in British Columbia (...

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Bibliographic Details
Published in:FACETS
Main Authors: Emiliano Di Cicco, Hugh W. Ferguson, Karia H. Kaukinen, Angela D. Schulze, Shaorong Li, Amy Tabata, Oliver P. Günther, Gideon Mordecai, Curtis A. Suttle, Kristina M. Miller
Format: Article in Journal/Newspaper
Language:English
Published: Canadian Science Publishing 2018
Subjects:
PRV
Atlantic salmon
chinook salmon
HSMI
jaundice/anemia
VDD
ISH
Education
L
Science
Q
British Columbia
Canada
Norway
Pacific
Salmo salar
Online Access:https://doi.org/10.1139/facets-2018-0008
https://doaj.org/article/ead5a5c1e97d400f98bed63f205f5382
Description
Summary:Piscine orthoreovirus Strain PRV-1 is the causative agent of heart and skeletal muscle inflammation (HSMI) in Atlantic salmon (Salmo salar Linnaeus, 1758). Given its high prevalence in net pen salmon, debate has arisen on whether PRV poses a risk to migratory salmon, especially in British Columbia (BC) where commercially important wild Pacific salmon are in decline. Various strains of PRV have been associated with diseases in Pacific salmon, including erythrocytic inclusion body syndrome (EIBS), HSMI-like disease, and jaundice/anemia in Japan, Norway, Chile and Canada. We examined the developmental pathway of HSMI and jaundice/anemia associated with PRV-1 in farmed Atlantic and chinook (Oncorhynchus tshawytscha (Walbaum, 1792)) salmon in BC, respectively. In situ hybridization localized PRV-1 within developing lesions in both diseases. The two diseases showed dissimilar pathological pathways, with inflammatory lesions in heart and skeletal muscle in Atlantic salmon and degenerative-necrotic lesions in kidney and liver in chinook salmon, plausibly explained by differences in PRV load tolerance in red blood cells. Viral genome sequencing revealed no consistent differences in PRV-1 variants intimately involved in the development of both diseases suggesting that migratory chinook salmon may be at more than a minimal risk of disease from exposure to the high levels of PRV occurring in salmon farms.

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