Increased transmissibility explains the third wave of infection by the 2009 H1N1 pandemic virus in England
Identifieur interne : 001817 ( Main/Curation ); précédent : 001816; suivant : 001818Increased transmissibility explains the third wave of infection by the 2009 H1N1 pandemic virus in England
Auteurs : Ilaria Dorigatti [Royaume-Uni] ; Simon Cauchemez [Royaume-Uni] ; Neil M. Ferguson [Royaume-Uni]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2013.
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Abstract
In the 2009 H1N1 pandemic, the United Kingdom experienced two waves of infection, the first in the late spring and the second in the autumn. Given the low level of susceptibility to the pandemic virus expected to be remaining in the population after the second wave, it was a surprise that a substantial third epidemic occurred in the UK population between November 2010 and February 2011, despite no evidence for any significant antigenic evolution of the pandemic virus. Here, we use a mathematical model of influenza transmission embedded within a Bayesian synthesis inferential framework to jointly analyze syndromic, virological, and serological surveillance data collected in England in 2009-2011 and thereby assess epidemiological mechanisms which might have generated the third wave. We find that substantially increased transmissibility of the H1N1pdm09 virus is required to reproduce the third wave, suggesting that the virus evolved and increased fitness in the human host by the end of 2010, or that the very cold weather experienced in the United Kingdom at that time enhanced transmission rates. We also find some evidence that the preexisting heterologous immunity which reduced attack rates in adults during 2009 had substantially decayed by the winter of 2010, thus increasing the susceptibility of the adult population to infection. Finally, our analysis suggests that a pandemic vaccination campaign targeting adults and school-age children could have mitigated or prevented the third wave even at moderate levels of coverage.
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Ferguson</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Medical Research Council Centre for Outbreak Analysis and Modelling, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, Norfolk Place</s1><s2>London W2 1PG</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Royaume-Uni</country><wicri:noRegion>London W2 1PG</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Proceedings of the National Academy of Sciences of the United States of America</title><title level="j" type="abbreviated">Proc. Natl. Acad. Sci. U. S. A.</title><idno type="ISSN">0027-8424</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Proceedings of the National Academy of Sciences of the United States of America</title><title level="j" type="abbreviated">Proc. Natl. Acad. Sci. U. S. A.</title><idno type="ISSN">0027-8424</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>2009</term><term>England</term><term>Epidemiology</term><term>Human</term><term>Influenza</term><term>Transmission from man to man</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Grippe</term><term>Transmission homme homme</term><term>2009</term><term>Angleterre</term><term>Homme</term><term>Epidémiologie</term><term>Influenzavirus A(H1N1)</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the 2009 H1N1 pandemic, the United Kingdom experienced two waves of infection, the first in the late spring and the second in the autumn. Given the low level of susceptibility to the pandemic virus expected to be remaining in the population after the second wave, it was a surprise that a substantial third epidemic occurred in the UK population between November 2010 and February 2011, despite no evidence for any significant antigenic evolution of the pandemic virus. Here, we use a mathematical model of influenza transmission embedded within a Bayesian synthesis inferential framework to jointly analyze syndromic, virological, and serological surveillance data collected in England in 2009-2011 and thereby assess epidemiological mechanisms which might have generated the third wave. We find that substantially increased transmissibility of the H1N1pdm09 virus is required to reproduce the third wave, suggesting that the virus evolved and increased fitness in the human host by the end of 2010, or that the very cold weather experienced in the United Kingdom at that time enhanced transmission rates. We also find some evidence that the preexisting heterologous immunity which reduced attack rates in adults during 2009 had substantially decayed by the winter of 2010, thus increasing the susceptibility of the adult population to infection. Finally, our analysis suggests that a pandemic vaccination campaign targeting adults and school-age children could have mitigated or prevented the third wave even at moderate levels of coverage.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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