Susceptibility to flavivirus-specific antiviral response of Oas1b affects the neurovirulence of the Far-Eastern subtype of tick-borne encephalitis virus
Identifieur interne : 000F07 ( Istex/Corpus ); précédent : 000F06; suivant : 000F08Susceptibility to flavivirus-specific antiviral response of Oas1b affects the neurovirulence of the Far-Eastern subtype of tick-borne encephalitis virus
Auteurs : Kentaro Yoshii ; Kanako Moritoh ; Noriyo Nagata ; Kana Yokozawa ; Mizuki Sakai ; Nobuya Sasaki ; Hiroaki Kariwa ; Takashi Agui ; Ikuo TakashimaSource :
- Archives of Virology [ 0304-8608 ] ; 2013-05-01.
Abstract
Abstract: Tick-borne encephalitis virus (TBEV) is a zoonotic agent that causes fatal encephalitis in humans. 2’-5’-oligoadenylate synthetase 1b (Oas1b) has been identified as a flavivirus resistance gene, but most inbred laboratory mice do not possess a functional Oas1b gene. In this study, a congenic strain carrying a functional Oas1b gene, B6.MSM-Oas, was used to evaluate the pathogenicity of Far-Eastern TBEV. Although intracerebral infection of B6.MSM-Oas mice by Oshima 5-10 resulted in limited signs of illness, infection by Sofjin-HO resulted in death with severe neurologic signs. While Oshima 5-10 was cleared from the brain, Sofjin-HO was not cleared despite a similar level of expression of the intact Oas1b gene. Necrotic neurons with viral antigens and inflammatory reactions were observed in the brain infected with Sofjin-HO. These data indicate that the different susceptibility to the antiviral activity of Oas1b resulted in a difference in neurovirulence in the two TBEV strains.
Url:
DOI: 10.1007/s00705-012-1579-1
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ISTEX:3CD5DB8D97A3A489F0E2E92B8C3B3B0E80AB8FD7Le document en format XML
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Takashima</name><affiliation><mods:affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Archives of Virology</title><title level="j" type="sub">Official Journal of the Virology Division of the International Union of Microbiological Societies</title><title level="j" type="abbrev">Arch Virol</title><idno type="ISSN">0304-8608</idno><idno type="eISSN">1432-8798</idno><imprint><publisher>Springer Vienna</publisher><pubPlace>Vienna</pubPlace><date type="published" when="2013-05-01">2013-05-01</date><biblScope unit="volume">158</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1039">1039</biblScope><biblScope unit="page" to="1046">1046</biblScope></imprint><idno 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In this study, a congenic strain carrying a functional Oas1b gene, B6.MSM-Oas, was used to evaluate the pathogenicity of Far-Eastern TBEV. Although intracerebral infection of B6.MSM-Oas mice by Oshima 5-10 resulted in limited signs of illness, infection by Sofjin-HO resulted in death with severe neurologic signs. While Oshima 5-10 was cleared from the brain, Sofjin-HO was not cleared despite a similar level of expression of the intact Oas1b gene. Necrotic neurons with viral antigens and inflammatory reactions were observed in the brain infected with Sofjin-HO. These data indicate that the different susceptibility to the antiviral activity of Oas1b resulted in a difference in neurovirulence in the two TBEV strains.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Kentaro Yoshii</name><affiliations><json:string>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</json:string><json:string>E-mail: kyoshii@vetmed.hokudai.ac.jp</json:string></affiliations></json:item><json:item><name>Kanako Moritoh</name><affiliations><json:string>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Noriyo Nagata</name><affiliations><json:string>Department of Pathology, National Institute of Infectious Diseases, 208-0011, Musashimurayama, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Kana Yokozawa</name><affiliations><json:string>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Mizuki Sakai</name><affiliations><json:string>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Nobuya Sasaki</name><affiliations><json:string>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Hiroaki Kariwa</name><affiliations><json:string>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Takashi Agui</name><affiliations><json:string>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Ikuo Takashima</name><affiliations><json:string>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item></author><articleId><json:string>1579</json:string><json:string>s00705-012-1579-1</json:string></articleId><arkIstex>ark:/67375/VQC-Z2LV7HMM-1</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Abstract: Tick-borne encephalitis virus (TBEV) is a zoonotic agent that causes fatal encephalitis in humans. 