Mutations in Polymerase Genes Enhanced the Virulence of 2009 Pandemic H1N1 Influenza Virus in Mice
Identifieur interne : 000704 ( Pmc/Checkpoint ); précédent : 000703; suivant : 000705Mutations in Polymerase Genes Enhanced the Virulence of 2009 Pandemic H1N1 Influenza Virus in Mice
Auteurs : Wenfei Zhu ; Yun Zhu ; Kun Qin ; Zaijiang Yu ; Rongbao Gao ; Huiyan Yu ; Jianfang Zhou ; Yuelong ShuSource :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
Influenza A virus can infect a wide variety of animal species with illness ranging from mild to severe, and is a continual cause for concern. Genetic mutations that occur either naturally or during viral adaptation in a poorly susceptible host are key mechanisms underlying the evolution and virulence of influenza A virus. Here, the variants containing PA-A36T or PB2-H357N observed in the mouse-adapted descendants of 2009 pandemic H1N1 virus (pH1N1), A/Sichuan/1/2009 (SC), were characterized. Both mutations enhanced polymerase activity in mammalian cells. These effects were confirmed using recombinant SC virus containing polymerase genes with wild type (WT) or mutant PA or PB2. The PA-A36T mutant showed enhanced growth property compared to the WT in both human A549 cells and porcine PK15 cells
Url:
DOI: 10.1371/journal.pone.0033383
PubMed: 22438920
PubMed Central: 3305307
Affiliations:
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Mutations in Polymerase Genes Enhanced the Virulence of 2009 Pandemic H1N1 Influenza Virus in Mice</title>
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<front><div type="abstract" xml:lang="en"><p>Influenza A virus can infect a wide variety of animal species with illness ranging from mild to severe, and is a continual cause for concern. Genetic mutations that occur either naturally or during viral adaptation in a poorly susceptible host are key mechanisms underlying the evolution and virulence of influenza A virus. Here, the variants containing PA-A36T or PB2-H357N observed in the mouse-adapted descendants of 2009 pandemic H1N1 virus (pH1N1), A/Sichuan/1/2009 (SC), were characterized. Both mutations enhanced polymerase activity in mammalian cells. These effects were confirmed using recombinant SC virus containing polymerase genes with wild type (WT) or mutant PA or PB2. The PA-A36T mutant showed enhanced growth property compared to the WT in both human A549 cells and porcine PK15 cells <italic>in vitro</italic>
, without significant effect on viral propagation in murine LA-4 cells and pathogenicity in mice; however, it did enhance the lung virus titer. PB2-H357N variant demonstrated growth ability comparable to the WT in A549 cells, but replicated well in PK15, LA-4 cells and in mice with an enhanced pathogenic phenotype. Despite such mutations are rare in nature, they could be observed in avian H5 and H7 subtype viruses which were currently recognized to pose potential threat to human. Our findings indicated that pH1N1 may adapt well in mammals when acquiring these mutations. Therefore, future molecular epidemiological surveillance should include scrutiny of both markers because of their potential impact on pathogenesis.</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">22438920</article-id>
<article-id pub-id-type="pmc">3305307</article-id>
<article-id pub-id-type="publisher-id">PONE-D-11-15459</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0033383</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Biology</subject>
<subj-group><subject>Genetics</subject>
</subj-group>
<subj-group><subject>Microbiology</subject>
<subj-group><subject>Virology</subject>
</subj-group>
</subj-group>
<subj-group><subject>Model Organisms</subject>
<subj-group><subject>Animal Models</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Medicine</subject>
<subj-group><subject>Infectious Diseases</subject>
<subj-group><subject>Viral Diseases</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group subj-group-type="Discipline-v2"><subject>Veterinary Science</subject>
<subj-group><subject>Veterinary Diseases</subject>
<subj-group><subject>Zoonotic Diseases</subject>
</subj-group>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Mutations in Polymerase Genes Enhanced the Virulence of 2009 Pandemic H1N1 Influenza Virus in Mice</article-title>
<alt-title alt-title-type="running-head">PB2-H357N Increased the Virulence of 2009H1N1pdm</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Zhu</surname>
<given-names>Wenfei</given-names>
</name>
</contrib>
<contrib contrib-type="author" equal-contrib="yes"><name><surname>Zhu</surname>
<given-names>Yun</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Qin</surname>
