Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
Identifieur interne : 001003 ( Ncbi/Merge ); précédent : 001002; suivant : 001004Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility
Auteurs : Sanjay Mukherjee [Inde] ; Veena C. Vipat [Inde] ; Akhilesh C. Mishra [Inde] ; Shailesh D. Pawar [Inde] ; Alok K. Chakrabarti [Inde]Source :
- Virology Journal [ 1743-422X ] ; 2011.
Descripteurs français
- KwdFr :
- Grippe humaine (génétique), Grippe humaine (immunologie), Grippe humaine (transmission), Grippe humaine (épidémiologie), Humains, Immunité innée, Inde (épidémiologie), Lignée cellulaire, Pandémies, Régulation de l'expression des gènes, Régulation de l'expression des gènes viraux, Sous-type H1N1 du virus de la grippe A (génétique), Sous-type H1N1 du virus de la grippe A (immunologie).
- MESH :
- génétique : Grippe humaine, Sous-type H1N1 du virus de la grippe A.
- immunologie : Grippe humaine, Sous-type H1N1 du virus de la grippe A.
- épidémiologie : Grippe humaine, Inde.
- Humains, Immunité innée, Lignée cellulaire, Pandémies, Régulation de l'expression des gènes, Régulation de l'expression des gènes viraux.
- Wicri :
- geographic : Inde.
English descriptors
- KwdEn :
- Cell Line, Gene Expression Regulation, Gene Expression Regulation, Viral, Humans, Immunity, Innate, India (epidemiology), Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (immunology), Influenza, Human (epidemiology), Influenza, Human (genetics), Influenza, Human (immunology), Influenza, Human (transmission), Pandemics.
- MESH :
- geographic , epidemiology : India.
- epidemiology : Influenza, Human.
- genetics : Influenza A Virus, H1N1 Subtype, Influenza, Human.
- immunology : Influenza A Virus, H1N1 Subtype, Influenza, Human.
- transmission : Influenza, Human.
- Cell Line, Gene Expression Regulation, Gene Expression Regulation, Viral, Humans, Immunity, Innate, Pandemics.
Abstract
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.
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.
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.
Url:
DOI: 10.1186/1743-422X-8-140
PubMed: 21439068
PubMed Central: 3076257
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PMC:3076257Le document en format XML
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<series><title level="j">Virology Journal</title>
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<term>Gene Expression Regulation</term>
<term>Gene Expression Regulation, Viral</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>India (epidemiology)</term>
<term>Influenza A Virus, H1N1 Subtype (genetics)</term>
<term>Influenza A Virus, H1N1 Subtype (immunology)</term>
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<term>Influenza, Human (immunology)</term>
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<term>Pandemics</term>
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<term>Grippe humaine (immunologie)</term>
<term>Grippe humaine (transmission)</term>
<term>Grippe humaine (épidémiologie)</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Inde (épidémiologie)</term>
<term>Lignée cellulaire</term>
<term>Pandémies</term>
<term>Régulation de l'expression des gènes</term>
<term>Régulation de l'expression des gènes viraux</term>
<term>Sous-type H1N1 du virus de la grippe A (génétique)</term>
<term>Sous-type H1N1 du virus de la grippe A (immunologie)</term>
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<keywords scheme="MESH" type="geographic" qualifier="epidemiology" xml:lang="en"><term>India</term>
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<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Influenza, Human</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza, Human</term>
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<term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Grippe humaine</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza, Human</term>
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<term>Gene Expression Regulation, Viral</term>
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<term>Lignée cellulaire</term>
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<term>Régulation de l'expression des gènes</term>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>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.</p>
</sec>
<sec><title>Results</title>
<p>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.</p>
</sec>
<sec><title>Conclusion</title>
<p>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.</p>
</sec>
</div>
</front>
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<series><title level="j">Virology Journal</title>
