Characterization of the 1918 “Spanish” Influenza Virus Matrix Gene Segment
Identifieur interne : 000375 ( Pmc/Curation ); précédent : 000374; suivant : 000376Characterization of the 1918 “Spanish” Influenza Virus Matrix Gene Segment
Auteurs : Ann H. Reid [États-Unis] ; Thomas G. Fanning [États-Unis] ; Thomas A. Janczewski [États-Unis] ; Sherman Mccall [États-Unis] ; Jeffery K. Taubenberger [États-Unis]Source :
- Journal of Virology [ 0022-538X ] ; 2002.
Abstract
The coding region of influenza A virus RNA segment 7 from the 1918 pandemic virus, consisting of the open reading frames of the two matrix genes M1 and M2, has been sequenced. While this segment is highly conserved among influenza virus strains, the 1918 sequence does not match any previously sequenced influenza virus strains. The 1918 sequence matches the consensus over the M1 RNA-binding domains and nuclear localization signal and the highly conserved transmembrane domain of M2. Amino acid changes that correlate with high yield and pathogenicity in animal models were not found in the 1918 strain. Phylogenetic analyses suggest that both genes were mammalian adapted and that the 1918 sequence is very similar to the common ancestor of all subsequent human and classical swine matrix segments. The 1918 sequence matches other mammalian strains at 4 amino acids in the extracellular domain of M2 that differ consistently between avian and mammalian strains, suggesting that the matrix segment may have been circulating in human strains for at least several years before 1918.
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DOI: 10.1128/JVI.76.21.10717-10723.2002
PubMed: 12368314
PubMed Central: 136643
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Reid</name><affiliation wicri:level="2"><nlm:aff id="aff0">Division of Molecular Pathology, Department of Cellular Pathology and Genetics, Armed Forces Institute of Pathology, Rockville, Maryland 20850-3125</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Division of Molecular Pathology, Department of Cellular Pathology and Genetics, Armed Forces Institute of Pathology, Rockville</wicri:cityArea></affiliation></author><author><name sortKey="Fanning, Thomas G" sort="Fanning, Thomas G" uniqKey="Fanning T" first="Thomas G." last="Fanning">Thomas G. 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Taubenberger</name><affiliation wicri:level="2"><nlm:aff id="aff0">Division of Molecular Pathology, Department of Cellular Pathology and Genetics, Armed Forces Institute of Pathology, Rockville, Maryland 20850-3125</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Division of Molecular Pathology, Department of Cellular Pathology and Genetics, Armed Forces Institute of Pathology, Rockville</wicri:cityArea></affiliation></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="2002">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The coding region of influenza A virus RNA segment 7 from the 1918 pandemic virus, consisting of the open reading frames of the two matrix genes M1 and M2, has been sequenced. While this segment is highly conserved among influenza virus strains, the 1918 sequence does not match any previously sequenced influenza virus strains. The 1918 sequence matches the consensus over the M1 RNA-binding domains and nuclear localization signal and the highly conserved transmembrane domain of M2. Amino acid changes that correlate with high yield and pathogenicity in animal models were not found in the 1918 strain. Phylogenetic analyses suggest that both genes were mammalian adapted and that the 1918 sequence is very similar to the common ancestor of all subsequent human and classical swine matrix segments. The 1918 sequence matches other mammalian strains at 4 amino acids in the extracellular domain of M2 that differ consistently between avian and mammalian strains, suggesting that the matrix segment may have been circulating in human strains for at least several years before 1918.</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="publisher-id">jvi</journal-id><journal-title>Journal of Virology</journal-title><issn pub-type="ppub">0022-538X</issn><issn pub-type="epub">1098-5514</issn><publisher><publisher-name>American Society for Microbiology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">12368314</article-id><article-id pub-id-type="pmc">136643</article-id><article-id pub-id-type="publisher-id">0952</article-id><article-id pub-id-type="doi">10.1128/JVI.76.21.10717-10723.2002</article-id><article-categories><subj-group subj-group-type="heading"><subject>Recombination and Evolution</subject></subj-group></article-categories><title-group><article-title>Characterization of the 1918 “Spanish” Influenza Virus Matrix Gene Segment</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Reid</surname><given-names>Ann H.</given-names></name><xref ref-type="aff" rid="aff0"></xref><xref ref-type="corresp" rid="cor1">*</xref></contrib><contrib contrib-type="author"><name><surname>Fanning</surname><given-names>Thomas G.</given-names></name><xref ref-type="aff" rid="aff0"></xref></contrib><contrib contrib-type="author"><name><surname>Janczewski</surname><given-names>Thomas A.</given-names></name><xref ref-type="aff" rid="aff0"></xref></contrib><contrib contrib-type="author"><name><surname>McCall</surname><given-names>Sherman</given-names></name><xref ref-type="aff" rid="aff0"></xref></contrib><contrib contrib-type="author"><name><surname>Taubenberger</surname><given-names>Jeffery K.</given-names></name><xref ref-type="aff" rid="aff0"></xref></contrib></contrib-group><aff id="aff0">Division of Molecular Pathology, Department of Cellular Pathology and Genetics, Armed Forces Institute of Pathology, Rockville, Maryland 20850-3125</aff><author-notes><fn id="cor1"><label>*</label><p>Corresponding author. Mailing address: Armed Forces Institute of Pathology, Department of Cellular Pathology and Genetics, 1413 Research Blvd., Building 101, Rm. 1057, Rockville, MD 20850-3125. Phone: (301) 319-0288. Fax: (301) 295-9507. E-mail: <email>Reid@afip.osd.mil</email>.</p></fn></author-notes><pub-date pub-type="ppub"><month>11</month><year>2002</year></pub-date><volume>76</volume><issue>21</issue><fpage>10717</fpage><lpage>10723</lpage><history><date date-type="received"><day>10</day><month>5</month><year>2002</year></date><date date-type="accepted"><day>29</day><month>7</month><year>2002</year></date></history><copyright-statement>Copyright © 2002, American Society for Microbiology</copyright-statement><copyright-year>2002</copyright-year><abstract><p>The coding region of influenza A virus RNA segment 7 from the 1918 pandemic virus, consisting of the open reading frames of the two matrix genes M1 and M2, has been sequenced. While this segment is highly conserved among influenza virus strains, the 1918 sequence does not match any previously sequenced influenza virus strains. The 1918 sequence matches the consensus over the M1 RNA-binding domains and nuclear localization signal and the highly conserved transmembrane domain of M2. Amino acid changes that correlate with high yield and pathogenicity in animal models were not found in the 1918 strain. Phylogenetic analyses suggest that both genes were mammalian adapted and that the 1918 sequence is very similar to the common ancestor of all subsequent human and classical swine matrix segments. The 1918 sequence matches other mammalian strains at 4 amino acids in the extracellular domain of M2 that differ consistently between avian and mammalian strains, suggesting that the matrix segment may have been circulating in human strains for at least several years before 1918.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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