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Seroprevalence Following the Second Wave of Pandemic 2009 H1N1 Influenza in Pittsburgh, PA, USA

Identifieur interne : 000B12 ( Pmc/Curation ); précédent : 000B11; suivant : 000B13

Seroprevalence Following the Second Wave of Pandemic 2009 H1N1 Influenza in Pittsburgh, PA, USA

Auteurs : Shanta M. Zimmer [États-Unis] ; Corey J. Crevar [États-Unis] ; Donald M. Carter [États-Unis] ; James H. Stark [États-Unis] ; Brendan M. Giles [États-Unis] ; Richard K. Zimmerman [États-Unis] ; Stephen M. Ostroff [États-Unis] ; Bruce Y. Lee [États-Unis] ; Donald S. Burke [États-Unis] ; Ted M. Ross [États-Unis]

Source :

RBID : PMC:2904390

Abstract

Background

In April 2009, a new pandemic strain of influenza infected thousands of persons in Mexico and the United States and spread rapidly worldwide. During the ensuing summer months, cases ebbed in the Northern Hemisphere while the Southern Hemisphere experienced a typical influenza season dominated by the novel strain. In the fall, a second wave of pandemic H1N1 swept through the United States, peaking in most parts of the country by mid October and returning to baseline levels by early December. The objective was to determine the seroprevalence of antibodies against the pandemic 2009 H1N1 influenza strain by decade of birth among Pittsburgh-area residents.

Methods and Findings

Anonymous blood samples were obtained from clinical laboratories and categorized by decade of birth from 1920–2009. Using hemagglutination-inhibition assays, approximately 100 samples per decade (n = 846) were tested from blood samples drawn on hospital and clinic patients in mid-November and early December 2009. Age specific seroprevalences against pandemic H1N1 (A/California/7/2009) were measured and compared to seroprevalences against H1N1 strains that had previously circulated in the population in 2007, 1957, and 1918. (A/Brisbane/59/2007, A/Denver/1/1957, and A/South Carolina/1/1918). Stored serum samples from healthy, young adults from 2008 were used as a control group (n = 100). Seroprevalences against pandemic 2009 H1N1 influenza varied by age group, with children age 10–19 years having the highest seroprevalence (45%), and persons age 70–79 years having the lowest (5%). The baseline seroprevalence among control samples from 18–24 year-olds was 6%. Overall seroprevalence against pandemic H1N1 across all age groups was approximately 21%.

Conclusions

After the peak of the second wave of 2009 H1N1, HAI seroprevalence results suggest that 21% of persons in the Pittsburgh area had become infected and developed immunity. Extrapolating to the entire US population, we estimate that at least 63 million persons became infected in 2009. As was observed among clinical cases, this sero-epidemiological study revealed highest infection rates among school-age children.


