Genetic characterization of an adapted pandemic 2009 H1N1 influenza virus that reveals improved replication rates in human lung epithelial cells.
Identifieur interne : 000554 ( PubMed/Corpus ); précédent : 000553; suivant : 000555Genetic characterization of an adapted pandemic 2009 H1N1 influenza virus that reveals improved replication rates in human lung epithelial cells.
Auteurs : Xenia Wörmann ; Markus Lesch ; Robert-William Welke ; Konstantin Okonechnikov ; Mirshat Abdurishid ; Christian Sieben ; Andreas Geissner ; Volker Brinkmann ; Markus Kastner ; Andreas Karner ; Rong Zhu ; Peter Hinterdorfer ; Chakkumkal Anish ; Peter H. Seeberger ; Andreas Herrmann ; Thomas F. Meyer ; Alexander KarlasSource :
- Virology [ 1096-0341 ] ; 2016.
English descriptors
- KwdEn :
- Adaptation, Physiological (genetics), Animals, Chickens, Dogs, Epithelial Cells (virology), Gene Expression, Hemagglutinin Glycoproteins, Influenza Virus (chemistry), Hemagglutinin Glycoproteins, Influenza Virus (genetics), Hemagglutinin Glycoproteins, Influenza Virus (metabolism), High-Throughput Nucleotide Sequencing, Host-Pathogen Interactions, Humans, Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (growth & development), Madin Darby Canine Kidney Cells, Mice, Mice, Inbred BALB C, Models, Molecular, Protein Structure, Secondary, Protein Structure, Tertiary, RNA, Viral (genetics), RNA, Viral (metabolism), Receptors, Virus (genetics), Receptors, Virus (metabolism), Reverse Genetics, Serial Passage, Virus Replication (genetics).
- MESH :
- chemical , chemistry : Hemagglutinin Glycoproteins, Influenza Virus.
- genetics : Adaptation, Physiological, Hemagglutinin Glycoproteins, Influenza Virus, Influenza A Virus, H1N1 Subtype, RNA, Viral, Receptors, Virus, Virus Replication.
- growth & development : Influenza A Virus, H1N1 Subtype.
- chemical , metabolism : Hemagglutinin Glycoproteins, Influenza Virus, RNA, Viral, Receptors, Virus.
- virology : Epithelial Cells.
- Animals, Chickens, Dogs, Gene Expression, High-Throughput Nucleotide Sequencing, Host-Pathogen Interactions, Humans, Madin Darby Canine Kidney Cells, Mice, Mice, Inbred BALB C, Models, Molecular, Protein Structure, Secondary, Protein Structure, Tertiary, Reverse Genetics, Serial Passage.
Abstract
The 2009 influenza pandemic originated from a swine-origin H1N1 virus, which, although less pathogenic than anticipated, may acquire additional virulence-associated mutations in the future. To estimate the potential risk, we sequentially passaged the isolate A/Hamburg/04/2009 in A549 human lung epithelial cells. After passage 6, we observed a 100-fold increased replication rate. High-throughput sequencing of viral gene segments identified five dominant mutations, whose contribution to the enhanced growth was analyzed by reverse genetics. The increased replication rate was pinpointed to two mutations within the hemagglutinin (HA) gene segment (HA1 D130E, HA2 I91L), near the receptor binding site and the stem domain. The adapted virus also replicated more efficiently in mice in vivo. Enhanced replication rate correlated with increased fusion pH of the HA protein and a decrease in receptor affinity. Our data might be relevant for surveillance of pre-pandemic strains and development of high titer cell culture strains for vaccine production.
