Generation of a neutralization-resistant variant of HIV-1 is due to selection for a point mutation in the envelope gene
Identifieur interne : 001F07 ( Istex/Corpus ); précédent : 001F06; suivant : 001F08Generation of a neutralization-resistant variant of HIV-1 is due to selection for a point mutation in the envelope gene
Auteurs : Marvin S. Reitz Jr. ; Carolyn Wilson ; Christine Naugle ; Robert C. Gallo ; Marjorie Robert-GuroffSource :
- Cell [ 0092-8674 ] ; 1988.
English descriptors
- Teeft :
- Acid substitution, Active clone, Amino, Amino acid sequence, Amino acids, Antiserum, Assay, Clone, Complete medium, Complete nucleotide sequence, Continuous presence, Control viruses, Cysteine residues, Differential hybridization, Dimarzo veronese, Disease progression, Envelope glycoprotein, Envelope proteins, Epitope, Experimental procedures, Fragment, Gallo, Genetic variation, Genomic diversity, Genomic library, Glycoprotein, Human serum, Human virus type, Hxb2d, Hxb2d clone, Hxb2d sequence, Hxb2d virus, Immune selection, Immunodeficiency syndrome, Lambda, Lambda clone, Lambda phage, Large envelope glycoprotein, Large envelope protein, Molecular clone, Monoclonal antibodies, Monoclonal antibody, Mxb2, Mxb2 recombinants, Neutralizability, Neutralization, Neutralization assays, Neutralization behavior, Neutralization resistance, Neutralizing, Neutralizing antibodies, Neutralizing antibody, Neutralizing antisera, Neutralizing antiserum, Neutralizing epitope, Normal serum, Parental, Parental virus, Parental virus population, Point mutation, Recombinant, Recombinant virus, Recombinant viruses, Resistant variant, Restriction enzyme analyses, Same antiserum, Second clone, Second neutralizing serum, Secondary structure, Sstl, Sstl fragment, Sstl site, Substitution, Tissue culture fluids, Transmembrane, Transmembrane envelope protein, Transmembrane protein, Variant, Variant virus, Viral, Virol, Virus, Virus population, Visna virus, Xhol site.
Abstract
Abstract: Transmission and growth of HIV-1 produced from the biologically active clone HTLV-III/HXB2D in the constant presence of a neutralizing antiserum yielded a viral population specifically resistant to neutralization by the same antiserum. Molecular clones MX-1 and -2, containing the entire envelope gene, were obtained from cultures of the resistant variant. The coding regions for the large envelope protein and most of the transmembrane envelope protein of two such clones were substituted for the homologous segment of HXB2D. Infectious viruses from these constructs were also specifically resistant to neutralization by the selecting antiserum. The exchanged fragment contained only one base change, resulting in an Ala→Thr replacement at position 582. When this substitution was introduced into HXB2D it conferred the resistant phenotype. Thus, small differences may be selected for in vivo by the host immune response and result in relatively large differences in susceptibility of the virus to such a response.
Url:
DOI: 10.1016/0092-8674(88)90179-1
Links to Exploration step
ISTEX:4D41DF71F903FD557B4FAD2D67102F440076D534Le document en format XML
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Reitz Jr.</name><affiliation><mods:affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</mods:affiliation></affiliation></author><author><name sortKey="Wilson, Carolyn" sort="Wilson, Carolyn" uniqKey="Wilson C" first="Carolyn" last="Wilson">Carolyn Wilson</name><affiliation><mods:affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</mods:affiliation></affiliation></author><author><name sortKey="Naugle, Christine" sort="Naugle, Christine" uniqKey="Naugle C" first="Christine" last="Naugle">Christine Naugle</name><affiliation><mods:affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</mods:affiliation></affiliation></author><author><name sortKey="Gallo, Robert C" sort="Gallo, Robert C" uniqKey="Gallo R" first="Robert C." last="Gallo">Robert C. 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Molecular clones MX-1 and -2, containing the entire envelope gene, were obtained from cultures of the resistant variant. The coding regions for the large envelope protein and most of the transmembrane envelope protein of two such clones were substituted for the homologous segment of HXB2D. Infectious viruses from these constructs were also specifically resistant to neutralization by the selecting antiserum. The exchanged fragment contained only one base change, resulting in an Ala→Thr replacement at position 582. When this substitution was introduced into HXB2D it conferred the resistant phenotype. 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Reitz, Jr.