Incomplete replication of human parainfluenza virus type 4 in LLC-MK2 cells and in L929 cells
Identifieur interne : 000990 ( Istex/Corpus ); précédent : 000989; suivant : 000991Incomplete replication of human parainfluenza virus type 4 in LLC-MK2 cells and in L929 cells
Auteurs : Hiroshi Komada ; Hisae Inoue ; Chihiro Yamabayashi ; Morihiro Ito ; Mitsuo Kawano ; Machiko Nishio ; Masato Tsurudome ; Yuji Kozuka ; Naoya Noda ; Kazuyoshi Namba ; Myles O'Brien ; Yasuhiko ItoSource :
- Medical Microbiology and Immunology [ 0300-8584 ] ; 2000-06-01.
English descriptors
- KwdEn :
Abstract
Abstract: Human parainfluenza virus type 4A (hPIV-4A) and type 4B (hPIV-4B) were tested for their ability to replicate in the monkey kidney LLC-MK2 cell line (MK2 cells) and the murine L929 cell line (L929 cells). These cells are normally non-permissive for replication of hPIV-4; however, treatment with acetylated trypsin led to virus replication in MK2 cells, but was less effective for L929 cells. Endogenously produced interferon (IFN) played no role in virus replication in L929 cells. Synthesis of virus-specific polypeptides was suppressed in L929 cells. WhereasNP-mRNA and HN-mRNA were detected in MK2 cells, no HN-mRNA was detected in L929 cells. These results indicate that hPIV-4 can infect both MK2 cells and L929 cells. In MK2 cells, when protease exists in the extracellular medium, hPIV-4 exhibits multistep growth. In L929 cells, however, the cause of incomplete replication might be lack of other unknown factors.
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DOI: 10.1007/s004300000037
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ISTEX:ED266053F87B394B8DBB70DB63B7CB6860247878Le document en format XML
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Medical Science, 510-0293, Suzuka, Mie, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yamabayashi, Chihiro" sort="Yamabayashi, Chihiro" uniqKey="Yamabayashi C" first="Chihiro" last="Yamabayashi">Chihiro Yamabayashi</name><affiliation><mods:affiliation>Department of Microbiology, Suzuka University of Medical Science, 510-0293, Suzuka, Mie, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ito, Morihiro" sort="Ito, Morihiro" uniqKey="Ito M" first="Morihiro" last="Ito">Morihiro Ito</name><affiliation><mods:affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kawano, Mitsuo" sort="Kawano, Mitsuo" uniqKey="Kawano M" first="Mitsuo" last="Kawano">Mitsuo Kawano</name><affiliation><mods:affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</mods:affiliation></affiliation></author><author><name 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cell line</term><term>LLC-MK2 cell line</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Human parainfluenza virus type 4A (hPIV-4A) and type 4B (hPIV-4B) were tested for their ability to replicate in the monkey kidney LLC-MK2 cell line (MK2 cells) and the murine L929 cell line (L929 cells). These cells are normally non-permissive for replication of hPIV-4; however, treatment with acetylated trypsin led to virus replication in MK2 cells, but was less effective for L929 cells. Endogenously produced interferon (IFN) played no role in virus replication in L929 cells. Synthesis of virus-specific polypeptides was suppressed in L929 cells. WhereasNP-mRNA and HN-mRNA were detected in MK2 cells, no HN-mRNA was detected in L929 cells. These results indicate that hPIV-4 can infect both MK2 cells and L929 cells. In MK2 cells, when protease exists in the extracellular medium, hPIV-4 exhibits multistep growth. In L929 cells, however, the cause of incomplete replication might be lack of other unknown factors.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Hiroshi Komada</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Hisae Inoue</name><affiliations><json:string>Department of Microbiology, Suzuka University of Medical Science, 510-0293, Suzuka, Mie, Japan</json:string></affiliations></json:item><json:item><name>Chihiro Yamabayashi</name><affiliations><json:string>Department of Microbiology, Suzuka University of Medical Science, 510-0293, Suzuka, Mie, Japan</json:string></affiliations></json:item><json:item><name>Morihiro Ito</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Mitsuo Kawano</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Machiko Nishio</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Masato Tsurudome</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Yuji Kozuka</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Naoya Noda</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Kazuyoshi