Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.
Identifieur interne : 000514 ( Main/Exploration ); précédent : 000513; suivant : 000515Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.
Auteurs : Changmeng Xu [République populaire de Chine] ; Mi Wang [République populaire de Chine] ; Zhongbao Song [République populaire de Chine] ; Zhijian Wang [République populaire de Chine] ; Qianyu Liu [République populaire de Chine] ; Ping Jiang [République populaire de Chine] ; Juan Bai [République populaire de Chine] ; Yufeng Li [République populaire de Chine] ; Xianwei Wang [République populaire de Chine]Source :
- Virus research [ 1872-7492 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Autophagie (MeSH), Autophagosomes (métabolisme), Autophagosomes (ultrastructure), Herpèsvirus porcin de type 1 (physiologie), Herpèsvirus porcin de type 1 (ultrastructure), Lignée cellulaire (MeSH), Maladie d'Aujeszky (virologie), Marqueurs biologiques (MeSH), Réplication virale (MeSH), Souris (MeSH), Survie cellulaire (MeSH), Transduction du signal (MeSH).
- MESH :
- métabolisme : Autophagosomes.
- physiologie : Herpèsvirus porcin de type 1.
- virologie : Maladie d'Aujeszky.
- Animaux, Autophagie, Autophagosomes, Herpèsvirus porcin de type 1, Lignée cellulaire, Marqueurs biologiques, Réplication virale, Souris, Survie cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Autophagosomes (metabolism), Autophagosomes (ultrastructure), Autophagy (MeSH), Biomarkers (MeSH), Cell Line (MeSH), Cell Survival (MeSH), Herpesvirus 1, Suid (physiology), Herpesvirus 1, Suid (ultrastructure), Mice (MeSH), Pseudorabies (virology), Signal Transduction (MeSH), Virus Replication (MeSH).
- MESH :
- chemical : Biomarkers.
- metabolism : Autophagosomes.
- physiology : Herpesvirus 1, Suid.
- ultrastructure : Autophagosomes, Herpesvirus 1, Suid.
- virology : Pseudorabies.
- Animals, Autophagy, Cell Line, Cell Survival, Mice, Signal Transduction, Virus Replication.
Abstract
Autophagy of cytoplasmic components plays an essential role in the pathogenic infection process. Furthermore, research suggests that autophagy is an extremely important component of the innate immune response. Our study aimed to reveal the effect of virus-induced autophagy on pseudorabies virus (PRV) replication. Our results confirmed that light chain 3 (LC3)-I was converted into LC3-II after PRV infection; this transition is considered an important indicator of autophagy. Transmission electron microscopy (TEM) revealed that PRV infection could notably increase the number of autophagosomes in mouse neuro-2a (N2a) cells. In addition, LC3-II accumulated in response to chloroquine (CQ) treatment, indicating that PRV infection induced a complete autophagic flux response. Furthermore, our analyses verified differences in the magnitude of autophagy induction by two different PRV isolates, LA and ZJ01. Subsequent analysis showed that the induction of autophagy by rapamycin facilitated PRV replication, while inhibition of autophagy by 3-methyladenine (3-MA) reduced PRV replication. These results indicated that PRV induced autophagy via the classical Beclin-1-Atg7-Atg5 pathway to enhance viral replication in N2a cells in vitro.
DOI: 10.1016/j.virusres.2018.02.004
PubMed: 29452162
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Medicine, Nanjing Agricultural University, Nanjing 210095, China. 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last="Wang">Mi Wang</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Song, Zhongbao" sort="Song, Zhongbao" uniqKey="Song Z" first="Zhongbao" last="Song">Zhongbao Song</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Zhijian" sort="Wang, Zhijian" uniqKey="Wang Z" first="Zhijian" last="Wang">Zhijian Wang</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Qianyu" sort="Liu, Qianyu" uniqKey="Liu Q" first="Qianyu" last="Liu">Qianyu Liu</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Jiang, Ping" sort="Jiang, Ping" uniqKey="Jiang P" first="Ping" last="Jiang">Ping Jiang</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Bai, Juan" sort="Bai, Juan" uniqKey="Bai J" first="Juan" last="Bai">Juan Bai</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Li, Yufeng" sort="Li, Yufeng" uniqKey="Li Y" first="Yufeng" last="Li">Yufeng Li</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Xianwei" sort="Wang, Xianwei" uniqKey="Wang X" first="Xianwei" last="Wang">Xianwei Wang</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China. Electronic address: xwwang@njau.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095</wicri:regionArea><wicri:noRegion>Nanjing 210095</wicri:noRegion></affiliation></author></analytic><series><title level="j">Virus research</title><idno type="eISSN">1872-7492</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Autophagosomes (metabolism)</term><term>Autophagosomes (ultrastructure)</term><term>Autophagy (MeSH)</term><term>Biomarkers (MeSH)</term><term>Cell Line (MeSH)</term><term>Cell Survival (MeSH)</term><term>Herpesvirus 1, Suid (physiology)</term><term>Herpesvirus 1, Suid (ultrastructure)</term><term>Mice (MeSH)</term><term>Pseudorabies (virology)</term><term>Signal Transduction (MeSH)</term><term>Virus Replication (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Autophagie (MeSH)</term><term>Autophagosomes (métabolisme)</term><term>Autophagosomes (ultrastructure)</term><term>Herpèsvirus porcin de type 1 (physiologie)</term><term>Herpèsvirus porcin de type 1 (ultrastructure)</term><term>Lignée cellulaire (MeSH)</term><term>Maladie d'Aujeszky (virologie)</term><term>Marqueurs biologiques (MeSH)</term><term>Réplication virale (MeSH)</term><term>Souris (MeSH)</term><term>Survie cellulaire (MeSH)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biomarkers</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Autophagosomes</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Herpèsvirus porcin de type 1</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Herpesvirus 1, Suid</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Autophagosomes</term><term>Herpesvirus 1, Suid</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Maladie d'Aujeszky</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Pseudorabies</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>Cell Line</term><term>Cell Survival</term><term>Mice</term><term>Signal Transduction</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Autophagosomes</term><term>Herpèsvirus