Summary of a Meeting on the Origin of Pandemic Influenza Viruses
Identifieur interne : 000210 ( Istex/Corpus ); précédent : 000209; suivant : 000211Summary of a Meeting on the Origin of Pandemic Influenza Viruses
Auteurs : W. Graeme Laver ; Robert G. Webster ; C. M. ChuSource :
- Journal of Infectious Diseases [ 0022-1899 ] ; 1984.
Abstract
Influenza type A virus periodically undergoes major antigenic shifts in which the hemagglutinin (HAG) and sometimes the neuraminidase (NA) antigens are replaced by HAG and NA antigens of another subtype. Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these “new” influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10–12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1–3]. In addition, studies of the genome of the HINI virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. This finding suggests that the virus existed in an animal reservoir during this period [4, 5].
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DOI: 10.1093/infdis/149.1.108
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Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these “new” influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10–12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1–3]. In addition, studies of the genome of the HINI virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. 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Bai</json:string><json:string>Chu Cell</json:string><json:string>Robert A. Lamb</json:string><json:string>Oswaldo Cruz</json:string><json:string>G. Pereira</json:string><json:string>B. L. Lu</json:string><json:string>Gillian Air</json:string><json:string>G. Q. Wang</json:string><json:string>Guo</json:string><json:string>Researchers</json:string><json:string>Y. D. Hou</json:string><json:string>Kuniaki Nerome</json:string><json:string>Y. T. Hou</json:string><json:string>C. M. Chu</json:string><json:string>Don C. Wiley</json:string><json:string>Richard Compans</json:string><json:string>Peter Palese</json:string><json:string>Kennedy Shortridge</json:string><json:string>George G. Brownlee</json:string><json:string>Robert G. Webster</json:string></persName><placeName><json:string>Birmingham</json:string><json:string>Miami</json:string><json:string>Singapore</json:string><json:string>Germany</json:string><json:string>Australia</json:string><json:string>Beijing</json:string><json:string>Bangkok</json:string><json:string>Hong Kong</json:string><json:string>Nashville</json:string><json:string>Canberra</json:string><json:string>Antigenicity</json:string><json:string>People's Republic of China</json:string><json:string>China</json:string><json:string>Shanghai</json:string><json:string>Japan</json:string><json:string>Tokyo</json:string><json:string>Rostock</json:string><json:string>York</json:string><json:string>Cambridge</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[23]</json:string><json:string>[18]</json:string><json:string>[22]</json:string><json:string>July 1968</json:string><json:string>[8]</json:string><json:string>[17]</json:string><json:string>[21]</json:string><json:string>[16]</json:string><json:string>[20]</json:string><json:string>[6, 7]</json:string><json:string>[26]</json:string><json:string>Both et al</json:string><json:string>[7]</json:string><json:string>[25]</json:string><json:string>[1-3]</json:string><json:string>[9]</json:string><json:string>August 1979</json:string><json:string>[24]</json:string><json:string>[19]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/HXZ-19CQCCSR-9</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - microbiology</json:string><json:string>2 - infectious diseases</json:string><json:string>2 - immunology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - microbiology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Infectious Diseases</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Immunology and Allergy</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1984</publicationDate><copyrightDate>1984</copyrightDate><doi><json:string>10.1093/infdis/149.1.108</json:string></doi><id>6B3E9D232A2EBEC8D9865366253F66076B48349E</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-19CQCCSR-9/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-19CQCCSR-9/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/HXZ-19CQCCSR-9/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Summary of a Meeting on the Origin of Pandemic Influenza Viruses</title><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>The University of Chicago Press</publisher><availability><licence>© 1984 by The University of Chicago</licence></availability><date