Surface glycoproteins determine the feature of the 2009 pandemic H1N1 virus
Identifieur interne : 000842 ( Ncbi/Merge ); précédent : 000841; suivant : 000843Surface glycoproteins determine the feature of the 2009 pandemic H1N1 virus
Auteurs : Jin Il Kim [Corée du Sud] ; Ilseob Lee [Corée du Sud] ; Sehee Park [Corée du Sud] ; Man-Seong Park [Corée du Sud]Source :
- BMB Reports [ 1976-6696 ] ; 2012.
Abstract
After the outbreak of the swine-origin influenza A H1N1 virus in April 2009, World Health Organization declared this novel H1N1 virus as the first pandemic influenza virus (2009 pH1N1) of the 21st century. To elucidate the characteristics of 2009 pH1N1, the growth properties of A/Korea/01/09 (K/09) was analyzed in cells. Interestingly, the maximal titer of K/09 was higher than that of a seasonal H1N1 virus isolated in Korea 2008 (S/08) though the RNP complex of K/09 was less competent than that of S/08. In addition, the NS1 protein of K/09 was determined as a weak interferon antagonist as compared to that of S/08. Thus, in order to confine genetic determinants of K/09, activities of two major surface glycoproteins were analyzed. Interestingly, K/09 possesses highly reactive NA proteins and weak HA cell-binding avidity. These findings suggest that the surface glycoproteins might be a key factor in the features of 2009 pH1N1. [BMB Reports 2012; 45(11): 653-658]
Url:
DOI: 10.5483/BMBRep.2012.45.11.137
PubMed: 23187005
PubMed Central: 4133798
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200-702</wicri:regionArea><wicri:noRegion>Chuncheon 200-702</wicri:noRegion></affiliation></author></analytic><series><title level="j">BMB Reports</title><idno type="ISSN">1976-6696</idno><idno type="eISSN">1976-670X</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>After the outbreak of the swine-origin influenza A H1N1 virus in April 2009, World Health Organization declared this novel H1N1 virus as the first pandemic influenza virus (2009 pH1N1) of the 21<sup>st</sup> century. To elucidate the characteristics of 2009 pH1N1, the growth properties of A/Korea/01/09 (K/09) was analyzed in cells. Interestingly, the maximal titer of K/09 was higher than that of a seasonal H1N1 virus isolated in Korea 2008 (S/08) though the RNP complex of K/09 was less competent than that of S/08. In addition, the NS1 protein of K/09 was determined as a weak interferon antagonist as compared to that of S/08. Thus, in order to confine genetic determinants of K/09, activities of two major surface glycoproteins were analyzed. Interestingly, K/09 possesses highly reactive NA proteins and weak HA cell-binding avidity. These findings suggest that the surface glycoproteins might be a key factor in the features of 2009 pH1N1. [BMB Reports 2012; 45(11): 653-658]</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Neumann, G" uniqKey="Neumann G">G. Neumann</name></author><author><name sortKey="Noda, T" uniqKey="Noda T">T. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">BMB Rep</journal-id><journal-id journal-id-type="iso-abbrev">BMB Rep</journal-id><journal-id journal-id-type="publisher-id">ksbmb</journal-id><journal-title-group><journal-title>BMB Reports</journal-title></journal-title-group><issn pub-type="ppub">1976-6696</issn><issn pub-type="epub">1976-670X</issn><publisher><publisher-name>Korean Society for Biochemistry and Molecular Biology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23187005</article-id><article-id pub-id-type="pmc">4133798</article-id><article-id pub-id-type="publisher-id">BMB-45-653</article-id><article-id pub-id-type="doi">10.5483/BMBRep.2012.45.11.137</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Articles</subject></subj-group></article-categories><title-group><article-title>Surface glycoproteins determine the feature of the 2009 pandemic H1N1 virus</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Kim</surname><given-names>Jin Il</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="corresp" rid="cor2">#</xref></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Ilseob</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="corresp" rid="cor2">#</xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>Sehee</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="corresp" rid="cor2">#</xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>Man-Seong</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Microbiology, Hallym University, Chuncheon 200-702, Korea</aff><aff id="A2"><label>2</label>Center for Medical Science Research, College of Medicine, Hallym University, Chuncheon 200-702, Korea</aff><author-notes><corresp id="cor1"><label>*</label>Corresponding author. Tel: +82-33-248-2632; Fax: +82-33-252-2843; E-mail: <email>ms0392@hallym.ac.kr</email></corresp><corresp id="cor2"><label>#</label>These authors contributed equally to this work.</corresp></author-notes><pub-date pub-type="ppub"><month>11</month><year>2012</year></pub-date><volume>45</volume><issue>11</issue><fpage>653</fpage><lpage>658</lpage><history><date date-type="received"><day>02</day><month>7</month><year>2012</year></date><date date-type="rev-recd"><day>04</day><month>7</month><year>2012</year></date><date date-type="accepted"><day>16</day><month>7</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2012, Korean Society for Biochemistry and Molecular Biology</copyright-statement><copyright-year>2012</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</ext-link>) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>After the outbreak of the swine-origin influenza A H1N1 virus in April 2009, World Health Organization declared this novel H1N1 virus as the first pandemic influenza virus (2009 pH1N1) of the 21<sup>st</sup> century. To elucidate the characteristics of 2009 pH1N1, the growth properties of A/Korea/01/09 (K/09) was analyzed in cells. Interestingly, the maximal titer of K/09 was higher than that of a seasonal H1N1 virus isolated in Korea 2008 (S/08) though the RNP complex of K/09 was less competent than that of S/08. In addition, the NS1 protein of K/09 was determined as a weak interferon antagonist as compared to that of S/08. Thus, in order to confine genetic determinants of K/09, activities of two major surface glycoproteins were analyzed. Interestingly, K/09 possesses highly reactive NA proteins and weak HA cell-binding avidity. These findings suggest that the surface glycoproteins might be a key factor in the features of 2009 pH1N1. [BMB Reports 2012; 45(11): 653-658]</p></abstract><kwd-group kwd-group-type="author"><kwd>Glycoprotein</kwd><kwd>Hemagglutinin</kwd><kwd>Influenza</kwd><kwd>Pandemic</kwd></kwd-group></article-meta></front></pmc><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Kim, Jin Il" sort="Kim, Jin Il" uniqKey="Kim J" first="Jin Il" last="Kim">Jin Il Kim</name></noRegion><name sortKey="Kim, Jin Il" sort="Kim, Jin Il" uniqKey="Kim J" first="Jin Il" last="Kim">Jin Il Kim</name><name sortKey="Lee, Ilseob" sort="Lee, Ilseob" uniqKey="Lee I" first="Ilseob" last="Lee">Ilseob Lee</name><name sortKey="Lee, Ilseob" sort="Lee, Ilseob" uniqKey="Lee I" first="Ilseob" last="Lee">Ilseob Lee</name><name sortKey="Park, Man Seong" sort="Park, Man Seong" uniqKey="Park M" first="Man-Seong" last="Park">Man-Seong Park</name><name sortKey="Park, Man Seong" sort="Park, Man Seong" uniqKey="Park M" first="Man-Seong" last="Park">Man-Seong Park</name><name sortKey="Park, Sehee" sort="Park, Sehee" uniqKey="Park S" first="Sehee" last="Park">Sehee Park</name><name sortKey="Park, Sehee" sort="Park, Sehee" uniqKey="Park S" first="Sehee" last="Park">Sehee Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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