Namba</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Myles O'Brien</name><affiliations><json:string>Mie Prefectural College of Nursing, 514-0116, Tsu, Mie, Japan</json:string></affiliations></json:item><json:item><name>Yasuhiko Ito</name><affiliations><json:string>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</json:string><json:string>E-mail: Ito@doc.medic.mie-u.ac.jp</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Key words Human parainfluenza virus type 4</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Incomplete replication</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LLC-MK2 cell line</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>L929 cell line</value></json:item></subject><articleId><json:string>1880185</json:string><json:string>Art1</json:string></articleId><arkIstex>ark:/67375/VQC-LG6BGWH2-H</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Abstract: Human parainfluenza virus type 4A (hPIV-4A) and type 4B (hPIV-4B) were tested for their ability to replicate in the monkey kidney LLC-MK2 cell line (MK2 cells) and the murine L929 cell line (L929 cells). These cells are normally non-permissive for replication of hPIV-4; however, treatment with acetylated trypsin led to virus replication in MK2 cells, but was less effective for L929 cells. Endogenously produced interferon (IFN) played no role in virus replication in L929 cells. Synthesis of virus-specific polypeptides was suppressed in L929 cells. WhereasNP-mRNA and HN-mRNA were detected in MK2 cells, no HN-mRNA was detected in L929 cells. These results indicate that hPIV-4 can infect both MK2 cells and L929 cells. In MK2 cells, when protease exists in the extracellular medium, hPIV-4 exhibits multistep growth. In L929 cells, however, the cause of incomplete replication might be lack of other unknown factors.</abstract><qualityIndicators><score>6.358</score><pdfWordCount>2642</pdfWordCount><pdfCharCount>15107</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>5</pdfPageCount><pdfPageSize>595 x 785 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>143</abstractWordCount><abstractCharCount>931</abstractCharCount><keywordCount>4</keywordCount></qualityIndicators><title>Incomplete replication of human parainfluenza virus type 4 in LLC-MK2 cells and in L929 cells</title><genre><json:string>research-article</json:string></genre><host><title>Medical Microbiology and 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These cells are normally non-permissive for replication of hPIV-4; however, treatment with acetylated trypsin led to virus replication in MK2 cells, but was less effective for L929 cells. Endogenously produced interferon (IFN) played no role in virus replication in L929 cells. Synthesis of virus-specific polypeptides was suppressed in L929 cells. WhereasNP-mRNA and HN-mRNA were detected in MK2 cells, no HN-mRNA was detected in L929 cells. These results indicate that hPIV-4 can infect both MK2 cells and L929 cells. In MK2 cells, when protease exists in the extracellular medium, hPIV-4 exhibits multistep growth. In L929 cells, however, the cause of incomplete replication might be lack of other unknown factors.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><item><term>Key words Human parainfluenza virus type 4</term></item><item><term>Incomplete replication</term></item><item><term>LLC-MK2 cell line</term></item><item><term>L929 cell line</term></item></list></keywords></textClass><textClass><keywords scheme="Journal-Subject-Group"><list><label>B</label><item><term>Biomedicine</term></item><label>B16003</label><item><term>Medical Microbiology</term></item><label>B14000</label><item><term>Immunology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-06-01">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/VQC-LG6BGWH2-H/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml 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Microbiology</JournalSubject><JournalSubject Type="Secondary" Priority="2" Code="B14000">Immunology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>188</VolumeIDStart><VolumeIDEnd>188</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueArticleCount>7</IssueArticleCount><IssueHistory><PrintDate><Year>2000</Year><Month>06</Month><Day>19</Day></PrintDate><CoverDate><Year>2000</Year><Month>06</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag Berlin Heidelberg</CopyrightHolderName><CopyrightYear>2000</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art1"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>1880185</ArticleID><ArticleDOI>10.1007/s004300000037</ArticleDOI><ArticleSequenceNumber>4</ArticleSequenceNumber><ArticleTitle