type="Copyright" when="1984">1984</date><date when="1984-01">1984</date></publicationStmt><notesStmt><note type="content-type" source="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="publication-type" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main" xml:lang="en">Summary of a Meeting on the Origin of Pandemic Influenza Viruses</title><author xml:id="author-0000"><persName><surname>Laver</surname><forename type="first">W. Graeme</forename></persName><affiliation><orgName type="institution">Department of Microbiology, John Curtin School of Medical Research, Australian National University</orgName><address><addrLine>Canberra, Australia</addrLine></address></affiliation><affiliation><orgName type="institution">St Jude's Children's Research Hospital</orgName><address><addrLine>Memphis, Tennessee</addrLine></address></affiliation><affiliation><orgName type="institution">Institute of Virology, Chinese Academy of Medical Sciences</orgName><address><addrLine>Beijing, China</addrLine></address></affiliation><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="department">John Curtin School of Medical Research</orgName><orgName type="institution">Australian National University</orgName><address><addrLine>Canberra, Australia</addrLine></address></affiliation><affiliation><orgName type="institution">St Jude's Children's Research Hospital</orgName><address><addrLine>Memphis, Tennessee</addrLine></address></affiliation><affiliation><orgName type="institution">Institute of Virology</orgName><orgName type="institution">Chinese Academy of Medical Sciences</orgName><address><addrLine>Beijing, China</addrLine></address></affiliation></author><author xml:id="author-0001"><persName><surname>Webster</surname><forename type="first">Robert G.</forename></persName><affiliation><orgName type="institution">Department of Microbiology, John Curtin School of Medical Research, Australian National University</orgName><address><addrLine>Canberra, Australia</addrLine></address></affiliation><affiliation><orgName type="institution">St Jude's Children's Research Hospital</orgName><address><addrLine>Memphis, Tennessee</addrLine></address></affiliation><affiliation><orgName type="institution">Institute of Virology, Chinese Academy of Medical Sciences</orgName><address><addrLine>Beijing, China</addrLine></address></affiliation><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="department">John Curtin School of Medical Research</orgName><orgName type="institution">Australian National University</orgName><address><addrLine>Canberra, Australia</addrLine></address></affiliation><affiliation><orgName type="institution">St Jude's Children's Research Hospital</orgName><address><addrLine>Memphis, Tennessee</addrLine></address></affiliation><affiliation><orgName type="institution">Institute of Virology</orgName><orgName type="institution">Chinese Academy of Medical Sciences</orgName><address><addrLine>Beijing, China</addrLine></address></affiliation></author><author xml:id="author-0002"><persName><surname>Chu</surname><forename type="first">C. M.</forename></persName><affiliation><orgName type="institution">Department of Microbiology, John Curtin School of Medical Research, Australian National University</orgName><address><addrLine>Canberra, Australia</addrLine></address></affiliation><affiliation><orgName type="institution">St Jude's Children's Research Hospital</orgName><address><addrLine>Memphis, Tennessee</addrLine></address></affiliation><affiliation><orgName type="institution">Institute of Virology, Chinese Academy of Medical Sciences</orgName><address><addrLine>Beijing, China</addrLine></address></affiliation><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="department">John Curtin School of Medical Research</orgName><orgName type="institution">Australian National University</orgName><address><addrLine>Canberra, Australia</addrLine></address></affiliation><affiliation><orgName type="institution">St Jude's Children's Research Hospital</orgName><address><addrLine>Memphis, Tennessee</addrLine></address></affiliation><affiliation><orgName type="institution">Institute of Virology</orgName><orgName type="institution">Chinese Academy of Medical Sciences</orgName><address><addrLine>Beijing, China</addrLine></address></affiliation></author><idno type="istex">6B3E9D232A2EBEC8D9865366253F66076B48349E</idno><idno type="ark">ark:/67375/HXZ-19CQCCSR-9</idno><idno type="DOI">10.1093/infdis/149.1.108</idno></analytic><monogr><title level="j" type="main">Journal of Infectious Diseases</title><title level="j" type="abbrev">J Infect Dis.