Newcastle disease virus triggers autophagy in U251 glioma cells to enhance virus replication
Identifieur interne : 000A43 ( Istex/Corpus ); précédent : 000A42; suivant : 000A44Newcastle disease virus triggers autophagy in U251 glioma cells to enhance virus replication
Auteurs : Chunchun Meng ; Zhizhi Zhou ; Ke Jiang ; Shengqing Yu ; Lijun Jia ; Yantao Wu ; Yanqing Liu ; Songshu Meng ; Chan DingSource :
- Archives of Virology [ 0304-8608 ] ; 2012-06-01.
Abstract
Abstract: Newcastle disease virus (NDV) can replicate in tumor cells and induce apoptosis in late stages of infection. However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (Atg5 and Beclin-1) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. Collectively, our data provide a unique example of a paramyxovirus that uses autophagy to enhance its production.
Url:
DOI: 10.1007/s00705-012-1270-6
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However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (Atg5 and Beclin-1) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. Collectively, our data provide a unique example of a paramyxovirus that uses autophagy to enhance its production.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Chunchun Meng</name><affiliations><json:string>Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 518 Ziyue Road, 200241, Shanghai, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Zhizhi Zhou</name><affiliations><json:string>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Ke Jiang</name><affiliations><json:string>College of Veterinary Medicine, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Shengqing Yu</name><affiliations><json:string>Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 518 Ziyue Road, 200241, Shanghai, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Lijun Jia</name><affiliations><json:string>Department of Immunology, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, 200032, Shanghai, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Yantao Wu</name><affiliations><json:string>College of Veterinary Medicine, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Yanqing Liu</name><affiliations><json:string>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</json:string></affiliations></json:item><json:item><name>Songshu Meng</name><affiliations><json:string>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</json:string><json:string>E-mail: ssmeng@yzu.edu.cn</json:string></affiliations></json:item><json:item><name>Chan Ding</name><affiliations><json:string>Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 518 Ziyue Road, 200241, Shanghai, People’s Republic of China</json:string><json:string>E-mail: shoveldeen@shvri.ac.cn</json:string></affiliations></json:item></author><articleId><json:string>1270</json:string><json:string>s00705-012-1270-6</json:string></articleId><arkIstex>ark:/67375/VQC-RKHHJRB0-Q</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Abstract: Newcastle disease virus (NDV) can replicate in tumor cells and induce apoptosis in late stages of infection. However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (Atg5 and Beclin-1) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. 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518 Ziyue Road, 200241, Shanghai, People’s Republic of China</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Lijun</forename><surname>Jia</surname></persName><affiliation>Department of Immunology, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, 200032, Shanghai, People’s Republic of China</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Yantao</forename><surname>Wu</surname></persName><affiliation>College of Veterinary Medicine, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Yanqing</forename><surname>Liu</surname></persName><affiliation>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation></author><author xml:id="author-0007" corresp="yes"><persName><forename 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However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (Atg5 and Beclin-1) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. Collectively, our data provide a unique example of a paramyxovirus that uses autophagy to enhance its production.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Virology</term></item><item><term>Infectious Diseases</term></item><item><term>Medical Microbiology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-10-02">Created</change><change when="2012-06-01">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-RKHHJRB0-Q/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not 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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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"><AuthorName DisplayOrder="Western"><GivenName>Chunchun</GivenName><FamilyName>Meng</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Zhizhi</GivenName><FamilyName>Zhou</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Ke</GivenName><FamilyName>Jiang</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Shengqing</GivenName><FamilyName>Yu</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>Lijun</GivenName><FamilyName>Jia</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Yantao</GivenName><FamilyName>Wu</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Yanqing</GivenName><FamilyName>Liu</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2" CorrespondingAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Songshu</GivenName><FamilyName>Meng</FamilyName></AuthorName><Contact><Phone>86-514-87972107</Phone><Fax>86-514-87991747</Fax><Email>ssmeng@yzu.edu.cn</Email></Contact></Author><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Chan</GivenName><FamilyName>Ding</FamilyName></AuthorName><Contact><Phone>86-21-34293441</Phone><Fax>86-21-54081818</Fax><Email>shoveldeen@shvri.ac.cn</Email></Contact></Author><Affiliation