Why Do Influenza Virus Subtypes Die Out? A Hypothesis
Identifieur interne : 000683 ( Ncbi/Merge ); précédent : 000682; suivant : 000684Why Do Influenza Virus Subtypes Die Out? A Hypothesis
Auteurs : Peter Palese ; Taia T. WangSource :
- mBio [ 2150-7511 ] ; 2011.
Abstract
Novel pandemic influenza viruses enter the human population with some regularity and can cause disease that is severe and widespread. The emergence of novel viruses, historically, has often been coupled with the disappearance of existing seasonal virus strains. Here, we propose that the elimination of seasonal strains during virus pandemics is a process mediated, at the population level, by humoral immunity. Specifically, we suggest that infection with a novel virus strain, in people previously exposed to influenza viruses, can elicit a memory B cell response against conserved hemagglutinin stalk epitopes and/or neuraminidase epitopes. The anti-stalk and/or anti-neuraminidase antibodies then act to diminish the clinical severity of disease caused by novel influenza viruses and to eliminate seasonal virus strains.
Url:
DOI: 10.1128/mBio.00150-11
PubMed: 21878571
PubMed Central: 3163940
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PMC:3163940Le document en format XML
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<p>Novel pandemic influenza viruses enter the human population with some regularity and can cause disease that is severe and widespread. The emergence of novel viruses, historically, has often been coupled with the disappearance of existing seasonal virus strains. Here, we propose that the elimination of seasonal strains during virus pandemics is a process mediated, at the population level, by humoral immunity. Specifically, we suggest that infection with a novel virus strain, in people previously exposed to influenza viruses, can elicit a memory B cell response against conserved hemagglutinin stalk epitopes and/or neuraminidase epitopes. The anti-stalk and/or anti-neuraminidase antibodies then act to diminish the clinical severity of disease caused by novel influenza viruses and to eliminate seasonal virus strains.</p>
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<article-id pub-id-type="doi">10.1128/mBio.00150-11</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Opinion/Hypothesis</subject>
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<title-group><article-title>Why Do Influenza Virus Subtypes Die Out? A Hypothesis</article-title>
<alt-title>Opinion/Hypothesis</alt-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Palese</surname>
<given-names>Peter</given-names>
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<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Taia T.</given-names>
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<aff id="aff1">Department of Microbiology, Mount Sinai School of Medicine, New York, New York, USA</aff>
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<author-notes><corresp id="cor1">Address correspondence to Peter Palese, <email>peter.palese@mssm.edu</email>
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<pub-date pub-type="epub"><day>30</day>
<month>8</month>
<year>2011</year>
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<pub-date pub-type="collection"><season>Sep-Oct</season>
<year>2011</year>
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<volume>2</volume>
<issue>5</issue>
<elocation-id>e00150-11</elocation-id>
<permissions><copyright-statement>Copyright © 2011 Palese et al. </copyright-statement>
<copyright-year>2011</copyright-year>
<copyright-holder>Palese and Wang</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0/"><license-p>This is an open-access article distributed under the terms of the <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0/">Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License</ext-link>
, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.</license-p>
</license>
</permissions>
<abstract><title>ABSTRACT</title>
<p>Novel pandemic influenza viruses enter the human population with some regularity and can cause disease that is severe and widespread. The emergence of novel viruses, historically, has often been coupled with the disappearance of existing seasonal virus strains. Here, we propose that the elimination of seasonal strains during virus pandemics is a process mediated, at the population level, by humoral immunity. Specifically, we suggest that infection with a novel virus strain, in people previously exposed to influenza viruses, can elicit a memory B cell response against conserved hemagglutinin stalk epitopes and/or neuraminidase epitopes. The anti-stalk and/or anti-neuraminidase antibodies then act to diminish the clinical severity of disease caused by novel influenza viruses and to eliminate seasonal virus strains.</p>
</abstract>
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