Abstract
BackgroundInfectious Pancreatic Necrosis (IPN) is a highly contagious birnavirus disease of farmed salmonid fish, which often causes high levels of morbidity and mortality. A large host genetic component to resistance has been previously described for Atlantic salmon (Salmo salar L.), which mediates high mortality rates in some families and zero mortality in others. However, the molecular and immunological basis for this resistance is not yet fully known. This manuscript describes a global comparison of the gene expression profiles of resistant and susceptible Atlantic salmon fry following challenge with the IPN virus.ResultsSalmon fry from two IPNV-resistant and two IPNV-susceptible full sibling families were challenged with the virus and sampled at 1 day, 7 days and 20 days post-challenge. Significant viral titre was observed in both resistant and susceptible fish at all timepoints, although generally at higher levels in susceptible fish. Gene expression profiles combined with gene ontology and pathway analyses demonstrated that while a clear immune response was observed in both resistant and susceptible fish, there were striking differences between the two phenotypes. The susceptible fish showed marked up-regulation of genes related to cytokine activity and inflammatory response that evidently failed to protect against the virus. In contrast, the resistant fish demonstrated a less pronounced immune response including up-regulation of genes relating to the M2 macrophage system.ConclusionsWhile only the susceptible phenotype shows appreciable mortality levels, both resistant and susceptible fish can become infected with IPNV. Susceptible fish are characterized by a much larger, yet ineffective, immune response, largely related to cytokine and inflammatory systems. Resistant fish demonstrate a more moderate, putative macrophage-mediated inflammatory response, which may contribute to their survival.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2600-y) contains supplementary material, which is available to authorized users.
Highlights
Infectious Pancreatic Necrosis (IPN) is a highly contagious birnavirus disease of farmed salmonid fish, which often causes high levels of morbidity and mortality
Moen et al [11] discovered SNPs associated with the putative quantitative trait locus (QTL) genotype (r2 0.57 – 0.58) in the cadherin-1 gene (CDH1) gene which encodes a protein that co-locates with the IPN virus in liver cells and can bind to the IPN virus in vitro. These results suggest a possible role for CDH1 in the entry of the virus to host cells and that a non-synonymous SNP in the CDH1 gene may form part of the underlying mechanism of the QTL
Infectious pancreatic necrosis virus (IPNV) immersion challenges for the gene expression study commenced immediately after these initial challenge experiments, using full siblings of the fry used in the mortality study
Summary
Infectious Pancreatic Necrosis (IPN) is a highly contagious birnavirus disease of farmed salmonid fish, which often causes high levels of morbidity and mortality. Infectious pancreatic necrosis virus (IPNV) is a pathogen of salmonid fish which can cause high mortality and morbidity of cultured Atlantic salmon (Salmo salar L.) and rainbow trout (Oncorhynchus mykiss) and is responsible for serious economic losses to the aquaculture industry. Vaccination can be used to protect post-smolt fish [2], but the control of freshwater outbreaks is dependent upon biosecurity in hatcheries and the level of innate resistance of the salmon fry. In this freshwater fry phase of the salmon life cycle, IPN outbreaks can result in near-complete population losses [1]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
