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Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1

Aquatic birds are the natural reservoir for most subtypes of influenza A, and a source of novel viruses with the potential to cause human pandemics, fatal zoonotic disease or devastating epizootics in poultry. It is well recognised that waterfowl typically show few clinical signs following influenza...

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Autores principales: Kuchipudi, Suresh V, Dunham, Stephen P, Nelli, Rahul, White, Gavin A, Coward, Vivien J, Slomka, Marek J, Brown, Ian H, Chang, Kin Chow
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257048/
https://www.ncbi.nlm.nih.gov/pubmed/21423263
http://dx.doi.org/10.1038/icb.2011.17
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author Kuchipudi, Suresh V
Dunham, Stephen P
Nelli, Rahul
White, Gavin A
Coward, Vivien J
Slomka, Marek J
Brown, Ian H
Chang, Kin Chow
author_facet Kuchipudi, Suresh V
Dunham, Stephen P
Nelli, Rahul
White, Gavin A
Coward, Vivien J
Slomka, Marek J
Brown, Ian H
Chang, Kin Chow
author_sort Kuchipudi, Suresh V
collection PubMed
description Aquatic birds are the natural reservoir for most subtypes of influenza A, and a source of novel viruses with the potential to cause human pandemics, fatal zoonotic disease or devastating epizootics in poultry. It is well recognised that waterfowl typically show few clinical signs following influenza A infection, in contrast, terrestrial poultry such as chickens may develop severe disease with rapid death following infection with highly pathogenic avian influenza. This study examined the cellular response to influenza infection in primary cells derived from resistant (duck) and susceptible (chicken) avian hosts. Paradoxically, we observed that duck cells underwent rapid cell death following infection with low pathogenic avian H2N3, classical swine H1N1 and ‘classical' highly pathogenic H5N1 viruses. Dying cells showed morphological features of apoptosis, increased DNA fragmentation and activation of caspase 3/7. Following infection of chicken cells, cell death occurred less rapidly, accompanied by reduced DNA fragmentation and caspase activation. Duck cells produced similar levels of viral RNA but less infectious virus, in comparison with chicken cells. Such rapid cell death was not observed in duck cells infected with a contemporary Eurasian lineage H5N1 fatal to ducks. The induction of rapid death in duck cells may be part of a mechanism of host resistance to influenza A, with the loss of this response leading to increased susceptibility to emergent strains of H5N1. These studies provide novel insights that should help resolve the long-standing enigma of host–pathogen relationships for highly pathogenic and zoonotic avian influenza.
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spelling pubmed-32570482012-01-12 Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1 Kuchipudi, Suresh V Dunham, Stephen P Nelli, Rahul White, Gavin A Coward, Vivien J Slomka, Marek J Brown, Ian H Chang, Kin Chow Immunol Cell Biol Original Article Aquatic birds are the natural reservoir for most subtypes of influenza A, and a source of novel viruses with the potential to cause human pandemics, fatal zoonotic disease or devastating epizootics in poultry. It is well recognised that waterfowl typically show few clinical signs following influenza A infection, in contrast, terrestrial poultry such as chickens may develop severe disease with rapid death following infection with highly pathogenic avian influenza. This study examined the cellular response to influenza infection in primary cells derived from resistant (duck) and susceptible (chicken) avian hosts. Paradoxically, we observed that duck cells underwent rapid cell death following infection with low pathogenic avian H2N3, classical swine H1N1 and ‘classical' highly pathogenic H5N1 viruses. Dying cells showed morphological features of apoptosis, increased DNA fragmentation and activation of caspase 3/7. Following infection of chicken cells, cell death occurred less rapidly, accompanied by reduced DNA fragmentation and caspase activation. Duck cells produced similar levels of viral RNA but less infectious virus, in comparison with chicken cells. Such rapid cell death was not observed in duck cells infected with a contemporary Eurasian lineage H5N1 fatal to ducks. The induction of rapid death in duck cells may be part of a mechanism of host resistance to influenza A, with the loss of this response leading to increased susceptibility to emergent strains of H5N1. These studies provide novel insights that should help resolve the long-standing enigma of host–pathogen relationships for highly pathogenic and zoonotic avian influenza. Nature Publishing Group 2012-01 2011-03-22 /pmc/articles/PMC3257048/ /pubmed/21423263 http://dx.doi.org/10.1038/icb.2011.17 Text en Copyright © 2012 Australasian Society for Immunology Inc. http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Original Article
Kuchipudi, Suresh V
Dunham, Stephen P
Nelli, Rahul
White, Gavin A
Coward, Vivien J
Slomka, Marek J
Brown, Ian H
Chang, Kin Chow
Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1
title Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1
title_full Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1
title_fullStr Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1
title_full_unstemmed Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1
title_short Rapid death of duck cells infected with influenza: a potential mechanism for host resistance to H5N1
title_sort rapid death of duck cells infected with influenza: a potential mechanism for host resistance to h5n1
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257048/
https://www.ncbi.nlm.nih.gov/pubmed/21423263
http://dx.doi.org/10.1038/icb.2011.17
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