2’-5’-oligoadenylate synthetase 1b (Oas1b) has been identified as a flavivirus resistance gene, but most inbred laboratory mice do not possess a functional Oas1b gene. In this study, a congenic strain carrying a functional Oas1b gene, B6.MSM-Oas, was used to evaluate the pathogenicity of Far-Eastern TBEV. Although intracerebral infection of B6.MSM-Oas mice by Oshima 5-10 resulted in limited signs of illness, infection by Sofjin-HO resulted in death with severe neurologic signs. While Oshima 5-10 was cleared from the brain, Sofjin-HO was not cleared despite a similar level of expression of the intact Oas1b gene. Necrotic neurons with viral antigens and inflammatory reactions were observed in the brain infected with Sofjin-HO. 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VolumeType="Regular"><VolumeIDStart>158</VolumeIDStart><VolumeIDEnd>158</VolumeIDEnd><VolumeIssueCount>12</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular" OutputMedium="All"><IssueInfo IssueType="Regular" TocLevels="0"><IssueIDStart>5</IssueIDStart><IssueIDEnd>5</IssueIDEnd><IssueArticleCount>24</IssueArticleCount><IssueHistory><OnlineDate><Year>2013</Year><Month>4</Month><Day>25</Day></OnlineDate><PrintDate><Year>2013</Year><Month>4</Month><Day>24</Day></PrintDate><CoverDate><Year>2013</Year><Month>5</Month></CoverDate><PricelistYear>2013</PricelistYear></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag Wien</CopyrightHolderName><CopyrightYear>2013</CopyrightYear></IssueCopyright></IssueInfo><Article ID="s00705-012-1579-1" OutputMedium="All"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="Yes" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>1579</ArticleID><ArticleDOI>10.1007/s00705-012-1579-1</ArticleDOI><ArticleSequenceNumber>12</ArticleSequenceNumber><ArticleTitle Language="En" OutputMedium="All">Susceptibility to flavivirus-specific antiviral response of Oas1b affects the neurovirulence of the Far-Eastern subtype of tick-borne encephalitis virus</ArticleTitle><ArticleCategory>Original Article</ArticleCategory><ArticleFirstPage>1039</ArticleFirstPage><ArticleLastPage>1046</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2012</Year><Month>12</Month><Day>8</Day></RegistrationDate><Received><Year>2012</Year><Month>6</Month><Day>12</Day></Received><Accepted><Year>2012</Year><Month>10</Month><Day>10</Day></Accepted><OnlineDate><Year>2012</Year><Month>12</Month><Day>25</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag Wien</CopyrightHolderName><CopyrightYear>2012</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="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Kentaro</GivenName><FamilyName>Yoshii</FamilyName></AuthorName><Contact><Phone>+81-11-7065213</Phone><Fax>+81-11-7065213</Fax><Email>kyoshii@vetmed.hokudai.ac.jp</Email></Contact></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Kanako</GivenName><FamilyName>Moritoh</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Noriyo</GivenName><FamilyName>Nagata</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Kana</GivenName><FamilyName>Yokozawa</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Mizuki</GivenName><FamilyName>Sakai</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Nobuya</GivenName><FamilyName>Sasaki</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Hiroaki</GivenName><FamilyName>Kariwa</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Takashi</GivenName><FamilyName>Agui</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Ikuo</GivenName><FamilyName>Takashima</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine</OrgDivision><OrgName>Hokkaido University</OrgName><OrgAddress><Street>Kita-18 nishi-9, kita-ku</Street><City>Sapporo</City><State>Hokkaido</State><Postcode>060-0818</Postcode><Country Code="JP">Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine</OrgDivision><OrgName>Hokkaido University</OrgName><OrgAddress><City>Sapporo</City><State>Hokkaido</State><Postcode>060-0818</Postcode><Country Code="JP">Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Pathology</OrgDivision><OrgName>National Institute of Infectious Diseases</OrgName><OrgAddress><City>Musashimurayama</City><State>Tokyo</State><Postcode>208-0011</Postcode><Country Code="JP">Japan</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En" OutputMedium="All"><Heading>Abstract</Heading><Para>Tick-borne encephalitis virus (TBEV) is a zoonotic agent that causes fatal encephalitis in humans. 