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Newly Emergent Highly Pathogenic H5N9 Subtype Avian Influenza A Virus

Identifieur interne : 000056 ( Pmc/Corpus ); précédent : 000055; suivant : 000057

Newly Emergent Highly Pathogenic H5N9 Subtype Avian Influenza A Virus

Auteurs : Yang Yu ; Xingbo Wang ; Tao Jin ; Hailong Wang ; Weiying Si ; Hui Yang ; Jiusheng Wu ; Yan Yan ; Guang Liu ; Xiaoyu Sang ; Xiaopeng Wu ; Yuwei Gao ; Xianzhu Xia ; Xinfen Yu ; Jingcao Pan ; George F. Gao ; Jiyong Zhou

Source :

RBID : PMC:4524050

Abstract

ABSTRACT

The novel H7N9 avian influenza virus (AIV) was demonstrated to cause severe human respiratory infections in China. Here, we examined poultry specimens from live bird markets linked to human H7N9 infection in Hangzhou, China. Metagenomic sequencing revealed mixed subtypes (H5, H7, H9, N1, N2, and N9). Subsequently, AIV subtypes H5N9, H7N9, and H9N2 were isolated. Evolutionary analysis showed that the hemagglutinin gene of the novel H5N9 virus originated from A/Muscovy duck/Vietnam/LBM227/2012 (H5N1), which belongs to clade 2.3.2.1. The neuraminidase gene of the novel H5N9 virus originated from human-infective A/Hangzhou/1/2013 (H7N9). The six internal genes were similar to those of other H5N1, H7N9, and H9N2 virus strains. The virus harbored the PQRERRRKR/GL motif characteristic of highly pathogenic AIVs at the HA cleavage site. Receptor-binding experiments demonstrated that the virus binds α-2,3 sialic acid but not α-2,6 sialic acid. Identically, pathogenicity experiments also showed that the virus caused low mortality rates in mice. This newly isolated H5N9 virus is a highly pathogenic reassortant virus originating from H5N1, H7N9, and H9N2 subtypes. Live bird markets represent a potential transmission risk to public health and the poultry industry.

IMPORTANCE This investigation confirms that the novel H5N9 subtype avian influenza A virus is a reassortant strain originating from H5N1, H7N9, and H9N2 subtypes and is totally different from the H5N9 viruses reported before. The novel H5N9 virus acquired a highly pathogenic H5 gene and an N9 gene from human-infecting subtype H7N9 but caused low mortality rates in mice. Whether this novel H5N9 virus will cause human infections from its avian host and become a pandemic subtype is not known yet. It is therefore imperative to assess the risk of emergence of this novel reassortant virus with potential transmissibility to public health.