porcin de type 1</term><term>Lignée cellulaire</term><term>Marqueurs biologiques</term><term>Réplication virale</term><term>Souris</term><term>Survie cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy of cytoplasmic components plays an essential role in the pathogenic infection process. Furthermore, research suggests that autophagy is an extremely important component of the innate immune response. Our study aimed to reveal the effect of virus-induced autophagy on pseudorabies virus (PRV) replication. Our results confirmed that light chain 3 (LC3)-I was converted into LC3-II after PRV infection; this transition is considered an important indicator of autophagy. Transmission electron microscopy (TEM) revealed that PRV infection could notably increase the number of autophagosomes in mouse neuro-2a (N2a) cells. In addition, LC3-II accumulated in response to chloroquine (CQ) treatment, indicating that PRV infection induced a complete autophagic flux response. Furthermore, our analyses verified differences in the magnitude of autophagy induction by two different PRV isolates, LA and ZJ01. Subsequent analysis showed that the induction of autophagy by rapamycin facilitated PRV replication, while inhibition of autophagy by 3-methyladenine (3-MA) reduced PRV replication. These results indicated that PRV induced autophagy via the classical Beclin-1-Atg7-Atg5 pathway to enhance viral replication in N2a cells in vitro.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29452162</PMID><DateCompleted><Year>2018</Year><Month>09</Month><Day>20</Day></DateCompleted><DateRevised><Year>2018</Year><Month>09</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7492</ISSN><JournalIssue CitedMedium="Internet"><Volume>248</Volume><PubDate><Year>2018</Year><Month>03</Month><Day>15</Day></PubDate></JournalIssue><Title>Virus research</Title><ISOAbbreviation>Virus Res</ISOAbbreviation></Journal><ArticleTitle>Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.</ArticleTitle><Pagination><MedlinePgn>44-52</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0168-1702(17)30861-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.virusres.2018.02.004</ELocationID><Abstract><AbstractText>Autophagy of cytoplasmic components plays an essential role in the pathogenic infection process. Furthermore, research suggests that autophagy is an extremely important component of the innate immune response. Our study aimed to reveal the effect of virus-induced autophagy on pseudorabies virus (PRV) replication. Our results confirmed that light chain 3 (LC3)-I was converted into LC3-II after PRV infection; this transition is considered an important indicator of autophagy. Transmission electron microscopy (TEM) revealed that PRV infection could notably increase the number of autophagosomes in mouse neuro-2a (N2a) cells. In addition, LC3-II accumulated in response to chloroquine (CQ) treatment, indicating that PRV infection induced a complete autophagic flux response. Furthermore, our analyses verified differences in the magnitude of autophagy induction by two different PRV isolates, LA and ZJ01. Subsequent analysis showed that the induction of autophagy by rapamycin facilitated PRV replication, while inhibition of autophagy by 3-methyladenine (3-MA) reduced PRV replication. These results indicated that PRV induced autophagy via the classical Beclin-1-Atg7-Atg5 pathway to enhance viral replication in N2a cells in vitro.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Changmeng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Mi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Zhongbao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Zhijian</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Qianyu</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Ping</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yufeng</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xianwei</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China. Electronic address: xwwang@njau.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>02</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Virus Res</MedlineTA><NlmUniqueID>8410979</NlmUniqueID><ISSNLinking>0168-1702</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000071182" MajorTopicYN="N">Autophagosomes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011558" MajorTopicYN="N">Herpesvirus 1, Suid</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011557" MajorTopicYN="N">Pseudorabies</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="Y">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagic flux</Keyword><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">LC3</Keyword><Keyword MajorTopicYN="Y">Pseudorabies virus (PRV)</Keyword><Keyword MajorTopicYN="Y">Replication</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>11</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>02</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>02</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>2</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>9</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>2</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29452162</ArticleId><ArticleId IdType="pii">S0168-1702(17)30861-4</ArticleId><ArticleId IdType="doi">10.1016/j.virusres.2018.02.004</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Xu, Changmeng" sort="Xu, Changmeng" uniqKey="Xu C" first="Changmeng" last="Xu">Changmeng Xu</name></noRegion><name sortKey="Bai, Juan" sort="Bai, Juan" uniqKey="Bai J" first="Juan" last="Bai">Juan Bai</name><name sortKey="Jiang, Ping" sort="Jiang, Ping" uniqKey="Jiang P" first="Ping" last="Jiang">Ping Jiang</name><name sortKey="Li, Yufeng" sort="Li, Yufeng" uniqKey="Li Y" first="Yufeng" last="Li">Yufeng Li</name><name sortKey="Liu, Qianyu" sort="Liu, Qianyu" uniqKey="Liu Q" first="Qianyu" last="Liu">Qianyu Liu</name><name sortKey="Song, Zhongbao" sort="Song, Zhongbao" uniqKey="Song Z" first="Zhongbao" last="Song">Zhongbao Song</name><name sortKey="Wang, Mi" sort="Wang, Mi" uniqKey="Wang M" first="Mi" last="Wang">Mi Wang</name><name sortKey="Wang, Xianwei" sort="Wang, Xianwei" uniqKey="Wang X" first="Xianwei" last="Wang">Xianwei Wang</name><name sortKey="Wang, Zhijian" sort="Wang, Zhijian" uniqKey="Wang Z" first="Zhijian" last="Wang">Zhijian Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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