ID="Aff1"><OrgDivision>Shanghai Veterinary Research Institute</OrgDivision><OrgName>The Chinese Academy of Agricultural Sciences</OrgName><OrgAddress><Street>518 Ziyue Road</Street><City>Shanghai</City><Postcode>200241</Postcode><Country Code="CN">People’s Republic of China</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>College of Bioscience and Biotechnology</OrgDivision><OrgName>Yangzhou University</OrgName><OrgAddress><Street>48 Wenhuidong Road</Street><City>Yangzhou</City><Postcode>225009</Postcode><Country Code="CN">People’s Republic of China</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>College of Veterinary Medicine</OrgDivision><OrgName>Yangzhou University</OrgName><OrgAddress><Street>48 Wenhuidong Road</Street><City>Yangzhou</City><Postcode>225009</Postcode><Country Code="CN">People’s Republic of China</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Department of Immunology, Shanghai Medical College</OrgDivision><OrgName>Fudan University</OrgName><OrgAddress><Street>138 Yixueyuan Road</Street><City>Shanghai</City><Postcode>200032</Postcode><Country Code="CN">People’s Republic of China</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En" OutputMedium="All"><Heading>Abstract</Heading><Para>Newcastle disease virus (NDV) can replicate in tumor cells and induce apoptosis in late stages of infection. However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (<Emphasis Type="Italic">Atg5</Emphasis> and <Emphasis Type="Italic">Beclin-1</Emphasis>) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. Collectively, our data provide a unique example of a paramyxovirus that uses autophagy to enhance its production.</Para></Abstract><ArticleNote Type="Misc"><SimplePara>C. Meng and Z. Zhou contributed equally to this work.</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Newcastle disease virus triggers autophagy in U251 glioma cells to enhance virus replication</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Newcastle disease virus triggers autophagy in U251 glioma cells to enhance virus replication</title></titleInfo><name type="personal"><namePart type="given">Chunchun</namePart><namePart type="family">Meng</namePart><affiliation>Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 518 Ziyue Road, 200241, Shanghai, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Zhizhi</namePart><namePart type="family">Zhou</namePart><affiliation>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ke</namePart><namePart type="family">Jiang</namePart><affiliation>College of Veterinary Medicine, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shengqing</namePart><namePart type="family">Yu</namePart><affiliation>Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 518 Ziyue Road, 200241, Shanghai, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lijun</namePart><namePart type="family">Jia</namePart><affiliation>Department of Immunology, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, 200032, Shanghai, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yantao</namePart><namePart type="family">Wu</namePart><affiliation>College of Veterinary Medicine, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yanqing</namePart><namePart type="family">Liu</namePart><affiliation>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Songshu</namePart><namePart type="family">Meng</namePart><affiliation>College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhuidong Road, 225009, Yangzhou, People’s Republic of China</affiliation><affiliation>E-mail: ssmeng@yzu.edu.cn</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Chan</namePart><namePart type="family">Ding</namePart><affiliation>Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 518 Ziyue Road, 200241, Shanghai, People’s Republic of China</affiliation><affiliation>E-mail: shoveldeen@shvri.ac.cn</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">2011-10-02</dateCreated><dateIssued encoding="w3cdtf">2012-06-01</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: Newcastle disease virus (NDV) can replicate in tumor cells and induce apoptosis in late stages of infection. However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (Atg5 and Beclin-1) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. Collectively, our data provide a unique example of a paramyxovirus that uses autophagy to enhance its production.</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">2012-05-31</dateIssued><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Virology</topic><topic>Infectious Diseases</topic><topic>Medical Microbiology</topic></subject><identifier type="ISSN">0304-8608</identifier><identifier type="eISSN">1432-8798</identifier><identifier type="JournalID">705</identifier><identifier type="IssueArticleCount">28</identifier><identifier type="VolumeIssueCount">12</identifier><part><date>2012</date><detail type="volume"><number>157</number><caption>vol.</caption></detail><detail type="issue"><number>6</number><caption>no.</caption></detail><extent unit="pages"><start>1011</start><end>1018</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 2012</recordOrigin></recordInfo></relatedItem><identifier type="istex">1A493F302411893F95B8D8D71482CD0102E4B57B</identifier><identifier type="ark">ark:/67375/VQC-RKHHJRB0-Q</identifier><identifier type="DOI">10.1007/s00705-012-1270-6</identifier><identifier type="ArticleID">1270</identifier><identifier type="ArticleID">s00705-012-1270-6</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag, 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, 2012</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-RKHHJRB0-Q/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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