The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3)
Identifieur interne : 000B52 ( Istex/Corpus ); précédent : 000B51; suivant : 000B53The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3)
Auteurs : Anne Stokes ; Eveline L. Tierney ; Christina M. Sarris ; Brian R. Murphy ; Susan L. HallSource :
- Virus Research [ 0168-1702 ] ; 1993.
English descriptors
- Teeft :
- Amino, Amino acid, Amino acid changes, Amino acid substitutions, Attenuated, Attenuating mutations, Attenuation, Belshe, Complete nucleotide sequence, Genetic basis, Genome, Genome leader, Human parainfluenza virus type, Infectious diseases, Leader region, Mutant, Mutant viruses, Mutation, Newcastle disease virus, Nucleotide, Nucleotide changes, Nucleotide differences, Parainfluenza, Paramyxovirus, Phenotype, Piv3, Regulatory regions, Rhesus monkeys, Sabin, Sendai virus, Sequence analysis, Stokes, Substitution, Unique substitutions, Vaccine, Virol, Virology, Virus, Yellow fever.
Abstract
Abstract: Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.
Url:
DOI: 10.1016/0168-1702(93)90014-E
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Hall</name><affiliation><mods:affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Virus Research</title><title level="j" type="abbrev">VIRUS</title><idno type="ISSN">0168-1702</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="43">43</biblScope><biblScope unit="page" to="52">52</biblScope></imprint><idno type="ISSN">0168-1702</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0168-1702</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Amino</term><term>Amino acid</term><term>Amino acid changes</term><term>Amino acid substitutions</term><term>Attenuated</term><term>Attenuating mutations</term><term>Attenuation</term><term>Belshe</term><term>Complete nucleotide sequence</term><term>Genetic basis</term><term>Genome</term><term>Genome leader</term><term>Human parainfluenza virus type</term><term>Infectious diseases</term><term>Leader region</term><term>Mutant</term><term>Mutant viruses</term><term>Mutation</term><term>Newcastle disease virus</term><term>Nucleotide</term><term>Nucleotide changes</term><term>Nucleotide differences</term><term>Parainfluenza</term><term>Paramyxovirus</term><term>Phenotype</term><term>Piv3</term><term>Regulatory regions</term><term>Rhesus monkeys</term><term>Sabin</term><term>Sendai virus</term><term>Sequence analysis</term><term>Stokes</term><term>Substitution</term><term>Unique substitutions</term><term>Vaccine</term><term>Virol</term><term>Virology</term><term>Virus</term><term>Yellow fever</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>mutant</json:string><json:string>mutation</json:string><json:string>genome</json:string><json:string>piv3</json:string><json:string>parainfluenza</json:string><json:string>attenuated</json:string><json:string>vaccine</json:string><json:string>attenuation</json:string><json:string>amino</json:string><json:string>phenotype</json:string><json:string>belshe</json:string><json:string>sabin</json:string><json:string>virology</json:string><json:string>virol</json:string><json:string>stokes</json:string><json:string>paramyxovirus</json:string><json:string>amino acid substitutions</json:string><json:string>nucleotide</json:string><json:string>human parainfluenza virus type</json:string><json:string>amino acid changes</json:string><json:string>complete nucleotide sequence</json:string><json:string>sequence analysis</json:string><json:string>substitution</json:string><json:string>genetic basis</json:string><json:string>rhesus monkeys</json:string><json:string>genome leader</json:string><json:string>infectious diseases</json:string><json:string>amino acid</json:string><json:string>mutant viruses</json:string><json:string>virus</json:string><json:string>nucleotide differences</json:string><json:string>unique substitutions</json:string><json:string>regulatory regions</json:string><json:string>newcastle disease virus</json:string><json:string>sendai virus</json:string><json:string>attenuating mutations</json:string><json:string>yellow fever</json:string><json:string>nucleotide changes</json:string><json:string>leader region</json:string></teeft></keywords><author><json:item><name>Anne Stokes</name><affiliations><json:string>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</json:string></affiliations></json:item><json:item><name>Eveline L. Tierney</name><affiliations><json:string>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</json:string></affiliations></json:item><json:item><name>Christina M. Sarris</name><affiliations><json:string>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</json:string></affiliations></json:item><json:item><name>Brian R. Murphy</name><affiliations><json:string>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</json:string></affiliations></json:item><json:item><name>Susan L. Hall</name><affiliations><json:string>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Cold-adapted vaccine virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Human parainfluenza virus type 3, strain JS</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Nucleotide sequence</value></json:item></subject><arkIstex>ark:/67375/6H6-BKW2BC3J-W</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.</abstract><qualityIndicators><score>8.391</score><pdfWordCount>3463</pdfWordCount><pdfCharCount>20733</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>432 x 648 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>244</abstractWordCount><abstractCharCount>1559</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3)</title><pmid><json:string>8266719</json:string></pmid><pii><json:string>0168-1702(93)90014-E</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. 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Tierney</json:string><json:string>Susan</json:string><json:string>Christina M. Sarris</json:string><json:string>Val Add</json:string><json:string>Brian R. Murphy</json:string><json:string>L. Based</json:string><json:string>S.L. Hall</json:string></persName><placeName></placeName><ref_url></ref_url><ref_bibl><json:string>Crookshanks and Belshe, 1984</json:string><json:string>Peeples et al., 1988</json:string><json:string>Galinski et al., 1988</json:string><json:string>Poch et al., 1989</json:string><json:string>Buser and Montagnon, 1970</json:string><json:string>Fulginiti et al.