DOI: 10.1016/j.virol.2016.02.002
PubMed: 26914510
Links to Exploration step
pubmed:26914510Le document en format XML
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<author><name sortKey="Seeberger, Peter H" sort="Seeberger, Peter H" uniqKey="Seeberger P" first="Peter H" last="Seeberger">Peter H. Seeberger</name>
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<author><name sortKey="Herrmann, Andreas" sort="Herrmann, Andreas" uniqKey="Herrmann A" first="Andreas" last="Herrmann">Andreas Herrmann</name>
<affiliation><nlm:affiliation>Department of Biology, Molecular Biophysics, IRI Life Sciences, Humboldt-Universität zu Berlin, Germany.</nlm:affiliation>
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<author><name sortKey="Meyer, Thomas F" sort="Meyer, Thomas F" uniqKey="Meyer T" first="Thomas F" last="Meyer">Thomas F. Meyer</name>
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</affiliation>
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<term>Dogs</term>
<term>Epithelial Cells (virology)</term>
<term>Gene Expression</term>
<term>Hemagglutinin Glycoproteins, Influenza Virus (chemistry)</term>
<term>Hemagglutinin Glycoproteins, Influenza Virus (genetics)</term>
<term>Hemagglutinin Glycoproteins, Influenza Virus (metabolism)</term>
<term>High-Throughput Nucleotide Sequencing</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Influenza A Virus, H1N1 Subtype (genetics)</term>
<term>Influenza A Virus, H1N1 Subtype (growth & development)</term>
<term>Madin Darby Canine Kidney Cells</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Models, Molecular</term>
<term>Protein Structure, Secondary</term>
<term>Protein Structure, Tertiary</term>
<term>RNA, Viral (genetics)</term>
<term>RNA, Viral (metabolism)</term>
<term>Receptors, Virus (genetics)</term>
<term>Receptors, Virus (metabolism)</term>
<term>Reverse Genetics</term>
<term>Serial Passage</term>
<term>Virus Replication (genetics)</term>
</keywords>
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<term>Hemagglutinin Glycoproteins, Influenza Virus</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>RNA, Viral</term>
<term>Receptors, Virus</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hemagglutinin Glycoproteins, Influenza Virus</term>
<term>RNA, Viral</term>
<term>Receptors, Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term>
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<term>Chickens</term>
<term>Dogs</term>
<term>Gene Expression</term>
<term>High-Throughput Nucleotide Sequencing</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Madin Darby Canine Kidney Cells</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Models, Molecular</term>
<term>Protein Structure, Secondary</term>
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<front><div type="abstract" xml:lang="en">The 2009 influenza pandemic originated from a swine-origin H1N1 virus, which, although less pathogenic than anticipated, may acquire additional virulence-associated mutations in the future. To estimate the potential risk, we sequentially passaged the isolate A/Hamburg/04/2009 in A549 human lung epithelial cells. After passage 6, we observed a 100-fold increased replication rate. High-throughput sequencing of viral gene segments identified five dominant mutations, whose contribution to the enhanced growth was analyzed by reverse genetics. The increased replication rate was pinpointed to two mutations within the hemagglutinin (HA) gene segment (HA1 D130E, HA2 I91L), near the receptor binding site and the stem domain. The adapted virus also replicated more efficiently in mice in vivo. Enhanced replication rate correlated with increased fusion pH of the HA protein and a decrease in receptor affinity. Our data might be relevant for surveillance of pre-pandemic strains and development of high titer cell culture strains for vaccine production. </div>
</front>
</TEI>
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<DateCompleted><Year>2016</Year>
<Month>08</Month>
<Day>16</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>04</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0341</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>492</Volume>
<PubDate><Year>2016</Year>
<Month>May</Month>
</PubDate>
</JournalIssue>
<Title>Virology</Title>
<ISOAbbreviation>Virology</ISOAbbreviation>
</Journal>
<ArticleTitle>Genetic characterization of an adapted pandemic 2009 H1N1 influenza virus that reveals improved replication rates in human lung epithelial cells.</ArticleTitle>
<Pagination><MedlinePgn>118-29</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.virol.2016.02.002</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0042-6822(16)00045-3</ELocationID>
<Abstract><AbstractText>The 2009 influenza pandemic originated from a swine-origin H1N1 virus, which, although less pathogenic than anticipated, may acquire additional virulence-associated mutations in the future. To estimate the potential risk, we sequentially passaged the isolate A/Hamburg/04/2009 in A549 human lung epithelial cells. After passage 6, we observed a 100-fold increased replication rate. High-throughput sequencing of viral gene segments identified five dominant mutations, whose contribution to the enhanced growth was analyzed by reverse genetics. The increased replication rate was pinpointed to two mutations within the hemagglutinin (HA) gene segment (HA1 D130E, HA2 I91L), near the receptor binding site and the stem domain. The adapted virus also replicated more efficiently in mice in vivo. Enhanced replication rate correlated with increased fusion pH of the HA protein and a decrease in receptor affinity. Our data might be relevant for surveillance of pre-pandemic strains and development of high titer cell culture strains for vaccine production. </AbstractText>
<CopyrightInformation>Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wörmann</LastName>