</name><affiliations><json:string>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</json:string></affiliations></json:item><json:item><name>Carolyn Wilson</name><affiliations><json:string>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</json:string></affiliations></json:item><json:item><name>Christine Naugle</name><affiliations><json:string>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</json:string></affiliations></json:item><json:item><name>Robert C. Gallo</name><affiliations><json:string>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</json:string></affiliations></json:item><json:item><name>Marjorie Robert-Guroff</name><affiliations><json:string>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-5G0JMMW2-8</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Transmission and growth of HIV-1 produced from the biologically active clone HTLV-III/HXB2D in the constant presence of a neutralizing antiserum yielded a viral population specifically resistant to neutralization by the same antiserum. Molecular clones MX-1 and -2, containing the entire envelope gene, were obtained from cultures of the resistant variant. The coding regions for the large envelope protein and most of the transmembrane envelope protein of two such clones were substituted for the homologous segment of HXB2D. Infectious viruses from these constructs were also specifically resistant to neutralization by the selecting antiserum. The exchanged fragment contained only one base change, resulting in an Ala→Thr replacement at position 582. When this substitution was introduced into HXB2D it conferred the resistant phenotype. Thus, small differences may be selected for in vivo by the host immune response and result in relatively large differences in susceptibility of the virus to such a response.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>150</abstractWordCount><abstractCharCount>1025</abstractCharCount><keywordCount>0</keywordCount><score>8.8</score><pdfWordCount>5378</pdfWordCount><pdfCharCount>31863</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>634 x 828 pts</pdfPageSize></qualityIndicators><title>Generation of a neutralization-resistant variant of HIV-1 is due to selection for a point mutation in the envelope gene</title><pmid><json:string>2838179</json:string></pmid><pii><json:string>0092-8674(88)90179-1</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. USA</title><language><json:string>unknown</json:string></language><volume>82</volume><pages><first>5199</first><last>5202</last></pages></serie><host><title>Cell</title><language><json:string>unknown</json:string></language><publicationDate>1988</publicationDate><issn><json:string>0092-8674</json:string></issn><pii><json:string>S0092-8674(00)X0596-X</json:string></pii><volume>54</volume><issue>1</issue><pages><first>57</first><last>63</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1988</json:string></date><geogName></geogName><orgName><json:string>Stratagene, Inc., San Diego</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>S.C. Section</json:string><json:string>G. Franchini</json:string><json:string>Carolyn Wilson</json:string><json:string>Karen Farrell</json:string><json:string>Sophia Bryant</json:string><json:string>Robert C. Gallo</json:string><json:string>Christine Naugle</json:string><json:string>D. Virus</json:string></persName><placeName></placeName><ref_url></ref_url><ref_bibl><json:string>Sanger et al., 1977</json:string><json:string>Alizon et al., 1986</json:string><json:string>Weiss et al., 1985</json:string><json:string>Gamier et al., (1978)</json:string><json:string>Wong-Staal et al., 1985</json:string><json:string>Robey et al., 1986</json:string><json:string>Matsushita et al., 1988</json:string><json:string>Robert-Guroff et al., 1981</json:string><json:string>Robert-Guroff et al., 1986</json:string><json:string>Fisher et al., 1985</json:string><json:string>Osterhaus et al., 1985</json:string><json:string>Ratner et al., 1987</json:string><json:string>Hussain et al., 1987</json:string><json:string>Robert-Guroff et al., 1985</json:string><json:string>Ho et al., 1987</json:string><json:string>Scott et al., 1979</json:string><json:string>Stanley et al., 1987</json:string><json:string>Zoller and Smith (1983)</json:string><json:string>Hahn et al., 1986</json:string><json:string>Narayan et al., 1981</json:string><json:string>RobertGuroff et al., 1986</json:string><json:string>Hahn et al., 1985</json:string><json:string>Starcich et al., 1986</json:string><json:string>Chanh et al., 1986</json:string><json:string>Feinberg et al., 1986</json:string><json:string>Steeves et al., 1974</json:string><json:string>Queen and Korn (1984)</json:string><json:string>Gnann et al., 1987</json:string><json:string>Veronese et al., 1985</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-5G0JMMW2-8</json:string></ark><categories><wos><json:string>1 - 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Molecular clones MX-1 and -2, containing the entire envelope gene, were obtained from cultures of the resistant variant. The coding regions for the large envelope protein and most of the transmembrane envelope protein of two such clones were substituted for the homologous segment of HXB2D. Infectious viruses from these constructs were also specifically resistant to neutralization by the selecting antiserum. The exchanged fragment contained only one base change, resulting in an Ala→Thr replacement at position 582. When this substitution was introduced into HXB2D it conferred the resistant phenotype. Thus, small differences may be selected for in vivo by the host immune response and result in relatively large differences in susceptibility of the virus to such a response.