Language="En">Incomplete replication of human parainfluenza virus type 4 in LLC-MK2 cells and in L929 cells</ArticleTitle><ArticleCategory>ORIGINAL INVESTIGATION</ArticleCategory><ArticleFirstPage>185</ArticleFirstPage><ArticleLastPage>189</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2000</Year><Month>01</Month><Day>01</Day></RegistrationDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag Berlin Heidelberg</CopyrightHolderName><CopyrightYear>2000</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></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Hiroshi</GivenName><FamilyName>Komada</FamilyName></AuthorName></Author><Author AffiliationIDS="A2"><AuthorName DisplayOrder="Western"><GivenName>Hisae</GivenName><FamilyName>Inoue</FamilyName></AuthorName></Author><Author AffiliationIDS="A2"><AuthorName DisplayOrder="Western"><GivenName>Chihiro</GivenName><FamilyName>Yamabayashi</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Morihiro</GivenName><FamilyName>Ito</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Mitsuo</GivenName><FamilyName>Kawano</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Machiko</GivenName><FamilyName>Nishio</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Masato</GivenName><FamilyName>Tsurudome</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Yuji</GivenName><FamilyName>Kozuka</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Naoya</GivenName><FamilyName>Noda</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Kazuyoshi</GivenName><FamilyName>Namba</FamilyName></AuthorName></Author><Author AffiliationIDS="A3"><AuthorName DisplayOrder="Western"><GivenName>Myles</GivenName><FamilyName>O'Brien</FamilyName></AuthorName></Author><Author AffiliationIDS="A1"><AuthorName DisplayOrder="Western"><GivenName>Yasuhiko</GivenName><FamilyName>Ito</FamilyName></AuthorName><Contact><Fax>+81-50-2315008</Fax><Email>Ito@doc.medic.mie-u.ac.jp</Email></Contact></Author><Affiliation ID="A1"><OrgDivision>Department of Microbiology</OrgDivision><OrgName>Mie University School of Medicine</OrgName><OrgAddress><Postcode>514-8507</Postcode><City>Tsu</City><State>Mie</State><Country>Japan</Country></OrgAddress></Affiliation><Affiliation ID="A2"><OrgDivision>Department of Microbiology</OrgDivision><OrgName>Suzuka University of Medical Science</OrgName><OrgAddress><Postcode>510-0293</Postcode><City>Suzuka</City><State>Mie</State><Country>Japan</Country></OrgAddress></Affiliation><Affiliation ID="A3"><OrgName>Mie Prefectural College of Nursing</OrgName><OrgAddress><Postcode>514-0116</Postcode><City>Tsu</City><State>Mie</State><Country>Japan</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para> Human parainfluenza virus type 4A (hPIV-4A) and type 4B (hPIV-4B) were tested for their ability to replicate in the monkey kidney LLC-MK2 cell line (MK2 cells) and the murine L929 cell line (L929 cells). These cells are normally non-permissive for replication of hPIV-4; however, treatment with acetylated trypsin led to virus replication in MK2 cells, but was less effective for L929 cells. Endogenously produced interferon (IFN) played no role in virus replication in L929 cells. Synthesis of virus-specific polypeptides was suppressed in L929 cells. WhereasNP-mRNA and HN-mRNA were detected in MK2 cells, no HN-mRNA was detected in L929 cells. These results indicate that hPIV-4 can infect both MK2 cells and L929 cells. In MK2 cells, when protease exists in the extracellular medium, hPIV-4 exhibits multistep growth. In L929 cells, however, the cause of incomplete replication might be lack of other unknown factors.</Para></Abstract><KeywordGroup Language="En"><Keyword>Key words Human parainfluenza virus type 4</Keyword><Keyword>Incomplete replication</Keyword><Keyword>LLC-MK2 cell line</Keyword><Keyword>L929 cell line</Keyword></KeywordGroup><ArticleNote Type="Misc"><SimplePara>Received: 10 January 2000</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Incomplete replication of human parainfluenza virus type 4 in LLC-MK2 cells and in L929 cells</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Incomplete replication of human parainfluenza virus type 4 in LLC-MK2 cells and in L929 cells</title></titleInfo><name type="personal"><namePart type="given">Hiroshi</namePart><namePart type="family">Komada</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hisae</namePart><namePart type="family">Inoue</namePart><affiliation>Department of Microbiology, Suzuka