Temperature-sensitive mutants of influenza virus
Identifieur interne : 000405 ( Istex/Corpus ); précédent : 000404; suivant : 000406Temperature-sensitive mutants of influenza virus
Auteurs : Brian R. Murphy ; Susan B. Spring ; Douglas D. Richman ; Eveline L. Tierney ; Julius Kasel ; Robert M. ChanockSource :
- Virology [ 0042-6822 ] ; 1975.
English descriptors
- Teeft :
- Allantoic cavity, Chanock, Clone, Complementation, Complementation group, Complementation groups, Genetic, Genetic interaction, Genetic stability, Genome, Glycoprotein, Greater reduction, Hemagglutinin, Hemagglutinin glycoproteins, High titer, Hong virus, Honl, Honl virus, Influenza, Influenza virus, Lesion, Monolayer cultures, Mutant, Neuraminidase, Neuraminidase gene, Neuraminidase glycoprotein, Neuraminidase glycoproteins, Neuraminidase subtype, Pairwise matings, Parent virus, Plaque, Plaque formation, Poisson distribution, Present study, Recombinant, Recombinant clones, Recombinant viruses, Recombination, Same complementation group, Shutoff, Shutoff temperature, Surface antigens, Tissue culture, Vaccine, Virus, Virus genome, Virus titer, Virus vaccine.
Abstract
Abstract: The nature of the genetic defect(s) present in the influenza A/Hong Kong/1968-ts-1[E] (H3N2) candidate vaccine virus, was analyzed by transferring them by genetic recombination to a 1943 HON1 wild-type virus. Three classes of ts viruses bearing the HO hemagglutinin were identified. One class consisted of two clones of virus, R1 and R8, which underwent complementation-recombination with each other but not with the Hong Kong/1968 (H3N2)-ts-1[E] parent virus. The second class consisted of clones of virus, such as R4 and R11, that failed to undergo complementation-recombination with R1, with R8, or with the ts-1[E] parent. These data indicated that the parent Hong Kong ts-1[E] virus possessed two ts lesions that segregated independently of each other and were presumably on different segments of the influenza A virus genome. The third class of ts mutants consisted of a spontaneously occurring ts mutant, clone R9; this clone underwent complementation-recombination with the ts-1[E] parent and other HO-ts recombinants and was shown to belong to a complementation group different than clones R1 and R8. The ts defects present in the Hong Kong-ts-1[E] donor virus segregated independently of the genes that coded for the epidemiologically important surface antigens, i.e., the hemagglutinin and the neuraminidase glycoproteins. The implications of these findings for the development of a live attenuated influenza virus vaccine are discussed.
Url:
DOI: 10.1016/0042-6822(75)90225-1
Links to Exploration step
ISTEX:EA11C8075B2914DDDDD171445EC72E9113F5DE1BLe document en format XML
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Tierney</name><affiliation><mods:affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</mods:affiliation></affiliation></author><author><name sortKey="Kasel, Julius" sort="Kasel, Julius" uniqKey="Kasel J" first="Julius" last="Kasel">Julius Kasel</name><affiliation><mods:affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</mods:affiliation></affiliation></author><author><name sortKey="Chanock, Robert M" sort="Chanock, Robert M" uniqKey="Chanock R" first="Robert M" last="Chanock">Robert M. Chanock</name><affiliation><mods:affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1975">1975</date><biblScope unit="volume">66</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="533">533</biblScope><biblScope unit="page" to="541">541</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Allantoic cavity</term><term>Chanock</term><term>Clone</term><term>Complementation</term><term>Complementation group</term><term>Complementation groups</term><term>Genetic</term><term>Genetic interaction</term><term>Genetic stability</term><term>Genome</term><term>Glycoprotein</term><term>Greater reduction</term><term>Hemagglutinin</term><term>Hemagglutinin glycoproteins</term><term>High titer</term><term>Hong virus</term><term>Honl</term><term>Honl virus</term><term>Influenza</term><term>Influenza virus</term><term>Lesion</term><term>Monolayer cultures</term><term>Mutant</term><term>Neuraminidase</term><term>Neuraminidase gene</term><term>Neuraminidase glycoprotein</term><term>Neuraminidase glycoproteins</term><term>Neuraminidase subtype</term><term>Pairwise matings</term><term>Parent virus</term><term>Plaque</term><term>Plaque formation</term><term>Poisson distribution</term><term>Present study</term><term>Recombinant</term><term>Recombinant clones</term><term>Recombinant viruses</term><term>Recombination</term><term>Same complementation group</term><term>Shutoff</term><term>Shutoff temperature</term><term>Surface antigens</term><term>Tissue culture</term><term>Vaccine</term><term>Virus</term><term>Virus genome</term><term>Virus titer</term><term>Virus vaccine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The