Url:
DOI: 10.1371/journal.pone.0011601
PubMed: 20644650
PubMed Central: 2904390

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PMC:2904390

Le document en format XML

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<title>Background</title>
<p>In April 2009, a new pandemic strain of influenza infected thousands of persons in Mexico and the United States and spread rapidly worldwide. During the ensuing summer months, cases ebbed in the Northern Hemisphere while the Southern Hemisphere experienced a typical influenza season dominated by the novel strain. In the fall, a second wave of pandemic H1N1 swept through the United States, peaking in most parts of the country by mid October and returning to baseline levels by early December. The objective was to determine the seroprevalence of antibodies against the pandemic 2009 H1N1 influenza strain by decade of birth among Pittsburgh-area residents.</p>
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<p>Anonymous blood samples were obtained from clinical laboratories and categorized by decade of birth from 1920–2009. Using hemagglutination-inhibition assays, approximately 100 samples per decade (n = 846) were tested from blood samples drawn on hospital and clinic patients in mid-November and early December 2009. Age specific seroprevalences against pandemic H1N1 (A/California/7/2009) were measured and compared to seroprevalences against H1N1 strains that had previously circulated in the population in 2007, 1957, and 1918. (A/Brisbane/59/2007, A/Denver/1/1957, and A/South Carolina/1/1918). Stored serum samples from healthy, young adults from 2008 were used as a control group (n = 100). Seroprevalences against pandemic 2009 H1N1 influenza varied by age group, with children age 10–19 years having the highest seroprevalence (45%), and persons age 70–79 years having the lowest (5%). The baseline seroprevalence among control samples from 18–24 year-olds was 6%. Overall seroprevalence against pandemic H1N1 across all age groups was approximately 21%.</p>
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<p>After the peak of the second wave of 2009 H1N1, HAI seroprevalence results suggest that 21% of persons in the Pittsburgh area had become infected and developed immunity. Extrapolating to the entire US population, we estimate that at least 63 million persons became infected in 2009. As was observed among clinical cases, this sero-epidemiological study revealed highest infection rates among school-age children.</p>
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<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">PLoS One</journal-id>
<journal-id journal-id-type="iso-abbrev">PLoS ONE</journal-id>
<journal-id journal-id-type="publisher-id">plos</journal-id>
<journal-id journal-id-type="pmc">plosone</journal-id>
<journal-title-group>
<journal-title>PLoS ONE</journal-title>
</journal-title-group>
<issn pub-type="epub">1932-6203</issn>
<publisher>
<publisher-name>Public Library of Science</publisher-name>
<publisher-loc>San Francisco, USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">20644650</article-id>
<article-id pub-id-type="pmc">2904390</article-id>
<article-id pub-id-type="publisher-id">10-PONE-RA-16216R1</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0011601</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Research Article</subject>
</subj-group>
<subj-group subj-group-type="Discipline">
<subject>Immunology/Immune Response</subject>
<subject>Microbiology/Immunity to Infections</subject>
<subject>Virology/Emerging Viral Diseases</subject>
<subject>Infectious Diseases/Respiratory Infections</subject>
<subject>Respiratory Medicine/Respiratory Infections</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Seroprevalence Following the Second Wave of Pandemic 2009 H1N1 Influenza in Pittsburgh, PA, USA</article-title>
<alt-title alt-title-type="running-head">Second Wave of H1N1 Influenza</alt-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Zimmer</surname>
<given-names>Shanta M.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Crevar</surname>
<given-names>Corey J.</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Carter</surname>
<given-names>Donald M.</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Stark</surname>
<given-names>James H.</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Giles</surname>
<given-names>Brendan M.</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zimmerman</surname>
<given-names>Richard K.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Ostroff</surname>
<given-names>Stephen M.</given-names>
</name>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lee</surname>
<given-names>Bruce Y.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Burke</surname>
<given-names>Donald S.</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Ross</surname>
<given-names>Ted M.</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<xref ref-type="aff" rid="aff5">
<sup>5</sup>
</xref>
<xref ref-type="corresp" rid="cor1">
<sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="aff1">
<label>1</label>
<addr-line>School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America</addr-line>
</aff>
<aff id="aff2">
<label>2</label>
<addr-line>Center for Vaccine Research, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America</addr-line>
</aff>
<aff id="aff3">
<label>3</label>
<addr-line>Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America</addr-line>
</aff>
<aff id="aff4">
<label>4</label>
<addr-line>Pennsylvania Department of Health, Pittsburgh, Pennsylvania, United States of America</addr-line>
</aff>
<aff id="aff5">
<label>5</label>
<addr-line>Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America</addr-line>
</aff>
<contrib-group>
<contrib contrib-type="editor">
<name>
<surname>Kelly</surname>
<given-names>Kathleen A.</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
</contrib>
</contrib-group>
<aff id="edit1">University of California Los Angeles, United States of America</aff>
<author-notes>
<corresp id="cor1">* E-mail:
<email>tmr15@pitt.edu</email>
</corresp>
<fn fn-type="con">
<p>Conceived and designed the experiments: SMZ DSB TMR. Performed the experiments: CJC DMC JHS BMG. Analyzed the data: SMZ CJC DMC JHS BMG RZ SO BYL DSB TMR. Contributed reagents/materials/analysis tools: SMZ BMG RZ TMR. Wrote the paper: SMZ DSB TMR.</p>
</fn>
</author-notes>
<pub-date pub-type="collection">
<year>2010</year>
</pub-date>
<pub-date pub-type="epub">
<day>14</day>
<month>7</month>
<year>2010</year>
</pub-date>
<volume>5</volume>
<issue>7</issue>
<elocation-id>e11601</elocation-id>
<history>
<date date-type="received">
<day>10</day>
<month>2</month>
<year>2010</year>
</date>
<date date-type="accepted">
<day>8</day>
<month>6</month>
<year>2010</year>
</date>
</history>
<permissions>
<copyright-statement>Zimmer et al.</copyright-statement>
<copyright-year>2010</copyright-year>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/">
<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.</license-p>
</license>
</permissions>
<abstract>
<sec>
<title>Background</title>
<p>In April 2009, a new pandemic strain of influenza infected thousands of persons in Mexico and the United States and spread rapidly worldwide. During the ensuing summer months, cases ebbed in the Northern Hemisphere while the Southern Hemisphere experienced a typical influenza season dominated by the novel strain. In the fall, a second wave of pandemic H1N1 swept through the United States, peaking in most parts of the country by mid October and returning to baseline levels by early December. The objective was to determine the seroprevalence of antibodies against the pandemic 2009 H1N1 influenza strain by decade of birth among Pittsburgh-area residents.</p>
</sec>
<sec>
<title>Methods and Findings</title>
<p>Anonymous blood samples were obtained from clinical laboratories and categorized by decade of birth from 1920–2009. Using hemagglutination-inhibition assays, approximately 100 samples per decade (n = 846) were tested from blood samples drawn on hospital and clinic patients in mid-November and early December 2009. Age specific seroprevalences against pandemic H1N1 (A/California/7/2009) were measured and compared to seroprevalences against H1N1 strains that had previously circulated in the population in 2007, 1957, and 1918. (A/Brisbane/59/2007, A/Denver/1/1957, and A/South Carolina/1/1918). Stored serum samples from healthy, young adults from 2008 were used as a control group (n = 100). Seroprevalences against pandemic 2009 H1N1 influenza varied by age group, with children age 10–19 years having the highest seroprevalence (45%), and persons age 70–79 years having the lowest (5%). The baseline seroprevalence among control samples from 18–24 year-olds was 6%. Overall seroprevalence against pandemic H1N1 across all age groups was approximately 21%.</p>
</sec>
<sec>
<title>Conclusions</title>
<p>After the peak of the second wave of 2009 H1N1, HAI seroprevalence results suggest that 21% of persons in the Pittsburgh area had become infected and developed immunity. Extrapolating to the entire US population, we estimate that at least 63 million persons became infected in 2009. As was observed among clinical cases, this sero-epidemiological study revealed highest infection rates among school-age children.</p>
</sec>
</abstract>
<counts>
<page-count count="7"></page-count>
</counts>
</article-meta>
</front>
</pmc>
</record>

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