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Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility

BACKGROUND: The world has recently overcome the first influenza pandemic of the 21st century caused by a novel H1N1 virus (pH1N1) which is a triple reassortant comprising genes derived from avian, human, and swine influenza viruses and antigenically quite different from seasonal H1N1 strains. Althou...

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Autores principales: Mukherjee, Sanjay, Vipat, Veena C, Mishra, Akhilesh C, Pawar, Shailesh D, Chakrabarti, Alok K
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076257/
https://www.ncbi.nlm.nih.gov/pubmed/21439068
http://dx.doi.org/10.1186/1743-422X-8-140
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author Mukherjee, Sanjay
Vipat, Veena C
Mishra, Akhilesh C
Pawar, Shailesh D
Chakrabarti, Alok K
author_facet Mukherjee, Sanjay
Vipat, Veena C
Mishra, Akhilesh C
Pawar, Shailesh D
Chakrabarti, Alok K
author_sort Mukherjee, Sanjay
collection PubMed
description BACKGROUND: The world has recently overcome the first influenza pandemic of the 21st century caused by a novel H1N1 virus (pH1N1) which is a triple reassortant comprising genes derived from avian, human, and swine influenza viruses and antigenically quite different from seasonal H1N1 strains. Although the case fatality rates have decreased in many developed countries, the situation is still alarming in many developing countries including India where considerable numbers of new cases are appearing everyday. There is still a high morbidity and mortality of susceptible adult as well as young population without having underlying health issues due to the influenza infection. RESULTS: To achieve a better understanding of the risk posed by the pH1N1 and to understand its pathogenicity, we studied the host gene expression response to Indian isolate of pH1N1 infection and compared it with seasonal H1N1 infection. The response was studied at four different time points (4, 8, 16 and 24 h) post infection (hpi) in A549 cells using microarray platform. We found that pH1N1 induces immune response earlier than seasonal H1N1 viruses, but at the later stages of infection there is a suppression of host immune responses. The infection with pH1N1 resulted in considerable decrease in the expression of cytokine and other immune genes namely IL8, STAT1, B2 M and IL4 compared to seasonal H1N1. CONCLUSION: We propose that the inability to induce strong innate immune response could be a reason for the high transmissibility, pathogenicity and mortality caused by pH1N1 virus.
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spelling pubmed-30762572011-04-14 Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility Mukherjee, Sanjay Vipat, Veena C Mishra, Akhilesh C Pawar, Shailesh D Chakrabarti, Alok K Virol J Research BACKGROUND: The world has recently overcome the first influenza pandemic of the 21st century caused by a novel H1N1 virus (pH1N1) which is a triple reassortant comprising genes derived from avian, human, and swine influenza viruses and antigenically quite different from seasonal H1N1 strains. Although the case fatality rates have decreased in many developed countries, the situation is still alarming in many developing countries including India where considerable numbers of new cases are appearing everyday. There is still a high morbidity and mortality of susceptible adult as well as young population without having underlying health issues due to the influenza infection. RESULTS: To achieve a better understanding of the risk posed by the pH1N1 and to understand its pathogenicity, we studied the host gene expression response to Indian isolate of pH1N1 infection and compared it with seasonal H1N1 infection. The response was studied at four different time points (4, 8, 16 and 24 h) post infection (hpi) in A549 cells using microarray platform. We found that pH1N1 induces immune response earlier than seasonal H1N1 viruses, but at the later stages of infection there is a suppression of host immune responses. The infection with pH1N1 resulted in considerable decrease in the expression of cytokine and other immune genes namely IL8, STAT1, B2 M and IL4 compared to seasonal H1N1. CONCLUSION: We propose that the inability to induce strong innate immune response could be a reason for the high transmissibility, pathogenicity and mortality caused by pH1N1 virus. BioMed Central 2011-03-25 /pmc/articles/PMC3076257/ /pubmed/21439068 http://dx.doi.org/10.1186/1743-422X-8-140 Text en Copyright ©2011 Mukherjee 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
Mukherjee, Sanjay
Vipat, Veena C
Mishra, Akhilesh C
Pawar, Shailesh D
Chakrabarti, Alok K
Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
title Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
title_full Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
title_fullStr Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
title_full_unstemmed Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
title_short Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
title_sort pandemic (h1n1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076257/
https://www.ncbi.nlm.nih.gov/pubmed/21439068
http://dx.doi.org/10.1186/1743-422X-8-140
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