nature of the genetic defect(s) present in the influenza A/Hong Kong/1968-ts-1[E] (H3N2) candidate vaccine virus, was analyzed by transferring them by genetic recombination to a 1943 HON1 wild-type virus. Three classes of ts viruses bearing the HO hemagglutinin were identified. One class consisted of two clones of virus, R1 and R8, which underwent complementation-recombination with each other but not with the Hong Kong/1968 (H3N2)-ts-1[E] parent virus. The second class consisted of clones of virus, such as R4 and R11, that failed to undergo complementation-recombination with R1, with R8, or with the ts-1[E] parent. These data indicated that the parent Hong Kong ts-1[E] virus possessed two ts lesions that segregated independently of each other and were presumably on different segments of the influenza A virus genome. The third class of ts mutants consisted of a spontaneously occurring ts mutant, clone R9; this clone underwent complementation-recombination with the ts-1[E] parent and other HO-ts recombinants and was shown to belong to a complementation group different than clones R1 and R8. The ts defects present in the Hong Kong-ts-1[E] donor virus segregated independently of the genes that coded for the epidemiologically important surface antigens, i.e., the hemagglutinin and the neuraminidase glycoproteins. The implications of these findings for the development of a live attenuated influenza virus vaccine are discussed.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>clone</json:string><json:string>recombinant</json:string><json:string>mutant</json:string><json:string>neuraminidase</json:string><json:string>honl</json:string><json:string>hemagglutinin</json:string><json:string>influenza virus</json:string><json:string>influenza</json:string><json:string>recombination</json:string><json:string>shutoff</json:string><json:string>glycoprotein</json:string><json:string>complementation</json:string><json:string>recombinant viruses</json:string><json:string>lesion</json:string><json:string>genetic stability</json:string><json:string>chanock</json:string><json:string>shutoff temperature</json:string><json:string>genome</json:string><json:string>parent virus</json:string><json:string>virus</json:string><json:string>recombinant clones</json:string><json:string>plaque</json:string><json:string>vaccine</json:string><json:string>monolayer cultures</json:string><json:string>honl virus</json:string><json:string>pairwise matings</json:string><json:string>plaque formation</json:string><json:string>high titer</json:string><json:string>allantoic cavity</json:string><json:string>virus titer</json:string><json:string>genetic interaction</json:string><json:string>tissue culture</json:string><json:string>virus genome</json:string><json:string>complementation group</json:string><json:string>neuraminidase glycoproteins</json:string><json:string>neuraminidase subtype</json:string><json:string>virus vaccine</json:string><json:string>hong virus</json:string><json:string>poisson distribution</json:string><json:string>hemagglutinin glycoproteins</json:string><json:string>greater reduction</json:string><json:string>neuraminidase glycoprotein</json:string><json:string>present study</json:string><json:string>surface antigens</json:string><json:string>complementation groups</json:string><json:string>same complementation group</json:string><json:string>neuraminidase gene</json:string><json:string>genetic</json:string></teeft></keywords><author><json:item><name>Brian R Murphy</name><affiliations><json:string>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</json:string></affiliations></json:item><json:item><name>Susan B Spring</name><affiliations><json:string>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</json:string></affiliations></json:item><json:item><name>Douglas D Richman</name><affiliations><json:string>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</json:string></affiliations></json:item><json:item><name>Eveline L Tierney</name><affiliations><json:string>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</json:string></affiliations></json:item><json:item><name>Julius Kasel</name><affiliations><json:string>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</json:string></affiliations></json:item><json:item><name>Robert M Chanock</name><affiliations><json:string>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-BX38WFQ4-K</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: The nature of the genetic defect(s) present in the influenza A/Hong Kong/1968-ts-1[E] (H3N2) candidate vaccine virus, was analyzed by transferring them by genetic recombination to a 1943 HON1 wild-type virus. Three classes of ts viruses bearing the HO hemagglutinin were identified. One class consisted of two clones of virus, R1 and R8, which underwent complementation-recombination with each other but not with the Hong Kong/1968 (H3N2)-ts-1[E] parent virus. The second class consisted of clones of virus, such as R4 and R11, that failed to undergo complementation-recombination with R1, with R8, or with the ts-1[E] parent. These data indicated that the parent Hong Kong ts-1[E] virus possessed two ts lesions that segregated independently of each other and were presumably on different segments of the influenza A virus genome. The third class of ts mutants consisted of a spontaneously occurring ts mutant, clone R9; this clone underwent complementation-recombination with the ts-1[E] parent and other HO-ts recombinants and was shown to belong to a complementation group different than clones R1 and R8. The ts defects present in the Hong Kong-ts-1[E] donor virus segregated independently of the genes that coded for the epidemiologically important surface antigens, i.e., the hemagglutinin and the neuraminidase glycoproteins. The implications of these findings for the development of a live attenuated influenza virus vaccine are discussed.</abstract><qualityIndicators><score>8.653</score><pdfWordCount>4061</pdfWordCount><pdfCharCount>26777</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>504 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>216</abstractWordCount><abstractCharCount>1458</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Temperature-sensitive mutants of influenza virus</title><pmid><json:string>1171556</json:string></pmid><pii><json:string>0042-6822(75)90225-1</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Soc. Exp. Biol. Med.</title><language><json:string>unknown</json:string></language><volume>139</volume><pages><first>768</first><last>773</last></pages></serie><host><title>Virology</title><language><json:string>unknown</json:string></language><publicationDate>1975</publicationDate><issn><json:string>0042-6822</json:string></issn><pii><json:string>S0042-6822(00)X0734-9</json:string></pii><volume>66</volume><issue>2</issue><pages><first>533</first><last>541</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1968</json:string><json:string>1975</json:string><json:string>1965</json:string></date><geogName></geogName><orgName><json:string>University School of Medicine</json:string><json:string>Influenza Institute of Allergy Bethesda, Maryland</json:string><json:string>Academic Press, Inc.</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Marion Coleman</json:string><json:string>Hong Kong</json:string><json:string>The</json:string><json:string>Ann Arbor</json:string><json:string>Fred Davenport</json:string><json:string>HONG Ko</json:string><json:string>Ann ArborlMar</json:string><json:string>Robert Webster</json:string></persName><placeName></placeName><ref_url></ref_url><ref_bibl><json:string>Murphy et al., 1973</json:string><json:string>Murphy et al., 1972</json:string><json:string>March and Infectious 20014</json:string><json:string>Hirst, 1973</json:string><json:string>Richman et al., 1975</json:string><json:string>Kilbourne et al., 1967</json:string><json:string>Spring et al., 1975b</json:string><json:string>McCahon et al., 1971</json:string><json:string>Spring et al., 1975</json:string><json:string>Spring et al., 1975a</json:string><json:string>Aymard-Henry et al., 1973</json:string><json:string>McCahon et al.</json:string><json:string>Sugiura et al., 1972</json:string><json:string>Maassab et al., 1972</json:string><json:string>Mills and Chanock, 1971</json:string><json:string>Laver et al., 1966</json:string><json:string>Flammand and Pringle, 1971</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-BX38WFQ4-K</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</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 biologiques fondamentales et appliquees. psychologie</json:string><json:string>4 - microbiologie</json:string></inist></categories><publicationDate>1975</publicationDate><copyrightDate>1975</copyrightDate><doi><json:string>10.1016/0042-6822(75)90225-1</json:string></doi><id>EA11C8075B2914DDDDD171445EC72E9113F5DE1B</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-BX38WFQ4-K/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-BX38WFQ4-K/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-BX38WFQ4-K/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Temperature-sensitive mutants of influenza virus</title><title level="a" type="sub">VII. Transfer of the ts -1[E] lesions to a wild-type influenza A virus with the HON1 surface antigens</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1975</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Temperature-sensitive mutants of influenza virus</title><title level="a" type="sub">VII. Transfer of the ts -1[E] lesions to a wild-type influenza A virus with the HON1 surface antigens</title><author xml:id="author-0000"><persName><forename type="first">Brian R</forename><surname>Murphy</surname></persName><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Susan B</forename><surname>Spring</surname></persName><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Douglas D</forename><surname>Richman</surname></persName><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Eveline L</forename><surname>Tierney</surname></persName><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Julius</forename><surname>Kasel</surname></persName><note type="biography">Baylor University School of Medicine, Houston, Texas.