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Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight
Salmonid alphavirus (SAV) is an enveloped, single-stranded, positive sense RNA virus belonging to the family Togaviridae. It causes economically devastating disease in cultured salmonids. The characteristic features of SAV infection include severe histopathological changes in the heart, pancreas and...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705579/ https://www.ncbi.nlm.nih.gov/pubmed/26743442 http://dx.doi.org/10.1186/s13567-015-0300-2 |
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author | Herath, Tharangani K. Ferguson, Hugh W. Weidmann, Manfred W. Bron, James E. Thompson, Kimberly D. Adams, Alexandra Muir, Katherine F. Richards, Randolph H. |
author_facet | Herath, Tharangani K. Ferguson, Hugh W. Weidmann, Manfred W. Bron, James E. Thompson, Kimberly D. Adams, Alexandra Muir, Katherine F. Richards, Randolph H. |
author_sort | Herath, Tharangani K. |
collection | PubMed |
description | Salmonid alphavirus (SAV) is an enveloped, single-stranded, positive sense RNA virus belonging to the family Togaviridae. It causes economically devastating disease in cultured salmonids. The characteristic features of SAV infection include severe histopathological changes in the heart, pancreas and skeletal muscles of diseased fish. Although the presence of virus has been reported in a wider range of tissues, the mechanisms responsible for viral tissue tropism and for lesion development during the disease are not clearly described or understood. Previously, we have described membrane-dependent morphogenesis of SAV and associated apoptosis-mediated cell death in vitro. The aims of the present study were to explore ultrastructural changes associated with SAV infection in vivo. Cytolytic changes were observed in heart, but not in gill and head-kidney of virus-infected fish, although they still exhibited signs of SAV morphogenesis. Ultrastructural changes associated with virus replication were also noted in leukocytes in the head kidney of virus-infected fish. These results further describe the presence of degenerative lesions in the heart as expected, but not in the gills and in the kidney. |
format | Online Article Text |
id | pubmed-4705579 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-47055792016-01-09 Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight Herath, Tharangani K. Ferguson, Hugh W. Weidmann, Manfred W. Bron, James E. Thompson, Kimberly D. Adams, Alexandra Muir, Katherine F. Richards, Randolph H. Vet Res Research Article Salmonid alphavirus (SAV) is an enveloped, single-stranded, positive sense RNA virus belonging to the family Togaviridae. It causes economically devastating disease in cultured salmonids. The characteristic features of SAV infection include severe histopathological changes in the heart, pancreas and skeletal muscles of diseased fish. Although the presence of virus has been reported in a wider range of tissues, the mechanisms responsible for viral tissue tropism and for lesion development during the disease are not clearly described or understood. Previously, we have described membrane-dependent morphogenesis of SAV and associated apoptosis-mediated cell death in vitro. The aims of the present study were to explore ultrastructural changes associated with SAV infection in vivo. Cytolytic changes were observed in heart, but not in gill and head-kidney of virus-infected fish, although they still exhibited signs of SAV morphogenesis. Ultrastructural changes associated with virus replication were also noted in leukocytes in the head kidney of virus-infected fish. These results further describe the presence of degenerative lesions in the heart as expected, but not in the gills and in the kidney. BioMed Central 2016-01-08 2016 /pmc/articles/PMC4705579/ /pubmed/26743442 http://dx.doi.org/10.1186/s13567-015-0300-2 Text en © Herath et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Herath, Tharangani K. Ferguson, Hugh W. Weidmann, Manfred W. Bron, James E. Thompson, Kimberly D. Adams, Alexandra Muir, Katherine F. Richards, Randolph H. Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
title | Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
title_full | Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
title_fullStr | Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
title_full_unstemmed | Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
title_short | Pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
title_sort | pathogenesis of experimental salmonid alphavirus infection in vivo: an ultrastructural insight |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705579/ https://www.ncbi.nlm.nih.gov/pubmed/26743442 http://dx.doi.org/10.1186/s13567-015-0300-2 |
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