RapamycinFungusV1, Main, Exploration, bibRecord, 000356

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation.

Identifieur interne : 000356 ( Main/Exploration ); précédent : 000355; suivant : 000357

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation.

Auteurs : M S Gilardini Montani [Italie] ; R. Santarelli [Italie] ; M. Granato [Italie] ; R. Gonnella [Italie] ; M R Torrisi [Italie] ; A. Faggioni [Italie] ; M. Cirone [Italie]

Source :

Autophagy [ 1554-8635 ] ; 2019.

RBID : pubmed:30324853

Descripteurs français

English descriptors

Abstract

EBV has been reported to impair monocyte in vitro differentiation into dendritic cells (DCs) and reduce cell survival. In this study, we added another layer of knowledge to this topic and showed that these effects correlated with macroautophagy/autophagy, ROS and mitochondrial biogenesis reduction. Of note, autophagy and ROS, although strongly interconnected, have been separately reported to be induced by CSF2/GM-CSF (colony stimulating factor 2) and required for CSF2-IL4-driven monocyte in vitro differentiation into DCs. We show that EBV infects monocytes and initiates a feedback loop in which, by inhibiting autophagy, reduces ROS and through ROS reduction negatively influences autophagy. Mechanistically, autophagy reduction correlated with the downregulation of RAB7 and ATG5 expression and STAT3 activation, leading to the accumulation of SQSTM1/p62. The latter activated the SQSTM1-KEAP1- NFE2L2 axis and upregulated the anti-oxidant response, reducing ROS and further inhibiting autophagy. ROS decrease correlated also with the reduction of mitochondria, the main source of intracellular ROS, achieved by the downregulation of NRF1 and TFAM, mitochondrial biogenesis transcription factors. Interestingly, mitochondria supply membranes and ATP required for autophagy execution, thus their reduction may further reduce autophagy in EBV-infected monocytes. In conclusion, this study shows for the first time that the interconnected reduction of autophagy, intracellular ROS and mitochondria mediated by EBV switches monocyte differentiation into apoptosis, giving new insights into the mechanisms through which this virus reduces immune surveillance. Abbreviations: ACTB: actin beta; ATG5: autophagy related 5; BAF: bafilomycin A₁; BECN1: beclin 1; CAT: catalase; CSF2: colony stimulating factor 2; CT: control; CYCS (cytochrome C: somatic); DCs: dendritic cells; EBV: Epstein-Barr virus; GSR: glutathione-disulfide reductase; KEAP1: kelch like ECH associated protein 1; IL4: interleukin 4; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MET: metformin; NAC: N-acetylcysteine; NFE2L2/NRF2 nuclear factor: erythroid 2 like 2; NRF1 (nuclear respiratory factor 1); clPARP1: cleaved poly(ADP-ribose) polymerase; Rapa: Rapamycin; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1; TFAM: (transcription factor A: mitochondrial); TUBA1A: tubulin alpha 1a.

DOI: 10.1080/15548627.2018.1536530
PubMed: 30324853
PubMed Central: PMC6526866

Affiliations:

Italie

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000433
to stream Main, to step Curation: 000433

