PISCINE ORTHOREOVIRUS (PRV-1) AND PISCINE MYOCARDITIS VIRUS (PMCV) INFECTIONS DO NOT IMPAIR THERMAL OXYGEN-USE PERFORMANCE IN ATLANTIC SALMON Salmo salar

Introduction

Viral infections associated with severe cardiac pathologies represent one of the top health challenges in Atlantic salmon aquaculture in the North Atlantic. Piscine orthoreovirus genotype 1 (PRV-1) and Piscine myocarditis virus (PMCV), induce distinct patterns of cardiac inflammation (HSMI – Heart and Skeletal Muscle Inflammation and CMS – Cardiomyopathy Syndrome) that result in compromised animal welfare and substantial production losses at sea. The association of these diseases with cardiac inflammation and impaired blood circulation raises concerns regarding physiological tolerance to different types of stress. PRV-1 variants (PRV-1a, non-virulent) endemic to the West coast of Canada cause minimal physiological impairment to infected Atlantic salmon , but PRV-1 (PRV-1b, virulent) strains found in Norway reduce the capacity of infected fish to tolerate hypoxic conditions above 19^oC . However, there is currently no literature examining the impact of PRV-1 and PMCV infection on the metabolic oxygen demand at upper thermal ranges (CTmax), particularly at the current scenario of climate change, which can make the fish more susceptible to these potential impacts. Thus, our research aimed to investigate the standard (SMR) and maximum metabolic rate (MMR), upper thermal tolerance, and relative ventricular mass (RVM) of Atlantic salmon at the peak of PRV-1b and PMCV infection.

Materials and Methods

To assess the thermal oxygen-use performance, fish infected with PMCV and PRV-1b infection were placed in a controlled respirometry chamber. The experiments took place from 8-10 weeks post-challenge (wpc), when heart inflammation was projected to reach peak severity. Each afternoon one fish was selected from either a negative control, PRV-1b or PMCV infection tank and placed in a cylindrical respirometer to have their standard metabolic rate (SMR) calculated overnight at their holding temperature (14^oC) . The next morning, fish were given a critical thermal maximum (CTmax) test targeting a temperature increase of 3^oC per hour, with oxygen consumption recorded every increase of 1^oC, until fish lost equilibrium. The temperature reached at the loss of equilibrium was recorded as the CTmax. A total of 15 fish from each group were used across the three weeks of respirometry experiments. Fish remaining at the end of the 14wpc study were lethally sampled to have body weight and ventricle weight recorded for RVM calculations. Histology was also used to assess the timing and severity of cardiac lesions.

Results

At rest and under thermal challenge, viral infections failed to have a significant impact on the standard metabolic rate (SMR) and maximum metabolic rate (MMR) of post-smolt Atlantic salmon. However, the relative ventricular mass (RVM) of fish infected with PMCV was statistically higher than the negative control. The CTmax was also similar across study weeks. The trend in metabolic oxygen consumption (MO2) with increasing temperature and respiratory parameters can be found in Figure 1 and Table 1.

Discussion

Despite the expected impact of PRV-1b and PMCV infections on cardiac function, our results indicate that neither virus significantly altered SMR, MMR, or thermal oxygen-use performance under acute warming conditions. This suggests that infected fish maintained aerobic capacity even at upper thermal limits. The preservation of metabolic performance likely reflects the activation of compensatory mechanisms across several physiological adaptations. At the blood level, splenic contraction might increase hemoglobin (HGB) and hematocrit (HCT), thereby enhancing oxygen-carrying capacity. Ventilatory adjustments, including increased rate and amplitude, could improve oxygen uptake at the gill. Cardiovascular compensation through modulation of heart rate and stroke volume may sustain cardiac output despite inflammation, while acid–base regulation (via carbonic anhydrase activity and the Bohr and Root effects) likely facilitates efficient oxygen unloading at the tissues. Interestingly, the increased relative ventricular mass observed in PMCV-infected fish may represent a structural adaptation supporting cardiac output under inflammatory stress. Together, these responses may explain why no impairment in MO₂ or CTmax was detected, even at peak infection. Although hypoxia adaptations are different, these findings contrast with previous reports of reduced hypoxia tolerance in virulent PRV infections, suggesting that, under the conditions tested, Atlantic salmon can buffer the functional consequences of potential cardiac damage caused by PRV and PMCV during acute thermal challenges. However, the absence of performance impairment does not preclude subclinical limitations, particularly under chronic or multifactorial stressors, such as those encountered in field conditions.

Figure 1. Average Metabolic Oxygen Consumption (MO2) of Atlantic salmon from control, PMCV, or PRV-1b infection groups calculated in controlled respirometry experiments. Table 1. Average respirometry parameters.

Figure 1. Average Metabolic Oxygen Consumption (MO2) of Atlantic salmon from control, PMCV, or PRV-1b infection groups calculated in controlled respirometry experiments. Table 1. Average respirometry parameters.

Acknowledgment

This work was funded through an Alliance Grant (ALLRP) issued by the Natural Sciences and Engineering Research Council of Canada (NSERC) (File: ALLRP 608325 – 25) and Onda.

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