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Molecular characterization of H3N2 influenza A viruses isolated from Ontario swine in 2011 and 2012

Identifieur interne : 000209 ( Pmc/Curation ); précédent : 000208; suivant : 000210

Molecular characterization of H3N2 influenza A viruses isolated from Ontario swine in 2011 and 2012

Auteurs : Helena Grgi [Canada] ; Marcio Costa [Canada] ; Robert M. Friendship [Canada] ; Susy Carman ; Éva Nagy [Canada] ; Greg Wideman ; Scott Weese [Canada] ; Zvonimir Poljak [Canada]

Source :

RBID : PMC:4245826

Abstract

Background

Data about molecular diversity of commonly circulating type A influenza viruses in Ontario swine are scarce. Yet, this information is essential for surveillance of animal and public health, vaccine updates, and for understanding virus evolution and its large-scale spread.

Methods

The study population consisted of 21 swine herds with clinical problems due to respiratory disease. Nasal swabs from individual pigs were collected and tested by virus isolation in MDCK cells and by rtRT-PCR. All eight segments of 10 H3N2 viruses were sequenced using high-throughput sequencing and molecularly characterized.

Results

Within-herd prevalence ranged between 2 and 100%. Structurally, Ontario H3N2 viruses could be classified into three different groups. Group 1 was the most similar to the original trH3N2 virus from 2005. Group 2 was the most similar to the Ontario turkey H3N2 isolates with PB1 and NS genes originating from trH3N2 virus and M, PB2, PA and NP genes originating from the A(H1N1)pdm09 virus. All Group 3 internal genes were genetically related to A(H1N1)pdm09. Analysis of antigenic sites of HA1 showed that Group 1 had 8 aa changes within 4 antigenic sites, A(1), B(3), C(2) and E(2). The Group 2 viruses had 8 aa changes within 3 antigenic sites A(3), B(3) and C(2), while Group 3 viruses had 4 aa changes within 3 antigenic sites, B(1), D(1) and E(2), when compared to the cluster IV H3N2 virus [A/swine/Ontario/33853/2005/(H3N2)].

Conclusions

The characterization of the Ontario H3N2 viruses clearly indicates reassortment of gene segments between the North American swine trH3N2 from cluster IV and the A(H1N1)pdm09 virus.

Electronic supplementary material

The online version of this article (doi:10.1186/s12985-014-0194-z) contains supplementary material, which is available to authorized users.


