Analysis by Single-Gene Reassortment Demonstrates that the 1918 Influenza Virus Is Functionally Compatible with a Low-Pathogenicity Avian Influenza Virus in Mice
Identifieur interne : 000738 ( Pmc/Curation ); précédent : 000737; suivant : 000739Analysis by Single-Gene Reassortment Demonstrates that the 1918 Influenza Virus Is Functionally Compatible with a Low-Pathogenicity Avian Influenza Virus in Mice
Auteurs : Li Qi ; A. Sally Davis ; Brett W. Jagger ; Louis M. Schwartzman ; Eleca J. Dunham ; John C. Kash ; Jeffery K. TaubenbergerSource :
- Journal of Virology [ 0022-538X ] ; 2012.
Abstract
The 1918-1919 “Spanish” influenza pandemic is estimated to have caused 50 million deaths worldwide. Understanding the origin, virulence, and pathogenic properties of past pandemic influenza viruses, including the 1918 virus, is crucial for current public health preparedness and future pandemic planning. The origin of the 1918 pandemic virus has not been resolved, but its coding sequences are very like those of avian influenza virus. The proteins encoded by the 1918 virus differ from typical low-pathogenicity avian influenza viruses at only a small number of amino acids in each open reading frame. In this study, a series of chimeric 1918 influenza viruses were created in which each of the eight 1918 pandemic virus gene segments was replaced individually with the corresponding gene segment of a prototypical low-pathogenicity avian influenza (LPAI) H1N1 virus in order to investigate functional compatibility of the 1918 virus genome with gene segments from an LPAI virus and to identify gene segments and mutations important for mammalian adaptation. This set of eight “7:1” chimeric viruses was compared to the parental 1918 and LPAI H1N1 viruses in intranasally infected mice. Seven of the 1918 LPAI 7:1 chimeric viruses replicated and caused disease equivalent to the fully reconstructed 1918 virus. Only the chimeric 1918 virus containing the avian influenza PB2 gene segment was attenuated in mice. This attenuation could be corrected by the single E627K amino acid change, further confirming the importance of this change in mammalian adaptation and mouse pathogenicity. While the mechanisms of influenza virus host switch, and particularly mammalian host adaptation are still only partly understood, these data suggest that the 1918 virus, whatever its origin, is very similar to avian influenza virus.
Url:
DOI: 10.1128/JVI.00887-12
PubMed: 22718825
PubMed Central: 3416129
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000738
Links to Exploration step
PMC:3416129Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Analysis by Single-Gene Reassortment Demonstrates that the 1918 Influenza Virus Is Functionally Compatible with a Low-Pathogenicity Avian Influenza Virus in Mice</title>
<author><name sortKey="Qi, Li" sort="Qi, Li" uniqKey="Qi L" first="Li" last="Qi">Li Qi</name>
</author>
<author><name sortKey="Davis, A Sally" sort="Davis, A Sally" uniqKey="Davis A" first="A. Sally" last="Davis">A. Sally Davis</name>
</author>
<author><name sortKey="Jagger, Brett W" sort="Jagger, Brett W" uniqKey="Jagger B" first="Brett W." last="Jagger">Brett W. Jagger</name>
</author>
<author><name sortKey="Schwartzman, Louis M" sort="Schwartzman, Louis M" uniqKey="Schwartzman L" first="Louis M." last="Schwartzman">Louis M. Schwartzman</name>
</author>
<author><name sortKey="Dunham, Eleca J" sort="Dunham, Eleca J" uniqKey="Dunham E" first="Eleca J." last="Dunham">Eleca J. Dunham</name>
</author>
<author><name sortKey="Kash, John C" sort="Kash, John C" uniqKey="Kash J" first="John C." last="Kash">John C. Kash</name>
</author>
<author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K." last="Taubenberger">Jeffery K. Taubenberger</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">22718825</idno>
<idno type="pmc">3416129</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416129</idno>
<idno type="RBID">PMC:3416129</idno>
<idno type="doi">10.1128/JVI.00887-12</idno>
<date when="2012">2012</date>
<idno type="wicri:Area/Pmc/Corpus">000738</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000738</idno>
<idno type="wicri:Area/Pmc/Curation">000738</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000738</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Analysis by Single-Gene Reassortment Demonstrates that the 1918 Influenza Virus Is Functionally Compatible with a Low-Pathogenicity Avian Influenza Virus in Mice</title>
<author><name sortKey="Qi, Li" sort="Qi, Li" uniqKey="Qi L" first="Li" last="Qi">Li Qi</name>
</author>
<author><name sortKey="Davis, A Sally" sort="Davis, A Sally" uniqKey="Davis A" first="A. Sally" last="Davis">A. Sally Davis</name>
</author>
<author><name sortKey="Jagger, Brett W" sort="Jagger, Brett W" uniqKey="Jagger B" first="Brett W." last="Jagger">Brett W. Jagger</name>
</author>
<author><name sortKey="Schwartzman, Louis M" sort="Schwartzman, Louis M" uniqKey="Schwartzman L" first="Louis M." last="Schwartzman">Louis M. Schwartzman</name>
</author>
<author><name sortKey="Dunham, Eleca J" sort="Dunham, Eleca J" uniqKey="Dunham E" first="Eleca J." last="Dunham">Eleca J. Dunham</name>
</author>
<author><name sortKey="Kash, John C" sort="Kash, John C" uniqKey="Kash J" first="John C." last="Kash">John C. Kash</name>
</author>
<author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K." last="Taubenberger">Jeffery K. Taubenberger</name>
</author>
</analytic>
<series><title level="j">Journal of Virology</title>
<idno type="ISSN">0022-538X</idno>
