Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.
Identifieur interne : 000613 ( Main/Corpus ); précédent : 000612; suivant : 000614Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.
Auteurs : Changmeng Xu ; Mi Wang ; Zhongbao Song ; Zhijian Wang ; Qianyu Liu ; Ping Jiang ; Juan Bai ; Yufeng Li ; Xianwei WangSource :
- Virus research [ 1872-7492 ] ; 2018.
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
Links to Exploration step
pubmed:29452162Le document en format XML
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Electronic address: xwwang@njau.edu.cn.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:29452162</idno><idno type="pmid">29452162</idno><idno type="doi">10.1016/j.virusres.2018.02.004</idno><idno type="wicri:Area/Main/Corpus">000613</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000613</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.</title><author><name sortKey="Xu, Changmeng" sort="Xu, Changmeng" uniqKey="Xu C" first="Changmeng" last="Xu">Changmeng Xu</name><affiliation><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></affiliation></author><author><name sortKey="Wang, Mi" sort="Wang, Mi" uniqKey="Wang M" first="Mi" last="Wang">Mi Wang</name><affiliation><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></affiliation></author><author><name sortKey="Song, Zhongbao" sort="Song, Zhongbao" uniqKey="Song Z" first="Zhongbao" last="Song">Zhongbao Song</name><affiliation><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></affiliation></author><author><name sortKey="Wang, Zhijian" sort="Wang, Zhijian" uniqKey="Wang Z" first="Zhijian" last="Wang">Zhijian Wang</name><affiliation><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></affiliation></author><author><name sortKey="Liu, Qianyu" sort="Liu, Qianyu" uniqKey="Liu Q" first="Qianyu" last="Liu">Qianyu Liu</name><affiliation><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></affiliation></author><author><name sortKey="Jiang, Ping" sort="Jiang, Ping" uniqKey="Jiang P" first="Ping" last="Jiang">Ping Jiang</name><affiliation><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></affiliation></author><author><name sortKey="Bai, Juan" sort="Bai, Juan" uniqKey="Bai J" first="Juan" last="Bai">Juan Bai</name><affiliation><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></affiliation></author><author><name sortKey="Li, Yufeng" sort="Li, Yufeng" uniqKey="Li Y" first="Yufeng" last="Li">Yufeng Li</name><affiliation><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></affiliation></author><author><name sortKey="Wang, Xianwei" sort="Wang, Xianwei" uniqKey="Wang X" first="Xianwei" last="Wang">Xianwei Wang</name><affiliation><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></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="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="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="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></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></record>Pour manipuler ce document sous Unix (Dilib)
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