Le document en format XML

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<series><title level="j">Autophagy</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (genetics)</term>
<term>Autophagosomes (metabolism)</term>
<term>Autophagosomes (virology)</term>
<term>Autophagy (genetics)</term>
<term>Autophagy-Related Protein 5 (genetics)</term>
<term>Autophagy-Related Protein 5 (metabolism)</term>
<term>Cell Differentiation (genetics)</term>
<term>Cell Survival (genetics)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>DNA-Binding Proteins (metabolism)</term>
<term>Dendritic Cells (metabolism)</term>
<term>Dendritic Cells (virology)</term>
<term>Granulocyte-Macrophage Colony-Stimulating Factor (metabolism)</term>
<term>Herpesvirus 4, Human (physiology)</term>
<term>Humans (MeSH)</term>
<term>Interleukin-4 (metabolism)</term>
<term>Kelch-Like ECH-Associated Protein 1 (genetics)</term>
<term>Kelch-Like ECH-Associated Protein 1 (metabolism)</term>
<term>Mitochondria (metabolism)</term>
<term>Mitochondrial Proteins (genetics)</term>
<term>Mitochondrial Proteins (metabolism)</term>
<term>Monocytes (metabolism)</term>
<term>Monocytes (virology)</term>
<term>NF-E2-Related Factor 2 (genetics)</term>
<term>NF-E2-Related Factor 2 (metabolism)</term>
<term>RNA, Small Interfering (MeSH)</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>STAT3 Transcription Factor (genetics)</term>
<term>STAT3 Transcription Factor (metabolism)</term>
<term>Sequestosome-1 Protein (genetics)</term>
<term>Sequestosome-1 Protein (metabolism)</term>
<term>Signal Transduction (genetics)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
<term>rab GTP-Binding Proteins (genetics)</term>
<term>rab GTP-Binding Proteins (metabolism)</term>
</keywords>
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<term>Autophagie (génétique)</term>
<term>Autophagosomes (métabolisme)</term>
<term>Autophagosomes (virologie)</term>
<term>Cellules dendritiques (métabolisme)</term>
<term>Cellules dendritiques (virologie)</term>
<term>Différenciation cellulaire (génétique)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Facteur de stimulation des colonies de granulocytes et de macrophages (métabolisme)</term>
<term>Facteur de transcription STAT-3 (génétique)</term>
<term>Facteur de transcription STAT-3 (métabolisme)</term>
<term>Facteur-2 apparenté à NF-E2 (génétique)</term>
<term>Facteur-2 apparenté à NF-E2 (métabolisme)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Herpèsvirus humain de type 4 (physiologie)</term>
<term>Humains (MeSH)</term>
<term>Interleukine-4 (métabolisme)</term>
<term>Mitochondries (métabolisme)</term>
<term>Monocytes (métabolisme)</term>
<term>Monocytes (virologie)</term>
<term>Petit ARN interférent (MeSH)</term>
<term>Protéine-1 de type kelch associée à ECH (génétique)</term>
<term>Protéine-1 de type kelch associée à ECH (métabolisme)</term>
<term>Protéine-5 associée à l'autophagie (génétique)</term>
<term>Protéine-5 associée à l'autophagie (métabolisme)</term>
<term>Protéines G rab (génétique)</term>
<term>Protéines G rab (métabolisme)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de liaison à l'ADN (métabolisme)</term>
<term>Protéines mitochondriales (génétique)</term>
<term>Protéines mitochondriales (métabolisme)</term>
<term>Survie cellulaire (génétique)</term>
<term>Séquestosome-1 (génétique)</term>
<term>Séquestosome-1 (métabolisme)</term>
<term>Transduction du signal (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein 5</term>
<term>DNA-Binding Proteins</term>
<term>Kelch-Like ECH-Associated Protein 1</term>
<term>Mitochondrial Proteins</term>
<term>NF-E2-Related Factor 2</term>
<term>STAT3 Transcription Factor</term>
<term>Sequestosome-1 Protein</term>
<term>Transcription Factors</term>
<term>rab GTP-Binding Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Cell Differentiation</term>
<term>Cell Survival</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apoptose</term>
<term>Autophagie</term>
<term>Différenciation cellulaire</term>
<term>Facteur de transcription STAT-3</term>
<term>Facteur-2 apparenté à NF-E2</term>
<term>Facteurs de transcription</term>
<term>Protéine-1 de type kelch associée à ECH</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Protéines G rab</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines mitochondriales</term>
<term>Survie cellulaire</term>
<term>Séquestosome-1</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term>
<term>Autophagy-Related Protein 5</term>
<term>DNA-Binding Proteins</term>
<term>Dendritic Cells</term>
<term>Granulocyte-Macrophage Colony-Stimulating Factor</term>
<term>Interleukin-4</term>
<term>Kelch-Like ECH-Associated Protein 1</term>
<term>Mitochondria</term>
<term>Mitochondrial Proteins</term>
<term>Monocytes</term>
<term>NF-E2-Related Factor 2</term>
<term>Reactive Oxygen Species</term>
<term>STAT3 Transcription Factor</term>
<term>Sequestosome-1 Protein</term>
<term>Transcription Factors</term>
<term>rab GTP-Binding Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Autophagosomes</term>
<term>Cellules dendritiques</term>
<term>Espèces réactives de l'oxygène</term>
<term>Facteur de stimulation des colonies de granulocytes et de macrophages</term>
<term>Facteur de transcription STAT-3</term>
<term>Facteur-2 apparenté à NF-E2</term>
<term>Facteurs de transcription</term>
<term>Interleukine-4</term>
<term>Mitochondries</term>
<term>Monocytes</term>