<idno type="eISSN">1098-5514</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>The 1918-1919 “Spanish” influenza pandemic is estimated to have caused 50 million deaths worldwide. Understanding the origin, virulence, and pathogenic properties of past pandemic influenza viruses, including the 1918 virus, is crucial for current public health preparedness and future pandemic planning. The origin of the 1918 pandemic virus has not been resolved, but its coding sequences are very like those of avian influenza virus. The proteins encoded by the 1918 virus differ from typical low-pathogenicity avian influenza viruses at only a small number of amino acids in each open reading frame. In this study, a series of chimeric 1918 influenza viruses were created in which each of the eight 1918 pandemic virus gene segments was replaced individually with the corresponding gene segment of a prototypical low-pathogenicity avian influenza (LPAI) H1N1 virus in order to investigate functional compatibility of the 1918 virus genome with gene segments from an LPAI virus and to identify gene segments and mutations important for mammalian adaptation. This set of eight “7:1” chimeric viruses was compared to the parental 1918 and LPAI H1N1 viruses in intranasally infected mice. Seven of the 1918 LPAI 7:1 chimeric viruses replicated and caused disease equivalent to the fully reconstructed 1918 virus. Only the chimeric 1918 virus containing the avian influenza PB2 gene segment was attenuated in mice. This attenuation could be corrected by the single E627K amino acid change, further confirming the importance of this change in mammalian adaptation and mouse pathogenicity. While the mechanisms of influenza virus host switch, and particularly mammalian host adaptation are still only partly understood, these data suggest that the 1918 virus, whatever its origin, is very similar to avian influenza virus.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><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>
<journal-id journal-id-type="publisher-id">JVI</journal-id>
<journal-title-group><journal-title>Journal of Virology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0022-538X</issn>
<issn pub-type="epub">1098-5514</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
<publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">22718825</article-id>
<article-id pub-id-type="pmc">3416129</article-id>
<article-id pub-id-type="publisher-id">00887-12</article-id>
<article-id pub-id-type="doi">10.1128/JVI.00887-12</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Pathogenesis and Immunity</subject>
</subj-group>
</article-categories>
<title-group><article-title>Analysis by Single-Gene Reassortment Demonstrates that the 1918 Influenza Virus Is Functionally Compatible with a Low-Pathogenicity Avian Influenza Virus in Mice</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Qi</surname>
<given-names>Li</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Davis</surname>
<given-names>A. Sally</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Jagger</surname>
<given-names>Brett W.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Schwartzman</surname>
<given-names>Louis M.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Dunham</surname>
<given-names>Eleca J.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Kash</surname>
<given-names>John C.</given-names>
</name>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Taubenberger</surname>
<given-names>Jeffery K.</given-names>
</name>
</contrib>
<aff>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</aff>
</contrib-group>
<author-notes><corresp>Address correspondence to Jeffery K. Taubenberger, <email>taubenbergerj@niaid.nih.gov</email>
.</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>9</month>
<year>2012</year>
</pub-date>
<volume>86</volume>
<issue>17</issue>
<fpage>9211</fpage>
<lpage>9220</lpage>
<history><date date-type="received"><day>9</day>
<month>4</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>6</day>
<month>6</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2012, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2012</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zjv01712009211.pdf"></self-uri>
<abstract><p>The 1918-1919 “Spanish” influenza pandemic is estimated to have caused 50 million deaths worldwide. Understanding the origin, virulence, and pathogenic properties of past pandemic influenza viruses, including the 1918 virus, is crucial for current public health preparedness and future pandemic planning. The origin of the 1918 pandemic virus has not been resolved, but its coding sequences are very like those of avian influenza virus. The proteins encoded by the 1918 virus differ from typical low-pathogenicity avian influenza viruses at only a small number of amino acids in each open reading frame. In this study, a series of chimeric 1918 influenza viruses were created in which each of the eight 1918 pandemic virus gene segments was replaced individually with the corresponding gene segment of a prototypical low-pathogenicity avian influenza (LPAI) H1N1 virus in order to investigate functional compatibility of the 1918 virus genome with gene segments from an LPAI virus and to identify gene segments and mutations important for mammalian adaptation. This set of eight “7:1” chimeric viruses was compared to the parental 1918 and LPAI H1N1 viruses in intranasally infected mice. Seven of the 1918 LPAI 7:1 chimeric viruses replicated and caused disease equivalent to the fully reconstructed 1918 virus. Only the chimeric 1918 virus containing the avian influenza PB2 gene segment was attenuated in mice. This attenuation could be corrected by the single E627K amino acid change, further confirming the importance of this change in mammalian adaptation and mouse pathogenicity. While the mechanisms of influenza virus host switch, and particularly mammalian host adaptation are still only partly understood, these data suggest that the 1918 virus, whatever its origin, is very similar to avian influenza virus.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/PandemieGrippaleV1/Data/Pmc/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000738 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd -nk 000738 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= PandemieGrippaleV1 |flux= Pmc |étape= Curation |type= RBID |clé= PMC:3416129 |texte= Analysis by Single-Gene Reassortment Demonstrates that the 1918 Influenza Virus Is Functionally Compatible with a Low-Pathogenicity Avian Influenza Virus in Mice }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Curation/RBID.i -Sk "pubmed:22718825" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd \ | NlmPubMed2Wicri -a PandemieGrippaleV1
This area was generated with Dilib version V0.6.34. |