</json:string><json:string>Mink et al. (1991)</json:string><json:string>Sih et al., 1992</json:string><json:string>Hahn et al., 1987</json:string><json:string>Kim et al., 2969</json:string><json:string>Wolinsky and Wacham, 1990</json:string><json:string>Stokes et al., 1992</json:string><json:string>Cann et al., 1984</json:string><json:string>Belshe et al., 1992</json:string><json:string>Chanock and McIntosh, 1990</json:string><json:string>Preblud and Katz, 1988</json:string><json:string>Shioda et al., 1986</json:string><json:string>Westrop et al., 1989</json:string><json:string>Coelingh et al., 1989</json:string><json:string>German and Portner, 1989</json:string><json:string>Nomoto et al., 1982</json:string><json:string>Dimock and Collins, 1993</json:string><json:string>Tatem et al., 1992</json:string><json:string>Vella et al., 1969</json:string><json:string>Hall et al., 1992</json:string><json:string>Coelingh et al., 1988</json:string><json:string>Snyder et al., 1988</json:string><json:string>Belshe and Hissom, 1982</json:string><json:string>Clements et al., 1991</json:string><json:string>Ren et al., 1991</json:string><json:string>Galinski and Wechsler, 1990</json:string><json:string>Subbarao et al., 1992</json:string><json:string>Stec et al., 1991</json:string><json:string>Fulginiti et al., 1967</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-BKW2BC3J-W</json:string></ark><categories><wos><json:string>1 - 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Hall, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</p></note><affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</affiliation></author><idno type="istex">8240075AAD2A0A578AE71781C9F875156071EC58</idno><idno type="ark">ark:/67375/6H6-BKW2BC3J-W</idno><idno type="DOI">10.1016/0168-1702(93)90014-E</idno><idno type="PII">0168-1702(93)90014-E</idno></analytic><monogr><title level="j">Virus Research</title><title level="j" type="abbrev">VIRUS</title><idno type="pISSN">0168-1702</idno><idno type="PII">S0168-1702(00)X0109-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993"></date><biblScope unit="volume">30</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="43">43</biblScope><biblScope unit="page" to="52">52</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Cold-adapted vaccine virus</term></item><item><term>Human parainfluenza virus type 3, strain JS</term></item><item><term>Nucleotide sequence</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993">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-BKW2BC3J-W/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>VIRUS</jid><aid>9390014E</aid><ce:pii>0168-1702(93)90014-E</ce:pii><ce:doi>10.1016/0168-1702(93)90014-E</ce:doi><ce:copyright type="unknown" year="1993"></ce:copyright></item-info><head><ce:title>The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3)</ce:title><ce:author-group><ce:author><ce:given-name>Anne</ce:given-name><ce:surname>Stokes</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>Christina M.</ce:given-name><ce:surname>Sarris</ce:surname></ce:author><ce:author><ce:given-name>Brian R.</ce:given-name><ce:surname>Murphy</ce:surname></ce:author><ce:author><ce:given-name>Susan L.</ce:given-name><ce:surname>Hall</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Correspondence to: S.L. Hall, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="12" month="2" year="1993"></ce:date-received><ce:date-accepted day="14" month="5" year="1993"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (<ce:italic>wt</ce:italic>) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (<ce:italic>ca</ce:italic>), temperature-sensitive (<ce:italic>ts</ce:italic>), and attenuation (<ce:italic>att</ce:italic>) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype <ce:italic>wt</ce:italic> strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS <ce:italic>wt</ce:italic>. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Cold-adapted vaccine virus</ce:text></ce:keyword><ce:keyword><ce:text>Human parainfluenza virus type 3, strain JS</ce:text></ce:keyword><ce:keyword><ce:text>Nucleotide sequence</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3)</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>The complete nucleotide sequence of two cold-adapted, temperature-sensitive attenuated mutant vaccine viruses (cp12 and cp45) derived from the JS strain of human parainfluenza virus type 3 (PIV3)</title></titleInfo><name type="personal"><namePart type="given">Anne</namePart><namePart type="family">Stokes</namePart><affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, 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>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christina M.</namePart><namePart type="family">Sarris</namePart><affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Brian R.</namePart><namePart type="family">Murphy</namePart><affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susan L.</namePart><namePart type="family">Hall</namePart><affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA</affiliation><description>Correspondence to: S.L. Hall, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</description><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">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.</abstract><subject><genre>Keywords</genre><topic>Cold-adapted vaccine virus</topic><topic>Human parainfluenza virus type 3, strain JS</topic><topic>Nucleotide sequence</topic></subject><relatedItem type="host"><titleInfo><title>Virus Research</title></titleInfo><titleInfo type="abbreviated"><title>VIRUS</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">1993</dateIssued></originInfo><identifier type="ISSN">0168-1702</identifier><identifier type="PII">S0168-1702(00)X0109-8</identifier><part><date>1993</date><detail type="volume"><number>30</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>112</end></extent><extent unit="pages"><start>43</start><end>52</end></extent></part></relatedItem><identifier type="istex">8240075AAD2A0A578AE71781C9F875156071EC58</identifier><identifier type="ark">ark:/67375/6H6-BKW2BC3J-W</identifier><identifier type="DOI">10.1016/0168-1702(93)90014-E</identifier><identifier type="PII">0168-1702(93)90014-E</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-BKW2BC3J-W/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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