2’-5’-oligoadenylate synthetase 1b (<Emphasis Type="Italic">Oas1b</Emphasis>) has been identified as a flavivirus resistance gene, but most inbred laboratory mice do not possess a functional <Emphasis Type="Italic">Oas1b</Emphasis> gene. In this study, a congenic strain carrying a functional <Emphasis Type="Italic">Oas1b</Emphasis> gene, B6.MSM-<Emphasis Type="Italic">Oas</Emphasis>, was used to evaluate the pathogenicity of Far-Eastern TBEV. Although intracerebral infection of B6.MSM-<Emphasis Type="Italic">Oas</Emphasis> mice by Oshima 5-10 resulted in limited signs of illness, infection by Sofjin-HO resulted in death with severe neurologic signs. While Oshima 5-10 was cleared from the brain, Sofjin-HO was not cleared despite a similar level of expression of the intact <Emphasis Type="Italic">Oas1b</Emphasis> gene. Necrotic neurons with viral antigens and inflammatory reactions were observed in the brain infected with Sofjin-HO. These data indicate that the different susceptibility to the antiviral activity of Oas1b resulted in a difference in neurovirulence in the two TBEV strains.</Para></Abstract><AbbreviationGroup><Heading>Abbreviations</Heading><DefinitionList><DefinitionListEntry><Term>BHK</Term><Description><Para>Baby hamster kidney</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>B6</Term><Description><Para>C57BL/6J</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>CNS</Term><Description><Para>Central nervous system</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>FCS</Term><Description><Para>Fetal calf serum</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>LD<Subscript>50</Subscript></Term><Description><Para>50 % lethal dose</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>MEM</Term><Description><Para>Minimum essential medium</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>OAS</Term><Description><Para>2’-5’-oligoadenylate synthetase</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>Oas1b</Term><Description><Para>2’-5’-oligoadenylate synthetase 1b</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>pfu</Term><Description><Para>Plaque-forming unit</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>TBE</Term><Description><Para>Tick-borne encephalitis</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>TBEV</Term><Description><Para>Tick-borne encephalitis virus</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>TBST</Term><Description><Para>TBS containing 0.01% Tween 20</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>WNV</Term><Description><Para>West Nile virus</Para></Description></DefinitionListEntry></DefinitionList></AbbreviationGroup><ArticleNote Type="ESMHint"><Heading>Electronic supplementary material</Heading><SimplePara>The online version of this article (doi:<ExternalRef><RefSource>10.1007/s00705-012-1579-1</RefSource><RefTarget Address="10.1007/s00705-012-1579-1" TargetType="DOI"></RefTarget></ExternalRef>) contains supplementary material, which is available to authorized users.</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Susceptibility to flavivirus-specific antiviral response of Oas1b affects the neurovirulence of the Far-Eastern subtype of tick-borne encephalitis virus</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Susceptibility to flavivirus-specific antiviral response of Oas1b affects the neurovirulence of the Far-Eastern subtype of tick-borne encephalitis virus</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Kentaro</namePart><namePart type="family">Yoshii</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</affiliation><affiliation>E-mail: kyoshii@vetmed.hokudai.ac.