<term>Protéine-1 de type kelch associée à ECH</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Protéines G rab</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines mitochondriales</term>
<term>Séquestosome-1</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Herpèsvirus humain de type 4</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Herpesvirus 4, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Autophagosomes</term>
<term>Cellules dendritiques</term>
<term>Monocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Autophagosomes</term>
<term>Dendritic Cells</term>
<term>Monocytes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Humans</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Petit ARN interférent</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en">EBV has been reported to impair monocyte in vitro differentiation into dendritic cells (DCs) and reduce cell survival. In this study, we added another layer of knowledge to this topic and showed that these effects correlated with macroautophagy/autophagy, ROS and mitochondrial biogenesis reduction. Of note, autophagy and ROS, although strongly interconnected, have been separately reported to be induced by CSF2/GM-CSF (colony stimulating factor 2) and required for CSF2-IL4-driven monocyte in vitro differentiation into DCs. We show that EBV infects monocytes and initiates a feedback loop in which, by inhibiting autophagy, reduces ROS and through ROS reduction negatively influences autophagy. Mechanistically, autophagy reduction correlated with the downregulation of RAB7 and ATG5 expression and STAT3 activation, leading to the accumulation of SQSTM1/p62. The latter activated the SQSTM1-KEAP1- NFE2L2 axis and upregulated the anti-oxidant response, reducing ROS and further inhibiting autophagy. ROS decrease correlated also with the reduction of mitochondria, the main source of intracellular ROS, achieved by the downregulation of NRF1 and TFAM, mitochondrial biogenesis transcription factors. Interestingly, mitochondria supply membranes and ATP required for autophagy execution, thus their reduction may further reduce autophagy in EBV-infected monocytes. In conclusion, this study shows for the first time that the interconnected reduction of autophagy, intracellular ROS and mitochondria mediated by EBV switches monocyte differentiation into apoptosis, giving new insights into the mechanisms through which this virus reduces immune surveillance. Abbreviations: ACTB: actin beta; ATG5: autophagy related 5; BAF: bafilomycin A<sub>1</sub>
; BECN1: beclin 1; CAT: catalase; CSF2: colony stimulating factor 2; CT: control; CYCS (cytochrome C: somatic); DCs: dendritic cells; EBV: Epstein-Barr virus; GSR: glutathione-disulfide reductase; KEAP1: kelch like ECH associated protein 1; IL4: interleukin 4; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MET: metformin; NAC: N-acetylcysteine; NFE2L2/NRF2 nuclear factor: erythroid 2 like 2; NRF1 (nuclear respiratory factor 1); clPARP1: cleaved poly(ADP-ribose) polymerase; Rapa: Rapamycin; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1; TFAM: (transcription factor A: mitochondrial); TUBA1A: tubulin alpha 1a.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30324853</PMID>
<DateCompleted><Year>2020</Year>
<Month>05</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>05</Month>
<Day>11</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>15</Volume>
<Issue>4</Issue>
<PubDate><Year>2019</Year>
<Month>04</Month>
</PubDate>
</JournalIssue>
<Title>Autophagy</Title>
<ISOAbbreviation>Autophagy</ISOAbbreviation>
</Journal>
<ArticleTitle>EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation.</ArticleTitle>
<Pagination><MedlinePgn>652-667</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2018.1536530</ELocationID>
<Abstract><AbstractText>EBV has been reported to impair monocyte in vitro differentiation into dendritic cells (DCs) and reduce cell survival. In this study, we added another layer of knowledge to this topic and showed that these effects correlated with macroautophagy/autophagy, ROS and mitochondrial biogenesis reduction. Of note, autophagy and ROS, although strongly interconnected, have been separately reported to be induced by CSF2/GM-CSF (colony stimulating factor 2) and required for CSF2-IL4-driven monocyte in vitro differentiation into DCs. We show that EBV infects monocytes and initiates a feedback loop in which, by inhibiting autophagy, reduces ROS and through ROS reduction negatively influences autophagy. Mechanistically, autophagy reduction correlated with the downregulation of RAB7 and ATG5 expression and STAT3 activation, leading to the accumulation of SQSTM1/p62. The latter activated the SQSTM1-KEAP1- NFE2L2 axis and upregulated the anti-oxidant response, reducing ROS and further inhibiting autophagy. ROS decrease correlated also with the reduction of mitochondria, the main source of intracellular ROS, achieved by the downregulation of NRF1 and TFAM, mitochondrial biogenesis transcription factors. Interestingly, mitochondria supply membranes and ATP required for autophagy execution, thus their reduction may further reduce autophagy in EBV-infected monocytes. In conclusion, this study shows for the first time that the interconnected reduction of autophagy, intracellular ROS and mitochondria mediated by EBV switches monocyte differentiation into apoptosis, giving new insights into the mechanisms through which this virus reduces immune surveillance. Abbreviations: ACTB: actin beta; ATG5: autophagy related 5; BAF: bafilomycin A<sub>1</sub>