Url:
DOI: 10.1186/s12985-014-0194-z
PubMed: 25416300
PubMed Central: 4245826

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PMC:4245826

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Helena Grgi
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<nlm:aff id="Aff1">Department of Population Medicine, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2 W1 Canada</nlm:aff>
<wicri:noCountry code="subfield">Ontario N1G 2 W1 Canada</wicri:noCountry>
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Marcio Costa
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Robert M. Friendship
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Susy Carman
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Éva Nagy
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Greg Wideman
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Scott Weese
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Zvonimir Poljak
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<sec>
<title>Background</title>
<p>Data about molecular diversity of commonly circulating type A influenza viruses in Ontario swine are scarce. Yet, this information is essential for surveillance of animal and public health, vaccine updates, and for understanding virus evolution and its large-scale spread.</p>
</sec>
<sec>
<title>Methods</title>
<p>The study population consisted of 21 swine herds with clinical problems due to respiratory disease. Nasal swabs from individual pigs were collected and tested by virus isolation in MDCK cells and by rtRT-PCR. All eight segments of 10 H3N2 viruses were sequenced using high-throughput sequencing and molecularly characterized.</p>
</sec>
<sec>
<title>Results</title>
<p>Within-herd prevalence ranged between 2 and 100%. Structurally, Ontario H3N2 viruses could be classified into three different groups. Group 1 was the most similar to the original trH3N2 virus from 2005. Group 2 was the most similar to the Ontario turkey H3N2 isolates with PB1 and NS genes originating from trH3N2 virus and M, PB2, PA and NP genes originating from the A(H1N1)pdm09 virus. All Group 3 internal genes were genetically related to A(H1N1)pdm09. Analysis of antigenic sites of HA1 showed that Group 1 had 8 aa changes within 4 antigenic sites, A(1), B(3), C(2) and E(2). The Group 2 viruses had 8 aa changes within 3 antigenic sites A(3), B(3) and C(2), while Group 3 viruses had 4 aa changes within 3 antigenic sites, B(1), D(1) and E(2), when compared to the cluster IV H3N2 virus [A/swine/Ontario/33853/2005/(H3N2)].</p>
</sec>
<sec>
<title>Conclusions</title>
<p>The characterization of the Ontario H3N2 viruses clearly indicates reassortment of gene segments between the North American swine trH3N2 from cluster IV and the A(H1N1)pdm09 virus.</p>
</sec>
<sec>
<title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1186/s12985-014-0194-z) contains supplementary material, which is available to authorized users.</p>
</sec>
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<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Virol J</journal-id>
<journal-id journal-id-type="iso-abbrev">Virol. J</journal-id>
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<issn pub-type="epub">1743-422X</issn>
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<publisher-name>BioMed Central</publisher-name>
<publisher-loc>London</publisher-loc>
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<article-meta>
<article-id pub-id-type="pmid">25416300</article-id>
<article-id pub-id-type="pmc">4245826</article-id>
<article-id pub-id-type="publisher-id">194</article-id>
<article-id pub-id-type="doi">10.1186/s12985-014-0194-z</article-id>
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<subj-group subj-group-type="heading">
<subject>Research</subject>
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<title-group>
<article-title>Molecular characterization of H3N2 influenza A viruses isolated from Ontario swine in 2011 and 2012</article-title>
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<email>rfriends@uoguelph.ca</email>
</address>
<xref ref-type="aff" rid="Aff1"></xref>
<xref ref-type="aff" rid="Aff5"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Carman</surname>
<given-names>Susy</given-names>
</name>
<address>
<email>scarman@uoguelph.ca</email>
</address>
<xref ref-type="aff" rid="Aff3"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Nagy</surname>
<given-names>Éva</given-names>
</name>
<address>
<email>enagy@ovc.uoguelph.ca</email>
</address>
<xref ref-type="aff" rid="Aff2"></xref>
<xref ref-type="aff" rid="Aff5"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wideman</surname>
<given-names>Greg</given-names>
</name>
<address>
<email>gwideman@gmail.com</email>
</address>
<xref ref-type="aff" rid="Aff4"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Weese</surname>
<given-names>Scott</given-names>
</name>
<address>
<email>jsweese@uoguelph.ca</email>
</address>
<xref ref-type="aff" rid="Aff2"></xref>
<xref ref-type="aff" rid="Aff5"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Poljak</surname>
<given-names>Zvonimir</given-names>
</name>
<address>
<email>zpoljak@uoguelph.ca</email>
</address>
<xref ref-type="aff" rid="Aff1"></xref>
<xref ref-type="aff" rid="Aff5"></xref>
</contrib>
<aff id="Aff1">
<label></label>
Department of Population Medicine, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2 W1 Canada</aff>
<aff id="Aff2">
<label></label>
Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2 W1 Canada</aff>
<aff id="Aff3">
<label></label>
Animal Health Laboratory, University of Guelph, Guelph, Ontario N1H 6R8 Canada</aff>
<aff id="Aff4">
<label></label>
South-West Ontario Veterinary Services, Stratford, Ontario Canada</aff>
<aff id="Aff5">
<label></label>
Centre for Public Health and Zoonoses, University of Guelph, Guelph, Canada</aff>
</contrib-group>
<pub-date pub-type="epub">
<day>22</day>
<month>11</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>22</day>
<month>11</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="collection">
<year>2014</year>
</pub-date>
<volume>11</volume>
<elocation-id>194</elocation-id>
<history>
<date date-type="received">
<day>14</day>
<month>5</month>
<year>2014</year>
</date>
<date date-type="accepted">
<day>29</day>
<month>10</month>
<year>2014</year>
</date>
</history>
<permissions>
<copyright-statement>© Grgić et al.; licensee BioMed Central Ltd. 2014</copyright-statement>
<license license-type="open-access">
<license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0">http://creativecommons.org/licenses/by/4.0</ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>
) applies to the data made available in this article, unless otherwise stated.</license-p>
</license>
</permissions>
<abstract id="Abs1">
<sec>
<title>Background</title>
<p>Data about molecular diversity of commonly circulating type A influenza viruses in Ontario swine are scarce. Yet, this information is essential for surveillance of animal and public health, vaccine updates, and for understanding virus evolution and its large-scale spread.</p>
</sec>
<sec>
<title>Methods</title>
<p>The study population consisted of 21 swine herds with clinical problems due to respiratory disease. Nasal swabs from individual pigs were collected and tested by virus isolation in MDCK cells and by rtRT-PCR. All eight segments of 10 H3N2 viruses were sequenced using high-throughput sequencing and molecularly characterized.</p>
</sec>
<sec>
<title>Results</title>
<p>Within-herd prevalence ranged between 2 and 100%. Structurally, Ontario H3N2 viruses could be classified into three different groups. Group 1 was the most similar to the original trH3N2 virus from 2005. Group 2 was the most similar to the Ontario turkey H3N2 isolates with PB1 and NS genes originating from trH3N2 virus and M, PB2, PA and NP genes originating from the A(H1N1)pdm09 virus. All Group 3 internal genes were genetically related to A(H1N1)pdm09. Analysis of antigenic sites of HA1 showed that Group 1 had 8 aa changes within 4 antigenic sites, A(1), B(3), C(2) and E(2). The Group 2 viruses had 8 aa changes within 3 antigenic sites A(3), B(3) and C(2), while Group 3 viruses had 4 aa changes within 3 antigenic sites, B(1), D(1) and E(2), when compared to the cluster IV H3N2 virus [A/swine/Ontario/33853/2005/(H3N2)].</p>
</sec>
<sec>
<title>Conclusions</title>
<p>The characterization of the Ontario H3N2 viruses clearly indicates reassortment of gene segments between the North American swine trH3N2 from cluster IV and the A(H1N1)pdm09 virus.</p>
</sec>
<sec>
<title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1186/s12985-014-0194-z) contains supplementary material, which is available to authorized users.</p>
</sec>
</abstract>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>Influenza A virus</kwd>
<kwd>Triple-reassortant H3N2</kwd>
<kwd>Swine</kwd>
<kwd>454 sequencing</kwd>
<kwd>Phylogenetic analysis</kwd>
</kwd-group>
<custom-meta-group>
<custom-meta>
<meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2014</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>

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