</title><idno type="hwp">jinfdis</idno><idno type="publisher-id">jid</idno><idno type="pISSN">0022-1899</idno><idno type="eISSN">1537-6613</idno><imprint><publisher>The University of Chicago Press</publisher><date when="1984-01">1984</date><biblScope unit="vol">149</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="108">108</biblScope><biblScope unit="page" to="115">115</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-09"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract><p>Influenza type A virus periodically undergoes major antigenic shifts in which the hemagglutinin (HAG) and sometimes the neuraminidase (NA) antigens are replaced by HAG and NA antigens of another subtype. Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these “new” influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10–12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1–3]. In addition, studies of the genome of the HINI virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. This finding suggests that the virus existed in an animal reservoir during this period [4, 5].</p></abstract><textClass ana="subject"><keywords scheme="heading"><term>Institutional Report</term></keywords></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-09" who="#istex" xml:id="pub2tei">formatting</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2019-12-11">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-19CQCCSR-9/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup, element #text not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article">
<front>
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<journal-id journal-id-type="hwp">jinfdis</journal-id>
<journal-id journal-id-type="publisher-id">jid</journal-id>
<journal-title>Journal of Infectious Diseases</journal-title>
<abbrev-journal-title>J Infect Dis.</abbrev-journal-title>
<issn pub-type="ppub">0022-1899</issn>
<issn pub-type="epub">1537-6613</issn>
<publisher>
<publisher-name>The University of Chicago Press</publisher-name>
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<article-id pub-id-type="doi">10.1093/infdis/149.1.108</article-id>
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<subj-group subj-group-type="heading">
<subject>Institutional Report</subject>
<subj-group>
<subject>National Institutes of Health</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Summary of a Meeting on the Origin of Pandemic Influenza Viruses</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Laver</surname>
<given-names>W. Graeme</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Webster</surname>
<given-names>Robert G.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Chu</surname>
<given-names>C. M.</given-names>
</name>
</contrib>
<aff>From the <institution>Department of Microbiology, John Curtin School of Medical Research, Australian National University</institution>, <addr-line>Canberra, Australia</addr-line></aff>
<aff><institution>St Jude's Children's Research Hospital</institution>, <addr-line>Memphis, Tennessee</addr-line></aff>
<aff>the <institution>Institute of Virology, Chinese Academy of Medical Sciences</institution>, <addr-line>Beijing, China</addr-line></aff>
</contrib-group>
<author-notes>
<fn fn-type="other">
<p>Participants at this meeting included Gillian Air, Labs of Special Cancer Research, Birmingham, Ala; B. A. Askonas, National Institute for Medical Research, London; Z. S. Bai, Chinese Academy of Medical Sciences, Beijing; Gerry W. Both, Genetics Research Laboratories, North Ryde, Australia; George G. Brownlee, Oxford University, Oxford, England; H. S. Chen, Chinese Academy of Medical Sciences; C. M. Chu, Chinese Academy of Medical Sciences; Peter Colman, Commonwealth Scientific and Industrial Research Organization, Parkville, Australia; Richard Compans, University of Alabama Medical Center, Birmingham; Xin-chang Gong, Chinese Academy of Medical Sciences; Y. J. Guo, Chinese Academy of Medical Sciences; Virginia S. Hinshaw, St Jude's Children's Research Hospital, Memphis; Y. D. Hou, Chinese Academy of Medical Sciences; David C. Jackson, University of Melbourne, Parkville; Robert M. Krug, Memorial Sloan-Kettering Cancer Center, New York; C. J. Lai, National Institute of Allergy and Infectious Diseases, Bethesda, Md; Robert A. Lamb, Northwestern University, Evanston, Ill; W. Graeme Laver, Australian National University, Canberra, Australia; B. L. Lu, National Vaccine and Serum Institute, Beijing; Kuniaki Nerome, National Institute of Health, Tokyo; Peter Palese, Mt Sinai School of Medicine, New York; Helio G. Pereira, Fundaçåo Oswaldo Cruz, Rio de Janeiro; Chris Scholtissek, Institut für Virologie der Justus-Liebig-Universität, Giessen, West Germany; F. Z. Shen, Chinese Academy of Medical Sciences; Kennedy Shortridge, University of Hong Kong, Hong Kong; John Skehel, National Institute for Medical Research; C. Q. Wang, Chinese Academy of Medical Sciences; Colin Ward, Commonwealth Scientific and Industrial Research Organization; Robert G. Webster, St Jude's Children's Research Hospital; Don C. Wiley, Harvard University, Cambridge, Mass; Peter F. Wright, Vanderbilt University, Nashville, Tenn; and Y. H. Zhang, Chinese Academy of Medical Sciences.</p>