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kanako</namePart><namePart type="family">Moritoh</namePart><affiliation>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Noriyo</namePart><namePart type="family">Nagata</namePart><affiliation>Department of Pathology, National Institute of Infectious Diseases, 208-0011, Musashimurayama, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kana</namePart><namePart type="family">Yokozawa</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mizuki</namePart><namePart type="family">Sakai</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nobuya</namePart><namePart type="family">Sasaki</namePart><affiliation>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroaki</namePart><namePart type="family">Kariwa</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Agui</namePart><affiliation>Laboratory of Laboratory Animal Science and Medicine, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ikuo</namePart><namePart type="family">Takashima</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18 nishi-9, kita-ku, 060-0818, Sapporo, Hokkaido, Japan</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 Vienna</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">2012-06-12</dateCreated><dateIssued encoding="w3cdtf">2013-05-01</dateIssued><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Tick-borne encephalitis virus (TBEV) is a zoonotic agent that causes fatal encephalitis in humans. 2’-5’-oligoadenylate synthetase 1b (Oas1b) has been identified as a flavivirus resistance gene, but most inbred laboratory mice do not possess a functional Oas1b gene. In this study, a congenic strain carrying a functional Oas1b gene, B6.MSM-Oas, was used to evaluate the pathogenicity of Far-Eastern TBEV. Although intracerebral infection of B6.MSM-Oas mice by Oshima 5-10 resulted in limited signs of illness, infection by Sofjin-HO resulted in death with severe neurologic signs. While Oshima 5-10 was cleared from the brain, Sofjin-HO was not cleared despite a similar level of expression of the intact Oas1b gene. Necrotic neurons with viral antigens and inflammatory reactions were observed in the brain infected with Sofjin-HO. These data indicate that the different susceptibility to the antiviral activity of Oas1b resulted in a difference in neurovirulence in the two TBEV strains.</abstract><note>Original Article</note><relatedItem type="host"><titleInfo><title>Archives of Virology</title><subTitle>Official Journal of the Virology Division of the International Union of Microbiological Societies</subTitle></titleInfo><titleInfo type="abbreviated"><title>Arch Virol</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">2013-04-25</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><subject><genre>Journal-Subject-Collection</genre><topic authority="SpringerSubjectCodes" authorityURI="SC3">Biomedical and Life Sciences</topic></subject><subject><genre>Journal-Subject-Group</genre><topic authority="SpringerSubjectCodes" authorityURI="SCB">Biomedicine</topic><topic authority="SpringerSubjectCodes" authorityURI="SCB22003">Virology</topic><topic authority="SpringerSubjectCodes" authorityURI="SCB16003">Medical Microbiology</topic><topic authority="SpringerSubjectCodes" authorityURI="SCH33096">Infectious Diseases</topic></subject><identifier type="ISSN">0304-8608</identifier><identifier type="eISSN">1432-8798</identifier><identifier type="JournalID">705</identifier><identifier type="IssueArticleCount">24</identifier><identifier type="VolumeIssueCount">12</identifier><part><date>2013</date><detail type="volume"><number>158</number><caption>vol.</caption></detail><detail type="issue"><number>5</number><caption>no.</caption></detail><extent unit="pages"><start>1039</start><end>1046</end></extent></part><recordInfo><recordOrigin>Springer-Verlag Wien, 2013</recordOrigin></recordInfo></relatedItem><identifier type="istex">3CD5DB8D97A3A489F0E2E92B8C3B3B0E80AB8FD7</identifier><identifier type="ark">ark:/67375/VQC-Z2LV7HMM-1</identifier><identifier type="DOI">10.1007/s00705-012-1579-1</identifier><identifier type="ArticleID">1579</identifier><identifier type="ArticleID">s00705-012-1579-1</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag Wien, 2012</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 Wien, 2012</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-Z2LV7HMM-1/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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