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</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>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.</p>
</sec>
<sec><title>Results</title>
<p>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.</p>
</sec>
<sec><title>Conclusion</title>
<p>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.</p>
</sec>
</div>
</front>
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<pubmed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pandemic (H1N1) 2009 influenza virus induces weaker host immune responses in vitro: a possible mechanism of high transmissibility.</title>
<author><name sortKey="Mukherjee, Sanjay" sort="Mukherjee, Sanjay" uniqKey="Mukherjee S" first="Sanjay" last="Mukherjee">Sanjay Mukherjee</name>
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<country xml:lang="fr">Inde</country>
<wicri:regionArea>Microbial Containment Complex, National Institute of Virology, Sus Road, Pashan, Pune 411021</wicri:regionArea>
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<author><name sortKey="Vipat, Veena C" sort="Vipat, Veena C" uniqKey="Vipat V" first="Veena C" last="Vipat">Veena C. Vipat</name>
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<author><name sortKey="Mishra, Akhilesh C" sort="Mishra, Akhilesh C" uniqKey="Mishra A" first="Akhilesh C" last="Mishra">Akhilesh C. Mishra</name>
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<author><name sortKey="Pawar, Shailesh D" sort="Pawar, Shailesh D" uniqKey="Pawar S" first="Shailesh D" last="Pawar">Shailesh D. Pawar</name>
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<author><name sortKey="Chakrabarti, Alok K" sort="Chakrabarti, Alok K" uniqKey="Chakrabarti A" first="Alok K" last="Chakrabarti">Alok K. Chakrabarti</name>
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<author><name sortKey="Vipat, Veena C" sort="Vipat, Veena C" uniqKey="Vipat V" first="Veena C" last="Vipat">Veena C. Vipat</name>
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<author><name sortKey="Mishra, Akhilesh C" sort="Mishra, Akhilesh C" uniqKey="Mishra A" first="Akhilesh C" last="Mishra">Akhilesh C. Mishra</name>
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<author><name sortKey="Pawar, Shailesh D" sort="Pawar, Shailesh D" uniqKey="Pawar S" first="Shailesh D" last="Pawar">Shailesh D. Pawar</name>
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<author><name sortKey="Chakrabarti, Alok K" sort="Chakrabarti, Alok K" uniqKey="Chakrabarti A" first="Alok K" last="Chakrabarti">Alok K. Chakrabarti</name>
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<term>Gene Expression Regulation</term>
<term>Gene Expression Regulation, Viral</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>India (epidemiology)</term>
<term>Influenza A Virus, H1N1 Subtype (genetics)</term>
<term>Influenza A Virus, H1N1 Subtype (immunology)</term>
<term>Influenza, Human (epidemiology)</term>
<term>Influenza, Human (genetics)</term>
<term>Influenza, Human (immunology)</term>
<term>Influenza, Human (transmission)</term>
<term>Pandemics</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Grippe humaine (génétique)</term>
<term>Grippe humaine (immunologie)</term>
<term>Grippe humaine (transmission)</term>
<term>Grippe humaine (épidémiologie)</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Inde (épidémiologie)</term>
<term>Lignée cellulaire</term>
<term>Pandémies</term>
<term>Régulation de l'expression des gènes</term>
<term>Régulation de l'expression des gènes viraux</term>
<term>Sous-type H1N1 du virus de la grippe A (génétique)</term>
<term>Sous-type H1N1 du virus de la grippe A (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="geographic" qualifier="epidemiology" xml:lang="en"><term>India</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Grippe humaine</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Grippe humaine</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="transmission" xml:lang="en"><term>Influenza, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>Grippe humaine</term>
<term>Inde</term>
</keywords>
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<term>Gene Expression Regulation</term>
<term>Gene Expression Regulation, Viral</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Pandemics</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Immunité innée</term>
<term>Lignée cellulaire</term>
<term>Pandémies</term>
<term>Régulation de l'expression des gènes</term>
<term>Régulation de l'expression des gènes viraux</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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