Genetic characterization of simian immunodeficiency virus isolated from an African mandrill
Identifieur interne : 000109 ( Istex/Corpus ); précédent : 000108; suivant : 000110Genetic characterization of simian immunodeficiency virus isolated from an African mandrill
Auteurs : H. Sakai ; J. I. Sakuragi ; S. Sakuragi ; R. Shibata ; M. Hayami ; A. Ishimoto ; A. AdachiSource :
- Archives of Virology [ 0304-8608 ] ; 1992-03-01.
English descriptors
- KwdEn :
- Acid residues, Adachi, African mandrill, Aids virus, Amino, Amino acids, Assay, Cell lysates, Cells transfected, Clone, Coding exon, Deletion, Functional domains, Gene mutants, Genetic characterization, Genome, Hayami, Human immunodeficiency virus type, Immunodeficiency, Infectious clone, Lentiviruses, Molecular clones, Mutant, Negative control, Primate, Primate immunodeficiency viruses, Primate lentiviruses, Proc natl acad, Progeny, Progeny virions, Proviral, Retrovirus, Sakai, Sakai etal, Shibata, Simian, Simian immunodeficiency virus, Sivmnd, Transactivation, Transactivation potentials, Transfected, Transfection, Viral, Virol, Virus, Wild type, Wild type level.
- Teeft :
- Acid residues, Adachi, African mandrill, Aids virus, Amino, Amino acids, Assay, Cell lysates, Cells transfected, Clone, Coding exon, Deletion, Functional domains, Gene mutants, Genetic characterization, Genome, Hayami, Human immunodeficiency virus type, Immunodeficiency, Infectious clone, Lentiviruses, Molecular clones, Mutant, Negative control, Primate, Primate immunodeficiency viruses, Primate lentiviruses, Proc natl acad, Progeny, Progeny virions, Proviral, Retrovirus, Sakai, Sakai etal, Shibata, Simian, Simian immunodeficiency virus, Sivmnd, Transactivation, Transactivation potentials, Transfected, Transfection, Viral, Virol, Virus, Wild type, Wild type level.
Abstract
Summary: We constructed an infectious molecular clone of simian immunodeficiency virus from an African mandrill (SIVMND). Upon transfection, this clone directed the production of progeny virus particles infectious to and cytopathic for CD4+ human leukemia cells. Thirteen frameshift proviral mutants with an alteration in the eight open reading frames of SIVMND were generated by recombinant DNA techniques, and were analyzed biologically and biochemically. While mutations in the structural genesgag, pol, andenv abolished viral growth and induction of cytopathology, mutants of thevif, vpr, andnef genes were fully biologically active. Of thetat andrev mutants, only onerev mutant grew in CD4+ cells with delayed kinetics. In reporter-based transient expression systems, transactivation potentials of thetat andrev mutants were evaluated. A mutant lacking 2nd coding exon oftat gene exhibitedtat activity similar to that of the wild type clone. The infectiousrev mutant was partially defective forrev gene activity.
Url:
DOI: 10.1007/BF01309624
Links to Exploration step
ISTEX:ADCCF41D32E7E03E537CE2BDD7A93E3972A66664Le document en format XML
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Adachi</name><affiliations><json:string>Institute of Virus Research, Kyoto University, Kyoto, Japan</json:string></affiliations></json:item></author><articleId><json:string>BF01309624</json:string><json:string>Art1</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Summary: We constructed an infectious molecular clone of simian immunodeficiency virus from an African mandrill (SIVMND). Upon transfection, this clone directed the production of progeny virus particles infectious to and cytopathic for CD4+ human leukemia cells. Thirteen frameshift proviral mutants with an alteration in the eight open reading frames of SIVMND were generated by recombinant DNA techniques, and were analyzed biologically and biochemically. While mutations in the structural genesgag, pol, andenv abolished viral growth and induction of cytopathology, mutants of thevif, vpr, andnef genes were fully biologically active. Of thetat andrev mutants, only onerev mutant grew in CD4+ cells with delayed kinetics. In reporter-based transient expression systems, transactivation potentials of thetat andrev mutants were evaluated. A mutant lacking 2nd coding exon oftat gene exhibitedtat activity similar to that of the wild type clone. 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simian immunodeficiency virus isolated from an African mandrill</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><availability><p>Springer-Verlag, 1992</p></availability><date>1991-11-15</date></publicationStmt><notesStmt><note>Original Papers</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Genetic characterization of simian immunodeficiency virus isolated from an African mandrill</title><author xml:id="author-0000"><persName><forename type="first">H.</forename><surname>Sakai</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><author xml:id="author-0001"><persName><forename type="first">J.</forename><surname>Sakuragi</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><author xml:id="author-0002"><persName><forename type="first">S.