Abstract
The recent ubiquitous detection of PRV among salmonids has sparked international concern about the cardiorespiratory performance of infected wild and farmed salmon. Piscine orthoreovirus (PRV) has been shown to create substantial viremia in salmon by targeting erythrocytes for principle replication. In some instances, infections develop into heart and skeletal muscle inflammation (HSMI) or other pathological conditions affecting the respiratory system. Critical to assessing the seriousness of PRV infections are controlled infection studies that measure physiological impairment to critical life support systems. Respiratory performance is such a system and here multiple indices were measured to test the hypothesis that a low-virulence strain of PRV from Pacific Canada compromises the cardiorespiratory capabilities of Atlantic salmon. Contrary to this hypothesis, the oxygen affinity and carrying capacity of erythrocytes were unaffected by PRV despite the presence of severe viremia, minor heart pathology and transient cellular activation of antiviral response pathways. Similarly, PRV-infected fish had neither sustained nor appreciable differences in respiratory capabilities compared with control fish. The lack of functional harm to salmon infected with PRV in this instance highlights that, in an era of unprecedented virus discovery, detection of viral infection does not necessarily imply bodily harm and that viral load is not always a suitable predictor of disease within a host organism.
Highlights
Animal viruses are expected to inflict harm to the host cells they infect, either as a direct result of infection or as a product of host-directed apoptosis (Kaminskyy and Zhivotovsky, 2010)
Intraperitoneal injection of Piscine orthoreovirus (PRV) generated an anticipated high-load viremia in Atlantic salmon as evidenced by PRV transcriptional blood loads reaching a peak by 25 dpc at approximately 2.0 × 1010 mean reverse transcribed gRNA copies per mL of host blood and maintained above 3.0 × 109 mean copies per mL for the remainder of the study (Figure 1A)
While mild heart and/or skeletal muscle inflammation was diagnosed in PRVinfected salmon, a comparable prevalence and severity of heart inflammation occurred in the blood control (BC)-treatment group (p > 0.39) at 4, 25 and 148 dpc (Figure 1D and Supplementary Figure 1)
Summary
Animal viruses are expected to inflict harm to the host cells they infect, either as a direct result of infection or as a product of host-directed apoptosis (Kaminskyy and Zhivotovsky, 2010). Given that erythrocytes are primary targets for PRV infection and the heart is a principal organ associated with PRV disease (e.g., HSMI), it has been suggested that all PRV infections lead to respiratory impairments (Olsen et al, 2015; Takano et al, 2016; Lund et al, 2017; Di Cicco et al, 2018) and are of sufficient severity that if wild salmon become infected they might not be able to swim back to their spawning areas because of a presumed reduction in respiratory capabilities (Garseth et al, 2013; Morton et al, 2017; Di Cicco et al, 2018) This has sparked international concern for PRV’s potential to cause cardiorespiratory harm to both wild and farmed salmon populations. We incorporated an extreme acute hypoxic challenge into the late persistence phase of infection so as to maximize our likelihood for identifying PRV-associated respiratory harm
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