</note><affiliation>Baylor University School of Medicine, Houston, Texas.</affiliation><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Robert M</forename><surname>Chanock</surname></persName><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation></author><idno type="istex">EA11C8075B2914DDDDD171445EC72E9113F5DE1B</idno><idno type="ark">ark:/67375/6H6-BX38WFQ4-K</idno><idno type="DOI">10.1016/0042-6822(75)90225-1</idno><idno type="PII">0042-6822(75)90225-1</idno></analytic><monogr><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="pISSN">0042-6822</idno><idno type="PII">S0042-6822(00)X0734-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1975"></date><biblScope unit="volume">66</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="533">533</biblScope><biblScope unit="page" to="541">541</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1975</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The nature of the genetic defect(s) present in the influenza A/Hong Kong/1968-ts-1[E] (H3N2) candidate vaccine virus, was analyzed by transferring them by genetic recombination to a 1943 HON1 wild-type virus. Three classes of ts viruses bearing the HO hemagglutinin were identified. One class consisted of two clones of virus, R1 and R8, which underwent complementation-recombination with each other but not with the Hong Kong/1968 (H3N2)-ts-1[E] parent virus. The second class consisted of clones of virus, such as R4 and R11, that failed to undergo complementation-recombination with R1, with R8, or with the ts-1[E] parent. These data indicated that the parent Hong Kong ts-1[E] virus possessed two ts lesions that segregated independently of each other and were presumably on different segments of the influenza A virus genome. The third class of ts mutants consisted of a spontaneously occurring ts mutant, clone R9; this clone underwent complementation-recombination with the ts-1[E] parent and other HO-ts recombinants and was shown to belong to a complementation group different than clones R1 and R8. The ts defects present in the Hong Kong-ts-1[E] donor virus segregated independently of the genes that coded for the epidemiologically important surface antigens, i.e., the hemagglutinin and the neuraminidase glycoproteins. The implications of these findings for the development of a live attenuated influenza virus vaccine are discussed.</p></abstract></profileDesc><revisionDesc><change when="1975">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-BX38WFQ4-K/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YVIRO</jid><aid>75902251</aid><ce:pii>0042-6822(75)90225-1</ce:pii><ce:doi>10.1016/0042-6822(75)90225-1</ce:doi><ce:copyright type="unknown" year="1975"></ce:copyright></item-info><head><ce:title>Temperature-sensitive mutants of influenza virus</ce:title><ce:subtitle>VII. Transfer of the <ce:italic>ts</ce:italic>-1[E] lesions to a wild-type influenza A virus with the HON1 surface antigens</ce:subtitle><ce:author-group><ce:author><ce:given-name>Brian R</ce:given-name><ce:surname>Murphy</ce:surname></ce:author><ce:author><ce:given-name>Susan B</ce:given-name><ce:surname>Spring</ce:surname></ce:author><ce:author><ce:given-name>Douglas D</ce:given-name><ce:surname>Richman</ce:surname></ce:author><ce:author><ce:given-name>Eveline L</ce:given-name><ce:surname>Tierney</ce:surname></ce:author><ce:author><ce:given-name>Julius</ce:given-name><ce:surname>Kasel</ce:surname><ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Robert M</ce:given-name><ce:surname>Chanock</ce:surname></ce:author><ce:affiliation><ce:textfn>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Baylor University School of Medicine, Houston, Texas.</ce:note-para></ce:footnote></ce:author-group><ce:date-accepted day="21" month="3" year="1975"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The nature of the genetic defect(s) present in the influenza A/Hong Kong/1968-<ce:italic>ts</ce:italic>-1[E] (H3N2) candidate vaccine virus, was analyzed by transferring them by genetic recombination to a 1943 HON1 wild-type virus. Three classes of <ce:italic>ts</ce:italic> viruses bearing the HO hemagglutinin were identified. One class consisted of two clones of virus, R1 and R8, which underwent complementation-recombination with each other but not with the Hong Kong/1968 (H3N2)-<ce:italic>ts</ce:italic>-1[E] parent virus. The second class consisted of clones of virus, such as R4 and R11, that failed to undergo