title: Histology, immunocytochemistry and qRT-PCR analysis of Atlantic salmon, Salmo salar L., post-smolts following infection with infectious pancreatic necrosis virus (IPNV).
abstract: Infectious pancreatic necrosis (IPN) is a very serious viral disease in terms of its impact on production of Atlantic salmon, Salmo salar L., fry and post-smolts. Post-smolts of Atlantic salmon were injected with infectious pancreatic necrosis virus (IPNV) and cohabited with naive fish to produce natural infection. Cohabitant fish were sampled every 2 days, up to day 36 post-infection (p.i.). From 90 cohabitant fish, 11 (12.2%) were positive by immunohistochemistry (IHC). The first detection of IPNV by IHC occurred on day 16 p.i. which coincided with the onset of mortality in this group. Besides the pancreas, the liver was found to be a key target organ for IPNV. For the first time, the virus was observed in the islets of Langerhans and in the kidney corpuscles of Stannius which suggests that the virus could affect the fish's metabolism. The liver of two fish, which showed the most widespread presence of IPNV by IHC, had a pathology including focal necrosis and widespread presence of apoptotic hepatocytes, many of which did not stain for virus by IHC. Up-regulation of cytokine gene expression was found only in the IHC-positive (IHC+ve) fish and reflected the level of infection as determined by IHC positivity of the liver. In most fish, interferon (IFN), Mx, γIFN and γIP were up-regulated in liver and kidney, while only IFN and Mx were up-regulated in gill. IL1β and TNFα were not induced in any tissue. The gill showed variable levels of constitutive expression of IL1β and γIFN. The two fish with liver pathology had the highest level of IFN expression, especially relative to the level of Mx expression, in the liver compared with the other IHC+ve fish which did not have a liver pathology. The results suggest that following widespread infection of hepatocytes, the cells may over-produce IFN, resulting in apoptosis of neighbouring cells with subsequent death from liver failure.
authors.affiliation: Marine Scotland, Marine Laboratory, Aberdeen, Scotland, UK.
authors.forename: A E
authors.initials: AE
authors.lastname: Ellis
authors.forename: A
authors.initials: A
authors.lastname: Cavaco
authors.forename: A
authors.initials: A
authors.lastname: Petrie
authors.forename: K
authors.initials: K
authors.lastname: Lockhart
authors.forename: M
authors.initials: M
authors.lastname: Snow
authors.forename: B
authors.initials: B
authors.lastname: Collet
mesh_terms: D000818:Animals; D018175:Birnaviridae Infections / Q000473:pathology / Q000662:veterinary*; D016207:Cytokines / Q000378:metabolism; D005393:Fish Diseases / Q000473:pathology* / Q000821:virology*; D005880:Gills / Q000378:metabolism; D006653:Histology; D007150:Immunohistochemistry / Q000662:veterinary; D018061:Infectious pancreatic necrosis virus; D008099:Liver / Q000473:pathology / Q000821:virology; D010179:Pancreas / Q000473:pathology / Q000821:virology; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D020317:Salmo salar
chemical_list: D016207:Cytokines