<ForeName>Xenia</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lesch</LastName>
<ForeName>Markus</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany; Steinbeis Innovation gGmbH, Center for Systems Biomedicine, Falkensee, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Welke</LastName>
<ForeName>Robert-William</ForeName>
<Initials>RW</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Molecular Biophysics, IRI Life Sciences, Humboldt-Universität zu Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Okonechnikov</LastName>
<ForeName>Konstantin</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Abdurishid</LastName>
<ForeName>Mirshat</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sieben</LastName>
<ForeName>Christian</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Molecular Biophysics, IRI Life Sciences, Humboldt-Universität zu Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Geissner</LastName>
<ForeName>Andreas</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department for Biomolecular Systems, Max Planck Institute for Colloids and Interfaces, Potsdam, Germany; Institute of Chemistry and Biochemistry, Free University, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Brinkmann</LastName>
<ForeName>Volker</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kastner</LastName>
<ForeName>Markus</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute for Biophysics, Johannes Kepler University, Linz, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Karner</LastName>
<ForeName>Andreas</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Center for Advanced Bioanalysis GmbH (CBL), Linz, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Rong</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Institute for Biophysics, Johannes Kepler University, Linz, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hinterdorfer</LastName>
<ForeName>Peter</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Institute for Biophysics, Johannes Kepler University, Linz, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Anish</LastName>
<ForeName>Chakkumkal</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department for Biomolecular Systems, Max Planck Institute for Colloids and Interfaces, Potsdam, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Seeberger</LastName>
<ForeName>Peter H</ForeName>
<Initials>PH</Initials>
<AffiliationInfo><Affiliation>Department for Biomolecular Systems, Max Planck Institute for Colloids and Interfaces, Potsdam, Germany; Institute of Chemistry and Biochemistry, Free University, Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Herrmann</LastName>
<ForeName>Andreas</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Molecular Biophysics, IRI Life Sciences, Humboldt-Universität zu Berlin, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Meyer</LastName>
<ForeName>Thomas F</ForeName>
<Initials>TF</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany; Steinbeis Innovation gGmbH, Center for Systems Biomedicine, Falkensee, Germany. Electronic address: meyer@mpiib-berlin.mpg.de.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Karlas</LastName>
<ForeName>Alexander</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany; Steinbeis Innovation gGmbH, Center for Systems Biomedicine, Falkensee, Germany. Electronic address: karlas@mpiib-berlin.mpg.de.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>02</Month>
<Day>23</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Virology</MedlineTA>
<NlmUniqueID>0110674</NlmUniqueID>
<ISSNLinking>0042-6822</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019267">Hemagglutinin Glycoproteins, Influenza Virus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012367">RNA, Viral</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000222" MajorTopicYN="N">Adaptation, Physiological</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002645" MajorTopicYN="N">Chickens</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019267" MajorTopicYN="N">Hemagglutinin Glycoproteins, Influenza Virus</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059014" MajorTopicYN="N">High-Throughput Nucleotide Sequencing</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061985" MajorTopicYN="N">Madin Darby Canine Kidney Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008958" MajorTopicYN="N">Models, Molecular</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017433" MajorTopicYN="N">Protein Structure, Secondary</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017434" MajorTopicYN="N">Protein Structure, Tertiary</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012367" MajorTopicYN="N">RNA, Viral</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059386" MajorTopicYN="N">Reverse Genetics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012692" MajorTopicYN="N">Serial Passage</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">A/Hamburg/04/2009</Keyword>
<Keyword MajorTopicYN="N">Hemagglutinin</Keyword>
<Keyword MajorTopicYN="N">High-throughput sequencing</Keyword>
<Keyword MajorTopicYN="N">Reverse genetics</Keyword>
<Keyword MajorTopicYN="N">Viral adaptation</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>11</Month>
<Day>13</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2015</Year>
<Month>12</Month>
<Day>03</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>02</Month>
<Day>03</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2016</Year>
<Month>2</Month>
<Day>26</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2016</Year>
<Month>2</Month>
<Day>26</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2016</Year>
<Month>8</Month>
<Day>17</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">26914510</ArticleId>
<ArticleId IdType="pii">S0042-6822(16)00045-3</ArticleId>
<ArticleId IdType="doi">10.1016/j.virol.2016.02.002</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>
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