complementation-recombination with R1, with R8, or with the <ce:italic>ts</ce:italic>-1[E] parent. These data indicated that the parent Hong Kong <ce:italic>ts</ce:italic>-1[E] virus possessed two <ce:italic>ts</ce:italic> lesions that segregated independently of each other and were presumably on different segments of the influenza A virus genome. The third class of <ce:italic>ts</ce:italic> mutants consisted of a spontaneously occurring <ce:italic>ts</ce:italic> mutant, clone R9; this clone underwent complementation-recombination with the <ce:italic>ts</ce:italic>-1[E] parent and other HO-<ce:italic>ts</ce:italic> recombinants and was shown to belong to a complementation group different than clones R1 and R8. The <ce:italic>ts</ce:italic> defects present in the Hong Kong-<ce:italic>ts</ce:italic>-1[E] donor virus segregated independently of the genes that coded for the epidemiologically important surface antigens, i.e., the hemagglutinin and the neuraminidase glycoproteins. The implications of these findings for the development of a live attenuated influenza virus vaccine are discussed.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Temperature-sensitive mutants of influenza virus</title><subTitle>VII. Transfer of the ts -1[E] lesions to a wild-type influenza A virus with the HON1 surface antigens</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Temperature-sensitive mutants of influenza virus</title><subTitle>VII. Transfer of the ts-1[E] lesions to a wild-type influenza A virus with the HON1 surface antigens</subTitle></titleInfo><name type="personal"><namePart type="given">Brian R</namePart><namePart type="family">Murphy</namePart><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susan B</namePart><namePart type="family">Spring</namePart><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Douglas D</namePart><namePart type="family">Richman</namePart><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eveline L</namePart><namePart type="family">Tierney</namePart><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Julius</namePart><namePart type="family">Kasel</namePart><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation><description>Baylor University School of Medicine, Houston, Texas.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert M</namePart><namePart type="family">Chanock</namePart><affiliation>The Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1975</dateIssued><copyrightDate encoding="w3cdtf">1975</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The nature of the genetic defect(s) present in the influenza A/Hong Kong/1968-ts-1[E] (H3N2) candidate vaccine virus, was analyzed by transferring them by genetic recombination to a 1943 HON1 wild-type virus. Three classes of ts viruses bearing the HO hemagglutinin were identified. One class consisted of two clones of virus, R1 and R8, which underwent complementation-recombination with each other but not with the Hong Kong/1968 (H3N2)-ts-1[E] parent virus. The second class consisted of clones of virus, such as R4 and R11, that failed to undergo complementation-recombination with R1, with R8, or with the ts-1[E] parent. These data indicated that the parent Hong Kong ts-1[E] virus possessed two ts lesions that segregated independently of each other and were presumably on different segments of the influenza A virus genome. The third class of ts mutants consisted of a spontaneously occurring ts mutant, clone R9; this clone underwent complementation-recombination with the ts-1[E] parent and other HO-ts recombinants and was shown to belong to a complementation group different than clones R1 and R8. The ts defects present in the Hong Kong-ts-1[E] donor virus segregated independently of the genes that coded for the epidemiologically important surface antigens, i.e., the hemagglutinin and the neuraminidase glycoproteins. The implications of these findings for the development of a live attenuated influenza virus vaccine are discussed.</abstract><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><titleInfo type="abbreviated"><title>YVIRO</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1975</dateIssued></originInfo><identifier type="ISSN">0042-6822</identifier><identifier type="PII">S0042-6822(00)X0734-9</identifier><part><date>1975</date><detail type="volume"><number>66</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>347</start><end>632</end></extent><extent unit="pages"><start>533</start><end>541</end></extent></part></relatedItem><identifier type="istex">EA11C8075B2914DDDDD171445EC72E9113F5DE1B</identifier><identifier type="ark">ark:/67375/6H6-BX38WFQ4-K</identifier><identifier type="DOI">10.1016/0042-6822(75)90225-1</identifier><identifier type="PII">0042-6822(75)90225-1</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-BX38WFQ4-K/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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