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Research Document 2019/035

Characterization of piscine orthoreovirus (PRV) and associated diseases to inform pathogen transfer risk assessments in British Columbia

By Polinski, M. and Garver, K.

Abstract

Piscine orthoreovirus (PRV) is a common and pervasively distributed virus of salmon. In Canada, nearly all sea-farmed salmon likely become infected with PRV prior to harvest and the virus has been detected in archived specimens dating back to at least the mid 1980’s in British Columbia. Wild salmon (all species) also occasionally become infected with PRV. Detection is generally lower in wild populations than on farms, and not all salmon species are equally susceptible to PRV infection. Specifically, Sockeye Salmon appear mildly refractory compared to other species such as Atlantic Salmon. Among the wild Pacific salmon species in the Eastern Pacific, Coho and Chinook Salmon have the highest prevalence of PRV (approximately 9% and 6%, respectively); this prevalence appears independent from whether fish were collected from locations in close proximity to salmon farming or from areas devoid of salmon farming. The cumulative prevalence of PRV detected in Sockeye Salmon of Western North America over the past decade is approximately 1.5% based on the sampling of nearly 7,000 specimens of which more than 6,000 were collected from British Columbia stocks. Nonetheless, laboratory studies demonstrate that PRV infected Atlantic Salmon (dependent upon stage of infection) can transmit virus to cohabitating Sockeye Salmon; although the minimum exposure time, dose, and whether such transmission requirements would be reached in natural environs remain unknown. In some farmed salmon, PRV has caused disease – namely, cardiopathy and/or anemia – particularly in Europe and Japan. In farmed salmon of British Columbia, on rare occurrences, PRV has been detected in diseased Atlantic and Chinook salmon where the virus may have contributed to or caused the disease. This includes at least one instance of severe cardiopathy in farmed Atlantic Salmon and one instance of anemia in farmed Chinook Salmon in the past decade. If or when disease may manifest as a result of PRV infection is not well understood, appearing to require complex etiological factors that include host, virus, and environmental components. Both regional as well as viral strain-specific variations in virulence have been documented, and disease has, as yet, only been identified in farmed salmon populations. Important to discussions of PRV in Canada is that PRV in the Eastern Pacific appears less virulent in comparison to PRV in the Eastern Atlantic, and experimental infection of Sockeye and Atlantic Salmon with the PRV strain endemic to the Eastern Pacific has failed to manifest significant disease or impact respiratory function even though extreme systemic blood infections developed in both species. Furthermore, stressors such as smoltification, hypoxia, exhaustive chasing, or secondary viral (infectious hematopoietic necrosis virus) superinfection of salmon have not induced or enhanced this PRV virulence. Thus, neither the presence nor quantity of PRV generated during an infection is indicative of disease or physiological impairment in salmon of British Columbia.

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