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Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields
BACKGROUND: Massive mortalities have been observed in France since 2008 on spat and juvenile Pacific oysters, Crassostrea gigas. A herpes virus called OsHV-1, easily detectable by PCR, has been implicated in the mortalities as demonstrated by the results of numerous field studies linking mortality w...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766697/ https://www.ncbi.nlm.nih.gov/pubmed/23987141 http://dx.doi.org/10.1186/1471-2164-14-590 |
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author | Jouaux, Aude Lafont, Maxime Blin, Jean-Louis Houssin, Maryline Mathieu, Michel Lelong, Christophe |
author_facet | Jouaux, Aude Lafont, Maxime Blin, Jean-Louis Houssin, Maryline Mathieu, Michel Lelong, Christophe |
author_sort | Jouaux, Aude |
collection | PubMed |
description | BACKGROUND: Massive mortalities have been observed in France since 2008 on spat and juvenile Pacific oysters, Crassostrea gigas. A herpes virus called OsHV-1, easily detectable by PCR, has been implicated in the mortalities as demonstrated by the results of numerous field studies linking mortality with OsHV-1 prevalence. Moreover, experimental infections using viral particles have documented the pathogenicity of OsHV-1 but the physiological responses of host to pathogen are not well known. RESULTS: The aim of this study was to understand mechanisms brought into play against the virus during infection in the field. A microarray assay has been developed for a major part of the oyster genome and used for studying the host transcriptome across mortality on field. Spat with and without detectable OsHV-1 infection presenting or not mortality respectively were compared by microarray during mortality episodes. In this study, a number of genes are regulated in the response to pathogen infection on field and seems to argue to an implication of the virus in the observed mortality. The result allowed establishment of a hypothetic scheme of the host cell’s infection by, and response to, the pathogen. CONCLUSIONS: This response shows a “sensu stricto” innate immunity through genic regulation of the virus OsHV-1 life cycle, but also others biological processes resulting to complex interactions between host and pathogens in general. |
format | Online Article Text |
id | pubmed-3766697 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-37666972013-09-09 Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields Jouaux, Aude Lafont, Maxime Blin, Jean-Louis Houssin, Maryline Mathieu, Michel Lelong, Christophe BMC Genomics Research Article BACKGROUND: Massive mortalities have been observed in France since 2008 on spat and juvenile Pacific oysters, Crassostrea gigas. A herpes virus called OsHV-1, easily detectable by PCR, has been implicated in the mortalities as demonstrated by the results of numerous field studies linking mortality with OsHV-1 prevalence. Moreover, experimental infections using viral particles have documented the pathogenicity of OsHV-1 but the physiological responses of host to pathogen are not well known. RESULTS: The aim of this study was to understand mechanisms brought into play against the virus during infection in the field. A microarray assay has been developed for a major part of the oyster genome and used for studying the host transcriptome across mortality on field. Spat with and without detectable OsHV-1 infection presenting or not mortality respectively were compared by microarray during mortality episodes. In this study, a number of genes are regulated in the response to pathogen infection on field and seems to argue to an implication of the virus in the observed mortality. The result allowed establishment of a hypothetic scheme of the host cell’s infection by, and response to, the pathogen. CONCLUSIONS: This response shows a “sensu stricto” innate immunity through genic regulation of the virus OsHV-1 life cycle, but also others biological processes resulting to complex interactions between host and pathogens in general. BioMed Central 2013-08-29 /pmc/articles/PMC3766697/ /pubmed/23987141 http://dx.doi.org/10.1186/1471-2164-14-590 Text en Copyright © 2013 Jouaux et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Jouaux, Aude Lafont, Maxime Blin, Jean-Louis Houssin, Maryline Mathieu, Michel Lelong, Christophe Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields |
title | Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields |
title_full | Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields |
title_fullStr | Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields |
title_full_unstemmed | Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields |
title_short | Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields |
title_sort | physiological change under oshv-1 contamination in pacific oyster crassostrea gigas through massive mortality events on fields |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766697/ https://www.ncbi.nlm.nih.gov/pubmed/23987141 http://dx.doi.org/10.1186/1471-2164-14-590 |
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