<given-names>Kun</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Yu</surname>
<given-names>Zaijiang</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Gao</surname>
<given-names>Rongbao</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Yu</surname>
<given-names>Huiyan</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Zhou</surname>
<given-names>Jianfang</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
<xref ref-type="corresp" rid="cor1"><sup>*</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Shu</surname>
<given-names>Yuelong</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
<xref ref-type="corresp" rid="cor1"><sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="aff1"><addr-line>Chinese National Influenza Center, National Institute for Viral Disease Control and Prevention, China CDC, Beijing, People's Republic of China</addr-line>
</aff>
<contrib-group><contrib contrib-type="editor"><name><surname>Digard</surname>
<given-names>Paul</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
</contrib>
</contrib-group>
<aff id="edit1">University of Edinburgh, United Kingdom</aff>
<author-notes><corresp id="cor1">* E-mail: <email>jfz@cnic.org.cn</email>
(JFZ); <email>yshu@cnic.org.cn</email>
(YLS)</corresp>
<fn fn-type="con"><p>Analyzed the data: WFZ JFZ KQ YZ YLS. Contributed reagents/materials/analysis tools: YLS JFZ. Wrote the paper: WFZ JFZ. Designed the research: YLS JFZ KQ WFZ. Performed the research: WFZ YZ. Helped to construct partial plasmids and to perform partial research: KQ ZJY RBG HYY. Helped to revise the manuscript: KQ YLS.</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2012</year>
</pub-date>
<pub-date pub-type="epub"><day>15</day>
<month>3</month>
<year>2012</year>
</pub-date>
<volume>7</volume>
<issue>3</issue>
<elocation-id>e33383</elocation-id>
<history><date date-type="received"><day>9</day>
<month>8</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>13</day>
<month>2</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>Zhu et al.</copyright-statement>
<copyright-year>2012</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><p>Influenza A virus can infect a wide variety of animal species with illness ranging from mild to severe, and is a continual cause for concern. Genetic mutations that occur either naturally or during viral adaptation in a poorly susceptible host are key mechanisms underlying the evolution and virulence of influenza A virus. Here, the variants containing PA-A36T or PB2-H357N observed in the mouse-adapted descendants of 2009 pandemic H1N1 virus (pH1N1), A/Sichuan/1/2009 (SC), were characterized. Both mutations enhanced polymerase activity in mammalian cells. These effects were confirmed using recombinant SC virus containing polymerase genes with wild type (WT) or mutant PA or PB2. The PA-A36T mutant showed enhanced growth property compared to the WT in both human A549 cells and porcine PK15 cells <italic>in vitro</italic>
, without significant effect on viral propagation in murine LA-4 cells and pathogenicity in mice; however, it did enhance the lung virus titer. PB2-H357N variant demonstrated growth ability comparable to the WT in A549 cells, but replicated well in PK15, LA-4 cells and in mice with an enhanced pathogenic phenotype. Despite such mutations are rare in nature, they could be observed in avian H5 and H7 subtype viruses which were currently recognized to pose potential threat to human. Our findings indicated that pH1N1 may adapt well in mammals when acquiring these mutations. Therefore, future molecular epidemiological surveillance should include scrutiny of both markers because of their potential impact on pathogenesis.</p>
</abstract>
<counts><page-count count="7"></page-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Gao, Rongbao" sort="Gao, Rongbao" uniqKey="Gao R" first="Rongbao" last="Gao">Rongbao Gao</name>
<name sortKey="Qin, Kun" sort="Qin, Kun" uniqKey="Qin K" first="Kun" last="Qin">Kun Qin</name>
<name sortKey="Shu, Yuelong" sort="Shu, Yuelong" uniqKey="Shu Y" first="Yuelong" last="Shu">Yuelong Shu</name>
<name sortKey="Yu, Huiyan" sort="Yu, Huiyan" uniqKey="Yu H" first="Huiyan" last="Yu">Huiyan Yu</name>
<name sortKey="Yu, Zaijiang" sort="Yu, Zaijiang" uniqKey="Yu Z" first="Zaijiang" last="Yu">Zaijiang Yu</name>
<name sortKey="Zhou, Jianfang" sort="Zhou, Jianfang" uniqKey="Zhou J" first="Jianfang" last="Zhou">Jianfang Zhou</name>
<name sortKey="Zhu, Wenfei" sort="Zhu, Wenfei" uniqKey="Zhu W" first="Wenfei" last="Zhu">Wenfei Zhu</name>
<name sortKey="Zhu, Yun" sort="Zhu, Yun" uniqKey="Zhu Y" first="Yun" last="Zhu">Yun Zhu</name>
</noCountry>
</tree>
</affiliations>
</record>
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