Frontiers in immunology · 2026
Family-wise resistance to infectious salmon anemia suggests that early systemic recognition protects against disease but not viral transcription.
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Johnston Amber E, Bouchard Deborah A, Lifgren Demitri, Turner Sarah M, DeLap Daniel M, Polinski Mark P
Аннотация
INTRODUCTION: Infectious salmon anemia virus (ISAV), the causative agent of infectious salmon anemia (ISA), is one of the most regulated pathogens affecting Atlantic salmon aquaculture globally. Recent investigations suggest a linkage between the host genome and ISA resistance, identifying a potential for promoting resistance through selective breeding. Herein, we sought to explore the dynamics associated with phenotypic ISA and/or ISAV resistance to better mitigate ISA disease.
METHODS: Forty families of North American Atlantic salmon were challenged with ISAV to determine family-wise survival, with fish from each family distributed across 16 tanks (one fish per family per tank) and exposed via injection (n = 4 per family) or cohabitation (n = 12 per family). Four additional tanks (one fish/family/tank) were sampled at either early-onset (11 days post challenge), peak mortality (21 and 35 days post challenge), or resolution (49 days post challenge) phases of disease. Viral load was determined by RT-qPCR and host gene expression was determined by digital PCR in kidney, spleen, heart, and gill. Select spleen samples were also used for RNA sequencing (RNA-seq) transcriptomics.
RESULTS: The most resistant (N = 12) and susceptible (N = 13) families had a mean cumulative mortality of 34.3% and 78.5%, respectively. Selective breeding for growth and sea lice resistance (30 families) did not notably impact ISA resistance relative to randomly mated control families (10 families). However, ISA and ISAV resistance were not synonymous-phenotypic ISA-resistant and -susceptible fish were similarly burdened with virus in all organs screened. Gene expression and RNA-seq data identified early viral recognition, particularly in the kidney, as a marker for ISA resistance.
CONCLUSIONS: Selective breeding for enhanced growth and sea lice resistance did not appear to incidentally impact family-wise resistance to ISA. Phenotypic ISA resistance was at least partially linked to differential gene expression patterns in the kidney, highlighting early upregulation of antiviral, inflammatory, and endothelial growth factors of resistant fish. However, disease (ISA) resistance was not associated with reduced ISAV transcripts, which showed prolonged high loads in the spleen of all families during infection. These data support early recognition of ISAV in kidney as important in disease mitigation, even when ISAV replication is systemic.
METHODS: Forty families of North American Atlantic salmon were challenged with ISAV to determine family-wise survival, with fish from each family distributed across 16 tanks (one fish per family per tank) and exposed via injection (n = 4 per family) or cohabitation (n = 12 per family). Four additional tanks (one fish/family/tank) were sampled at either early-onset (11 days post challenge), peak mortality (21 and 35 days post challenge), or resolution (49 days post challenge) phases of disease. Viral load was determined by RT-qPCR and host gene expression was determined by digital PCR in kidney, spleen, heart, and gill. Select spleen samples were also used for RNA sequencing (RNA-seq) transcriptomics.
RESULTS: The most resistant (N = 12) and susceptible (N = 13) families had a mean cumulative mortality of 34.3% and 78.5%, respectively. Selective breeding for growth and sea lice resistance (30 families) did not notably impact ISA resistance relative to randomly mated control families (10 families). However, ISA and ISAV resistance were not synonymous-phenotypic ISA-resistant and -susceptible fish were similarly burdened with virus in all organs screened. Gene expression and RNA-seq data identified early viral recognition, particularly in the kidney, as a marker for ISA resistance.
CONCLUSIONS: Selective breeding for enhanced growth and sea lice resistance did not appear to incidentally impact family-wise resistance to ISA. Phenotypic ISA resistance was at least partially linked to differential gene expression patterns in the kidney, highlighting early upregulation of antiviral, inflammatory, and endothelial growth factors of resistant fish. However, disease (ISA) resistance was not associated with reduced ISAV transcripts, which showed prolonged high loads in the spleen of all families during infection. These data support early recognition of ISAV in kidney as important in disease mitigation, even when ISAV replication is systemic.