</forename><surname>Sakuragi</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><author xml:id="author-0003"><persName><forename type="first">R.</forename><surname>Shibata</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><author xml:id="author-0004"><persName><forename type="first">M.</forename><surname>Hayami</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><author xml:id="author-0005"><persName><forename type="first">A.</forename><surname>Ishimoto</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><author xml:id="author-0006"><persName><forename type="first">A.</forename><surname>Adachi</surname></persName><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation></author><idno type="istex">ADCCF41D32E7E03E537CE2BDD7A93E3972A66664</idno><idno type="DOI">10.1007/BF01309624</idno><idno type="ArticleID">BF01309624</idno><idno type="ArticleID">Art1</idno></analytic><monogr><title level="j">Archives of Virology</title><title level="j" type="abbrev">Archives of Virology</title><idno type="pISSN">0304-8608</idno><idno type="eISSN">1432-8798</idno><idno type="journal-ID">true</idno><idno type="issue-article-count">32</idno><idno type="volume-issue-count">4</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1992-03-01"></date><biblScope unit="volume">125</biblScope><biblScope unit="issue">1-4</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="14">14</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1991-11-15</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: We constructed an infectious molecular clone of simian immunodeficiency virus from an African mandrill (SIVMND). Upon transfection, this clone directed the production of progeny virus particles infectious to and cytopathic for CD4+ human leukemia cells. Thirteen frameshift proviral mutants with an alteration in the eight open reading frames of SIVMND were generated by recombinant DNA techniques, and were analyzed biologically and biochemically. While mutations in the structural genesgag, pol, andenv abolished viral growth and induction of cytopathology, mutants of thevif, vpr, andnef genes were fully biologically active. Of thetat andrev mutants, only onerev mutant grew in CD4+ cells with delayed kinetics. In reporter-based transient expression systems, transactivation potentials of thetat andrev mutants were evaluated. A mutant lacking 2nd coding exon oftat gene exhibitedtat activity similar to that of the wild type clone. The infectiousrev mutant was partially defective forrev gene activity.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Medical Microbiology</term></item><item><term>Virology</term></item><item><term>Infectious Diseases</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991-11-15">Created</change><change when="1992-03-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/ADCCF41D32E7E03E537CE2BDD7A93E3972A66664/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" 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TocLevels="0"><VolumeIDStart>125</VolumeIDStart><VolumeIDEnd>125</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Combined"><IssueInfo TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueArticleCount>32</IssueArticleCount><IssueHistory><CoverDate><DateString>1992</DateString><Year>1992</Year><Month>3</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1992</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art1"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01309624</ArticleID><ArticleDOI>10.1007/BF01309624</ArticleDOI><ArticleSequenceNumber>1</ArticleSequenceNumber><ArticleTitle Language="En">Genetic characterization of simian immunodeficiency virus isolated from an African mandrill</ArticleTitle><ArticleCategory>Original Papers</ArticleCategory><ArticleFirstPage>1</ArticleFirstPage><ArticleLastPage>14</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>2</Month><Day>28</Day></RegistrationDate><Received><Year>1991</Year><Month>11</Month><Day>15</Day></Received><Accepted><Year>1991</Year><Month>12</Month><Day>27</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1992</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>705</JournalID><VolumeIDStart>125</VolumeIDStart><VolumeIDEnd>125</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>4</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>H.</GivenName><FamilyName>Sakai</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>J.</GivenName><GivenName>-I.</GivenName><FamilyName>Sakuragi</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>S.</GivenName><FamilyName>Sakuragi</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>R.</GivenName><FamilyName>Shibata</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><FamilyName>Hayami</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>A.</GivenName><FamilyName>Ishimoto</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>A.