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H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks
Infection with H5N1 influenza virus is often fatal to poultry with death occurring in hours rather than days. However, whilst chickens may be acutely susceptible, ducks appear to be asymptomatic to H5N1. The mechanisms of disease pathogenesis are not well understood and the variation between differe...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Published by Elsevier B.V.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127704/ https://www.ncbi.nlm.nih.gov/pubmed/24657784 http://dx.doi.org/10.1016/j.virusres.2014.03.012 |
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author | Burggraaf, Simon Karpala, Adam J. Bingham, John Lowther, Sue Selleck, Paul Kimpton, Wayne Bean, Andrew G.D. |
author_facet | Burggraaf, Simon Karpala, Adam J. Bingham, John Lowther, Sue Selleck, Paul Kimpton, Wayne Bean, Andrew G.D. |
author_sort | Burggraaf, Simon |
collection | PubMed |
description | Infection with H5N1 influenza virus is often fatal to poultry with death occurring in hours rather than days. However, whilst chickens may be acutely susceptible, ducks appear to be asymptomatic to H5N1. The mechanisms of disease pathogenesis are not well understood and the variation between different species requires investigation to help explain these species differences. Here we investigated the expression of several key proinflammatory cytokines of chickens and ducks following infection with 2 highly pathogenic H5N1 (A/Muscovy duck/Vietnam/453/2004 (Vt453) and A/Duck/Indramayu/BBVW/109/2006 (Ind109)) and a low-pathogenic H5N3 influenza virus (A/Duck/Victoria/1462/2008 (Vc1462)). H5N1 viruses caused fatal infections in chickens as well as high viral loads and increased production of proinflammatory molecules when compared to ducks. Cytokines, including Interleukin 6 (IL6) and the acute phase protein Serum Amyloid A (SAA), were rapidly induced at 24 h post infection with H5N1. In contrast, low induction of these cytokines appeared in ducks and only at later times during the infection period. These observations support that hypercytokinemia may contribute to pathogenesis in chickens, whilst the lower cytokine response in ducks may be a factor in their apparent resistance to disease and decreased mortality. |
format | Online Article Text |
id | pubmed-7127704 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Published by Elsevier B.V. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71277042020-04-08 H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks Burggraaf, Simon Karpala, Adam J. Bingham, John Lowther, Sue Selleck, Paul Kimpton, Wayne Bean, Andrew G.D. Virus Res Article Infection with H5N1 influenza virus is often fatal to poultry with death occurring in hours rather than days. However, whilst chickens may be acutely susceptible, ducks appear to be asymptomatic to H5N1. The mechanisms of disease pathogenesis are not well understood and the variation between different species requires investigation to help explain these species differences. Here we investigated the expression of several key proinflammatory cytokines of chickens and ducks following infection with 2 highly pathogenic H5N1 (A/Muscovy duck/Vietnam/453/2004 (Vt453) and A/Duck/Indramayu/BBVW/109/2006 (Ind109)) and a low-pathogenic H5N3 influenza virus (A/Duck/Victoria/1462/2008 (Vc1462)). H5N1 viruses caused fatal infections in chickens as well as high viral loads and increased production of proinflammatory molecules when compared to ducks. Cytokines, including Interleukin 6 (IL6) and the acute phase protein Serum Amyloid A (SAA), were rapidly induced at 24 h post infection with H5N1. In contrast, low induction of these cytokines appeared in ducks and only at later times during the infection period. These observations support that hypercytokinemia may contribute to pathogenesis in chickens, whilst the lower cytokine response in ducks may be a factor in their apparent resistance to disease and decreased mortality. Published by Elsevier B.V. 2014-06-24 2014-03-19 /pmc/articles/PMC7127704/ /pubmed/24657784 http://dx.doi.org/10.1016/j.virusres.2014.03.012 Text en Crown copyright © 2014 Published by Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Burggraaf, Simon Karpala, Adam J. Bingham, John Lowther, Sue Selleck, Paul Kimpton, Wayne Bean, Andrew G.D. H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
title | H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
title_full | H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
title_fullStr | H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
title_full_unstemmed | H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
title_short | H5N1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
title_sort | h5n1 infection causes rapid mortality and high cytokine levels in chickens compared to ducks |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127704/ https://www.ncbi.nlm.nih.gov/pubmed/24657784 http://dx.doi.org/10.1016/j.virusres.2014.03.012 |
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