Studies on uptake and intracellular processing of infectious pancreatic necrosis virus by Atlantic cod scavenger endothelial cells

Abstract Previous work in our group has identified the scavenger endothelial cells (SECs) of heart endocardium in cod, Gadus morhua L., as the major site for elimination of both physiological and foreign macromolecular waste from the circulation. The present study was undertaken to establish the rol...

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Bibliographic Details
Published in:Journal of Fish Diseases
Main Authors: Martin‐Armas, M, Sommer, A‐I, Smedsrød, B
Format: Article in Journal/Newspaper
Language:English
Published: Wiley 2007
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Online Access:http://dx.doi.org/10.1111/j.1365-2761.2007.00857.x
https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-2761.2007.00857.x
https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2761.2007.00857.x
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Summary:Abstract Previous work in our group has identified the scavenger endothelial cells (SECs) of heart endocardium in cod, Gadus morhua L., as the major site for elimination of both physiological and foreign macromolecular waste from the circulation. The present study was undertaken to establish the role of cod SECs in the clearance of virus. We focused on infectious pancreatic necrosis virus (IPNV) as it is a well‐known virus with a broad host range, and causes significant economic losses in the salmon industry. Our results showed that cod SEC cultures infected by the IPNV produce high titres of new virus. Ligand‐receptor inhibition experiments suggested that the virus did not enter the cells through any of the major endocytosis receptors of cod SECs. Yet, the infection lowered the capacity of the cells to endocytose ligands via the scavenger receptor. Inhibitors of receptor recycling and vesicle acidification did not affect virus infectivity. The finding that SEC cultures prepared from 25% of the cod produced high titres of IPNV without being infected in the laboratory, suggests that SECs of cod may serve as reservoirs for IPNV in persistently infected cod.