Url:
DOI: 10.1128/JVI.00653-15
PubMed: 26085150
PubMed Central: 4524050

Links to Exploration step

PMC:4524050

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<name sortKey="Yan, Yan" sort="Yan, Yan" uniqKey="Yan Y" first="Yan" last="Yan">Yan Yan</name>
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<name sortKey="Liu, Guang" sort="Liu, Guang" uniqKey="Liu G" first="Guang" last="Liu">Guang Liu</name>
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<name sortKey="Gao, George F" sort="Gao, George F" uniqKey="Gao G" first="George F." last="Gao">George F. Gao</name>
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<div type="abstract" xml:lang="en">
<title>ABSTRACT</title>
<p>The novel H7N9 avian influenza virus (AIV) was demonstrated to cause severe human respiratory infections in China. Here, we examined poultry specimens from live bird markets linked to human H7N9 infection in Hangzhou, China. Metagenomic sequencing revealed mixed subtypes (H5, H7, H9, N1, N2, and N9). Subsequently, AIV subtypes H5N9, H7N9, and H9N2 were isolated. Evolutionary analysis showed that the hemagglutinin gene of the novel H5N9 virus originated from A/Muscovy duck/Vietnam/LBM227/2012 (H5N1), which belongs to clade 2.3.2.1. The neuraminidase gene of the novel H5N9 virus originated from human-infective A/Hangzhou/1/2013 (H7N9). The six internal genes were similar to those of other H5N1, H7N9, and H9N2 virus strains. The virus harbored the PQRERRRKR/GL motif characteristic of highly pathogenic AIVs at the HA cleavage site. Receptor-binding experiments demonstrated that the virus binds α-2,3 sialic acid but not α-2,6 sialic acid. Identically, pathogenicity experiments also showed that the virus caused low mortality rates in mice. This newly isolated H5N9 virus is a highly pathogenic reassortant virus originating from H5N1, H7N9, and H9N2 subtypes. Live bird markets represent a potential transmission risk to public health and the poultry industry. </p>
<p>
<bold>IMPORTANCE</bold>
This investigation confirms that the novel H5N9 subtype avian influenza A virus is a reassortant strain originating from H5N1, H7N9, and H9N2 subtypes and is totally different from the H5N9 viruses reported before. The novel H5N9 virus acquired a highly pathogenic H5 gene and an N9 gene from human-infecting subtype H7N9 but caused low mortality rates in mice. Whether this novel H5N9 virus will cause human infections from its avian host and become a pandemic subtype is not known yet. It is therefore imperative to assess the risk of emergence of this novel reassortant virus with potential transmissibility to public health.</p>
</div>
</front>
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<journal-id journal-id-type="nlm-ta">J Virol</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Virol</journal-id>
<journal-id journal-id-type="hwp">jvi</journal-id>
<journal-id journal-id-type="pmc">jvi</journal-id>
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<article-id pub-id-type="doi">10.1128/JVI.00653-15</article-id>
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<subject>Genetic Diversity and Evolution</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Newly Emergent Highly Pathogenic H5N9 Subtype Avian Influenza A Virus</article-title>
<alt-title alt-title-type="running-head">N9 in H5N9 AIV from Human-Infecting H7N9</alt-title>
<alt-title alt-title-type="short-authors">Yu et al.</alt-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Yu</surname>
<given-names>Yang</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wang</surname>
<given-names>Xingbo</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Jin</surname>
<given-names>Tao</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wang</surname>
<given-names>Hailong</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Si</surname>
<given-names>Weiying</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Yang</surname>
<given-names>Hui</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wu</surname>
<given-names>Jiusheng</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Yan</surname>
<given-names>Yan</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Liu</surname>
<given-names>Guang</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Sang</surname>
<given-names>Xiaoyu</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>c</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wu</surname>
<given-names>Xiaopeng</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>c</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Gao</surname>
<given-names>Yuwei</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>c</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Xia</surname>
<given-names>Xianzhu</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>c</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Yu</surname>
<given-names>Xinfen</given-names>
</name>
<xref ref-type="aff" rid="aff4">
<sup>d</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Pan</surname>
<given-names>Jingcao</given-names>
</name>
<xref ref-type="aff" rid="aff4">
<sup>d</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Gao</surname>
<given-names>George F.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
<xref ref-type="aff" rid="aff5">
<sup>e</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Zhou</surname>
<given-names>Jiyong</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>a</sup>
</xref>
</contrib>
<aff id="aff1">
<label>a</label>
Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University, Hangzhou, People's Republic of China</aff>
<aff id="aff2">
<label>b</label>
BGI-Shenzhen, Shenzhen, China</aff>
<aff id="aff3">
<label>c</label>
Changchun Institute of Veterinary Science, Chinese Academy of Agricultural Sciences, Changchun, China</aff>
<aff id="aff4">
<label>d</label>
Hangzhou Center for Disease Control and Prevention, Zhejiang, China</aff>
<aff id="aff5">
<label>e</label>
Chinese Center for Disease Control and Prevention, Beijing, China</aff>
</contrib-group>
<contrib-group>
<contrib contrib-type="editor">
<name>
<surname>Lyles</surname>
<given-names>D. S.</given-names>
</name>
<role>Editor</role>
</contrib>
</contrib-group>
<author-notes>
<corresp id="cor1">Address correspondence to Jiyong Zhou,
<email>jyzhou@zju.edu.cn</email>
.</corresp>
<fn fn-type="equal">
<p>Y. Yu, X. Wang, and T. Jin contributed equally to this work.</p>
</fn>
<fn fn-type="other">
<p>
<bold>Citation</bold>
Yu Y, Wang X, Jin T, Wang H, Si W, Yang H, Wu J, Yan Y, Liu G, Sang X, Wu X, Gao Y, Xia X, Yu X, Pan J, Gao GF, Zhou J. 2015. Newly emergent highly pathogenic H5N9 subtype avian influenza A virus. J Virol 89:8806–8815. doi:
<ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.1128/JVI.00653-15">10.1128/JVI.00653-15</ext-link>
.</p>
</fn>
</author-notes>
<pub-date pub-type="epub">
<day>17</day>
<month>6</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="collection">
<day>1</day>
<month>9</month>
<year>2015</year>
</pub-date>
<volume>89</volume>
<issue>17</issue>
<fpage>8806</fpage>
<lpage>8815</lpage>
<history>
<date date-type="received">
<day>16</day>
<month>3</month>
<year>2015</year>
</date>
<date date-type="accepted">
<day>4</day>
<month>6</month>
<year>2015</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2015</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri content-type="pdf" xlink:href="zjv01715008806.pdf"></self-uri>
<abstract>
<title>ABSTRACT</title>
<p>The novel H7N9 avian influenza virus (AIV) was demonstrated to cause severe human respiratory infections in China. Here, we examined poultry specimens from live bird markets linked to human H7N9 infection in Hangzhou, China. Metagenomic sequencing revealed mixed subtypes (H5, H7, H9, N1, N2, and N9). Subsequently, AIV subtypes H5N9, H7N9, and H9N2 were isolated. Evolutionary analysis showed that the hemagglutinin gene of the novel H5N9 virus originated from A/Muscovy duck/Vietnam/LBM227/2012 (H5N1), which belongs to clade 2.3.2.1. The neuraminidase gene of the novel H5N9 virus originated from human-infective A/Hangzhou/1/2013 (H7N9). The six internal genes were similar to those of other H5N1, H7N9, and H9N2 virus strains. The virus harbored the PQRERRRKR/GL motif characteristic of highly pathogenic AIVs at the HA cleavage site. Receptor-binding experiments demonstrated that the virus binds α-2,3 sialic acid but not α-2,6 sialic acid. Identically, pathogenicity experiments also showed that the virus caused low mortality rates in mice. This newly isolated H5N9 virus is a highly pathogenic reassortant virus originating from H5N1, H7N9, and H9N2 subtypes. Live bird markets represent a potential transmission risk to public health and the poultry industry. </p>
<p>
<bold>IMPORTANCE</bold>
This investigation confirms that the novel H5N9 subtype avian influenza A virus is a reassortant strain originating from H5N1, H7N9, and H9N2 subtypes and is totally different from the H5N9 viruses reported before. The novel H5N9 virus acquired a highly pathogenic H5 gene and an N9 gene from human-infecting subtype H7N9 but caused low mortality rates in mice. Whether this novel H5N9 virus will cause human infections from its avian host and become a pandemic subtype is not known yet. It is therefore imperative to assess the risk of emergence of this novel reassortant virus with potential transmissibility to public health.</p>
</abstract>
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<ref-count count="33"></ref-count>
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<word-count count="6667"></word-count>
</counts>
</article-meta>
</front>
</pmc>
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