</fn>
<fn fn-type="other">
<p>This meeting was sponsored by the Institute of Virology of the Chinese Academy of Medical Sciences and by the Australian National University. Partial support was provided by grant 1 R13 AI 19076-01 from the National Institute of Allergy and Infectious Diseases, the Australian National' University, the Australia-China Council, Burroughs-Wellcome Company, the Commonwealth Scientific and Industrial Research Organization, Merck Sharp and Dohme Research Laboratories, the Overseas Telecommunications Commission (Australia), and Flow Laboratories (Australia). The proceedings will be published by Elsevier/North-Holland.</p>
</fn>
<fn fn-type="other">
<p>Please address requests for reprints to Dr John R. LaMontagne, Development and Applications Branch, Microbiology and Infectious Diseases Program, National Institute of Allergy and Infectious Diseases, Room 750, Westwood Building, Bethesda, Maryland 20205.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub">
<month>1</month>
<year>1984</year>
</pub-date>
<volume>149</volume>
<issue>1</issue>
<fpage>108</fpage>
<lpage>115</lpage>
<copyright-statement>© 1984 by The University of Chicago</copyright-statement>
<copyright-year>1984</copyright-year>
<abstract>
<p>Influenza type A virus periodically undergoes major antigenic shifts in which the hemagglutinin (HAG) and sometimes the neuraminidase (NA) antigens are replaced by HAG and NA antigens of another subtype. Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these “new” influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10–12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1–3]. In addition, studies of the genome of the HINI virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. This finding suggests that the virus existed in an animal reservoir during this period [4, 5].</p>
</abstract>
</article-meta>
</front>
</article>
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Graeme</namePart><namePart type="family">Laver</namePart><affiliation>Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra, Australia, Memphis, Tennessee, Beijing, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert G.</namePart><namePart type="family">Webster</namePart><affiliation>Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra, Australia, Memphis, Tennessee, Beijing, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. 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Three such shifts have taken place since the virus was first isolated, and all appear to have occurred in China. The way in which these “new” influenza type A viruses suddenly appear (or reappear) in the human population is not known. At a meeting held in Beijing, China, on November 10–12, 1982, participants discussed the latest findings on the molecular biology of influenza viruses and on aspects of their ecology that may offer insight into the factors responsible for the origin of pandemic influenza viruses. Information obtained in earlier studies has provided some clues about how the antigenic shifts may occur. For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1–3]. In addition, studies of the genome of the HINI virus that appeared in Anshan, China, in 1977 have shown that this virus almost certainly underwent no replication for 27 years. This finding suggests that the virus existed in an animal reservoir during this period [4, 5].</abstract><note type="footnotes">Participants at this meeting included Gillian Air, Labs of Special Cancer Research, Birmingham, Ala; B. A. Askonas, National Institute for Medical Research, London; Z. S. Bai, Chinese Academy of Medical Sciences, Beijing; Gerry W. Both, Genetics Research Laboratories, North Ryde, Australia; George G. Brownlee, Oxford University, Oxford, England; H. S. Chen, Chinese Academy of Medical Sciences; C. M. Chu, Chinese Academy of Medical Sciences; Peter Colman, Commonwealth Scientific and Industrial Research Organization, Parkville, Australia; Richard Compans, University of Alabama Medical Center, Birmingham; Xin-chang Gong, Chinese Academy of Medical Sciences; Y. J. 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