</GivenName><FamilyName>Adachi</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Institute of Virus Research</OrgDivision><OrgName>Kyoto University</OrgName><OrgAddress><City>Kyoto</City><Country>Japan</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>We constructed an infectious molecular clone of simian immunodeficiency virus from an African mandrill (SIV<Subscript>MND</Subscript>). Upon transfection, this clone directed the production of progeny virus particles infectious to and cytopathic for CD4<Superscript>+</Superscript> human leukemia cells. Thirteen frameshift proviral mutants with an alteration in the eight open reading frames of SIV<Subscript>MND</Subscript> were generated by recombinant DNA techniques, and were analyzed biologically and biochemically. While mutations in the structural genes<Emphasis Type="Italic">gag, pol</Emphasis>, and<Emphasis Type="Italic">env</Emphasis> abolished viral growth and induction of cytopathology, mutants of the<Emphasis Type="Italic">vif, vpr</Emphasis>, and<Emphasis Type="Italic">nef</Emphasis> genes were fully biologically active. Of the<Emphasis Type="Italic">tat</Emphasis> and<Emphasis Type="Italic">rev</Emphasis> mutants, only one<Emphasis Type="Italic">rev</Emphasis> mutant grew in CD4<Superscript>+</Superscript> cells with delayed kinetics. In reporter-based transient expression systems, transactivation potentials of the<Emphasis Type="Italic">tat</Emphasis> and<Emphasis Type="Italic">rev</Emphasis> mutants were evaluated. A mutant lacking 2nd coding exon of<Emphasis Type="Italic">tat</Emphasis> gene exhibited<Emphasis Type="Italic">tat</Emphasis> activity similar to that of the wild type clone. The infectious<Emphasis Type="Italic">rev</Emphasis> mutant was partially defective for<Emphasis Type="Italic">rev</Emphasis> gene activity.</Para></Abstract></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Genetic characterization of simian immunodeficiency virus isolated from an African mandrill</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Genetic characterization of simian immunodeficiency virus isolated from an African mandrill</title></titleInfo><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Sakai</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="given">-I.</namePart><namePart type="family">Sakuragi</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Sakuragi</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Shibata</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Hayami</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Ishimoto</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Adachi</namePart><affiliation>Institute of Virus Research, Kyoto University, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1991-11-15</dateCreated><dateIssued encoding="w3cdtf">1992-03-01</dateIssued><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: We constructed an infectious molecular clone of simian immunodeficiency virus from an African mandrill (SIVMND). Upon transfection, this clone directed the production of progeny virus particles infectious to and cytopathic for CD4+ human leukemia cells. Thirteen frameshift proviral mutants with an alteration in the eight open reading frames of SIVMND were generated by recombinant DNA techniques, and were analyzed biologically and biochemically. While mutations in the structural genesgag, pol, andenv abolished viral growth and induction of cytopathology, mutants of thevif, vpr, andnef genes were fully biologically active. Of thetat andrev mutants, only onerev mutant grew in CD4+ cells with delayed kinetics. In reporter-based transient expression systems, transactivation potentials of thetat andrev mutants were evaluated. A mutant lacking 2nd coding exon oftat gene exhibitedtat activity similar to that of the wild type clone. The infectiousrev mutant was partially defective forrev gene activity.</abstract><note>Original Papers</note><relatedItem type="host"><titleInfo><title>Archives of Virology</title></titleInfo><titleInfo type="abbreviated"><title>Archives of Virology</title></titleInfo><genre type="journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1992-03-01</dateIssued><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Medical Microbiology</topic><topic>Virology</topic><topic>Infectious Diseases</topic></subject><identifier type="ISSN">0304-8608</identifier><identifier type="eISSN">1432-8798</identifier><identifier type="JournalID">705</identifier><identifier type="IssueArticleCount">32</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>1992</date><detail type="volume"><number>125</number><caption>vol.</caption></detail><detail type="issue"><number>1-4</number><caption>no.</caption></detail><extent unit="pages"><start>1</start><end>14</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1992</recordOrigin></recordInfo></relatedItem><identifier type="istex">ADCCF41D32E7E03E537CE2BDD7A93E3972A66664</identifier><identifier type="DOI">10.1007/BF01309624</identifier><identifier type="ArticleID">BF01309624</identifier><identifier type="ArticleID">Art1</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag, 1992</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1992</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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