</p></abstract></profileDesc><revisionDesc><change when="1988-04-12">Modified</change><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-5G0JMMW2-8/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>CELL</jid><aid>88901791</aid><ce:pii>0092-8674(88)90179-1</ce:pii><ce:doi>10.1016/0092-8674(88)90179-1</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>Generation of a neutralization-resistant variant of HIV-1 is due to selection for a point mutation in the envelope gene</ce:title><ce:author-group><ce:author><ce:given-name>Marvin S.</ce:given-name><ce:surname>Reitz</ce:surname><ce:suffix>Jr.</ce:suffix></ce:author><ce:author><ce:given-name>Carolyn</ce:given-name><ce:surname>Wilson</ce:surname></ce:author><ce:author><ce:given-name>Christine</ce:given-name><ce:surname>Naugle</ce:surname></ce:author><ce:author><ce:given-name>Robert C.</ce:given-name><ce:surname>Gallo</ce:surname></ce:author><ce:author><ce:given-name>Marjorie</ce:given-name><ce:surname>Robert-Guroff</ce:surname></ce:author><ce:affiliation><ce:textfn>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="18" month="12" year="1987"></ce:date-received><ce:date-revised day="12" month="4" year="1988"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Transmission and growth of HIV-1 produced from the biologically active clone HTLV-III/HXB2D in the constant presence of a neutralizing antiserum yielded a viral population specifically resistant to neutralization by the same antiserum. Molecular clones MX-1 and -2, containing the entire envelope gene, were obtained from cultures of the resistant variant. The coding regions for the large envelope protein and most of the transmembrane envelope protein of two such clones were substituted for the homologous segment of HXB2D. Infectious viruses from these constructs were also specifically resistant to neutralization by the selecting antiserum. The exchanged fragment contained only one base change, resulting in an Ala→Thr replacement at position 582. When this substitution was introduced into HXB2D it conferred the resistant phenotype. Thus, small differences may be selected for in vivo by the host immune response and result in relatively large differences in susceptibility of the virus to such a response.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Generation of a neutralization-resistant variant of HIV-1 is due to selection for a point mutation in the envelope gene</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Generation of a neutralization-resistant variant of HIV-1 is due to selection for a point mutation in the envelope gene</title></titleInfo><name type="personal"><namePart type="given">Marvin S.</namePart><namePart type="family">Reitz, Jr.</namePart><affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carolyn</namePart><namePart type="family">Wilson</namePart><affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Naugle</namePart><affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert C.</namePart><namePart type="family">Gallo</namePart><affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marjorie</namePart><namePart type="family">Robert-Guroff</namePart><affiliation>Laboratory of Tumor Cell Biology National Cancer Institute National Institutes of Health Bethesda, Maryland 20892, 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">1988</dateIssued><dateModified encoding="w3cdtf">1988-04-12</dateModified><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Transmission and growth of HIV-1 produced from the biologically active clone HTLV-III/HXB2D in the constant presence of a neutralizing antiserum yielded a viral population specifically resistant to neutralization by the same antiserum. Molecular clones MX-1 and -2, containing the entire envelope gene, were obtained from cultures of the resistant variant. The coding regions for the large envelope protein and most of the transmembrane envelope protein of two such clones were substituted for the homologous segment of HXB2D. Infectious viruses from these constructs were also specifically resistant to neutralization by the selecting antiserum. The exchanged fragment contained only one base change, resulting in an Ala→Thr replacement at position 582. When this substitution was introduced into HXB2D it conferred the resistant phenotype. Thus, small differences may be selected for in vivo by the host immune response and result in relatively large differences in susceptibility of the virus to such a response.</abstract><note type="content">Section title: Article</note><relatedItem type="host"><titleInfo><title>Cell</title></titleInfo><titleInfo type="abbreviated"><title>CELL</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">1988</dateIssued></originInfo><identifier type="ISSN">0092-8674</identifier><identifier type="PII">S0092-8674(00)X0596-X</identifier><part><date>1988</date><detail type="volume"><number>54</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>135</end></extent><extent unit="pages"><start>57</start><end>63</end></extent></part></relatedItem><identifier type="istex">4D41DF71F903FD557B4FAD2D67102F440076D534</identifier><identifier type="ark">ark:/67375/6H6-5G0JMMW2-8</identifier><identifier type="DOI">10.1016/0092-8674(88)90179-1</identifier><identifier type="PII">0092-8674(88)90179-1</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:/67375/6H6-5G0JMMW2-8/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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