University of Medical Science, 510-0293, Suzuka, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chihiro</namePart><namePart type="family">Yamabayashi</namePart><affiliation>Department of Microbiology, Suzuka University of Medical Science, 510-0293, Suzuka, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Morihiro</namePart><namePart type="family">Ito</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mitsuo</namePart><namePart type="family">Kawano</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Machiko</namePart><namePart type="family">Nishio</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masato</namePart><namePart type="family">Tsurudome</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yuji</namePart><namePart type="family">Kozuka</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naoya</namePart><namePart type="family">Noda</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazuyoshi</namePart><namePart type="family">Namba</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myles</namePart><namePart type="family">O'Brien</namePart><affiliation>Mie Prefectural College of Nursing, 514-0116, Tsu, Mie, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yasuhiko</namePart><namePart type="family">Ito</namePart><affiliation>Department of Microbiology, Mie University School of Medicine, 514-8507, Tsu, Mie, Japan</affiliation><affiliation>E-mail: Ito@doc.medic.mie-u.ac.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" 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>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateIssued encoding="w3cdtf">2000-06-01</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Human parainfluenza virus type 4A (hPIV-4A) and type 4B (hPIV-4B) were tested for their ability to replicate in the monkey kidney LLC-MK2 cell line (MK2 cells) and the murine L929 cell line (L929 cells). These cells are normally non-permissive for replication of hPIV-4; however, treatment with acetylated trypsin led to virus replication in MK2 cells, but was less effective for L929 cells. Endogenously produced interferon (IFN) played no role in virus replication in L929 cells. Synthesis of virus-specific polypeptides was suppressed in L929 cells. WhereasNP-mRNA and HN-mRNA were detected in MK2 cells, no HN-mRNA was detected in L929 cells. These results indicate that hPIV-4 can infect both MK2 cells and L929 cells. In MK2 cells, when protease exists in the extracellular medium, hPIV-4 exhibits multistep growth. In L929 cells, however, the cause of incomplete replication might be lack of other unknown factors.</abstract><note>ORIGINAL INVESTIGATION</note><subject lang="en"><topic>Key words Human parainfluenza virus type 4</topic><topic>Incomplete replication</topic><topic>LLC-MK2 cell line</topic><topic>L929 cell line</topic></subject><relatedItem type="host"><titleInfo><title>Medical Microbiology and Immunology</title></titleInfo><titleInfo type="abbreviated"><title>Med Microbiol Immunol</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>Springer</publisher><dateIssued encoding="w3cdtf">2000-06-01</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><subject><genre>Journal-Subject-Group</genre><topic authority="SpringerSubjectCodes" authorityURI="B">Biomedicine</topic><topic authority="SpringerSubjectCodes" authorityURI="B16003">Medical Microbiology</topic><topic authority="SpringerSubjectCodes" authorityURI="B14000">Immunology</topic></subject><identifier type="ISSN">0300-8584</identifier><identifier type="eISSN">1432-1831</identifier><identifier type="JournalID">430</identifier><identifier type="IssueArticleCount">7</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>2000</date><detail type="volume"><number>188</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="pages"><start>185</start><end>189</end></extent></part><recordInfo><recordOrigin>Springer-Verlag Berlin Heidelberg, 2000</recordOrigin></recordInfo></relatedItem><identifier type="istex">ED266053F87B394B8DBB70DB63B7CB6860247878</identifier><identifier type="ark">ark:/67375/VQC-LG6BGWH2-H</identifier><identifier type="DOI">10.1007/s004300000037</identifier><identifier type="ArticleID">1880185</identifier><identifier type="ArticleID">Art1</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag Berlin Heidelberg, 2000</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Springer-Verlag Berlin Heidelberg, 2000</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-LG6BGWH2-H/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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