; BECN1: beclin 1; CAT: catalase; CSF2: colony stimulating factor 2; CT: control; CYCS (cytochrome C: somatic); DCs: dendritic cells; EBV: Epstein-Barr virus; GSR: glutathione-disulfide reductase; KEAP1: kelch like ECH associated protein 1; IL4: interleukin 4; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MET: metformin; NAC: N-acetylcysteine; NFE2L2/NRF2 nuclear factor: erythroid 2 like 2; NRF1 (nuclear respiratory factor 1); clPARP1: cleaved poly(ADP-ribose) polymerase; Rapa: Rapamycin; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1; TFAM: (transcription factor A: mitochondrial); TUBA1A: tubulin alpha 1a.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gilardini Montani</LastName>
<ForeName>M S</ForeName>
<Initials>MS</Initials>
<AffiliationInfo><Affiliation>a Department of Experimental Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Rome , Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Santarelli</LastName>
<ForeName>R</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>a Department of Experimental Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Rome , Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Granato</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>a Department of Experimental Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Rome , Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gonnella</LastName>
<ForeName>R</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>a Department of Experimental Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Rome , Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Torrisi</LastName>
<ForeName>M R</ForeName>
<Initials>MR</Initials>
<AffiliationInfo><Affiliation>b Department of Clinical and Molecular Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Italy.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>c Sant'Andrea University Hospital , Azienda Ospedaliera Sant'Andrea , Rome , Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Faggioni</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>a Department of Experimental Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Rome , Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cirone</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>a Department of Experimental Medicine , Sapienza University of Rome, laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti , Rome , Italy.</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>10</Month>
<Day>23</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Autophagy</MedlineTA>
<NlmUniqueID>101265188</NlmUniqueID>
<ISSNLinking>1554-8627</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C502778">ATG5 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071187">Autophagy-Related Protein 5</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000631512">CSF2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C431364">KEAP1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000072019">Kelch-Like ECH-Associated Protein 1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D024101">Mitochondrial Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495635">NFE2L2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C099718">SQSTM1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D050796">STAT3 Transcription Factor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C494086">STAT3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071456">Sequestosome-1 Protein</NameOfSubstance>
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<NameOfSubstance UI="C499631">TFAM protein, human</NameOfSubstance>
</Chemical>
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<NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>152989-05-4</RegistryNumber>
<NameOfSubstance UI="C090531">rab7 protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>207137-56-2</RegistryNumber>
<NameOfSubstance UI="D015847">Interleukin-4</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>83869-56-1</RegistryNumber>
<NameOfSubstance UI="D016178">Granulocyte-Macrophage Colony-Stimulating Factor</NameOfSubstance>
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<Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber>
<NameOfSubstance UI="D020691">rab GTP-Binding Proteins</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071182" MajorTopicYN="N">Autophagosomes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016178" MajorTopicYN="N">Granulocyte-Macrophage Colony-Stimulating Factor</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004854" MajorTopicYN="N">Herpesvirus 4, Human</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015847" MajorTopicYN="N">Interleukin-4</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000072019" MajorTopicYN="N">Kelch-Like ECH-Associated Protein 1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D024101" MajorTopicYN="N">Mitochondrial Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051267" MajorTopicYN="N">NF-E2-Related Factor 2</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050796" MajorTopicYN="N">STAT3 Transcription Factor</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071456" MajorTopicYN="N">Sequestosome-1 Protein</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020691" MajorTopicYN="N">rab GTP-Binding Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">ATG5</Keyword>
<Keyword MajorTopicYN="Y">EBV</Keyword>
<Keyword MajorTopicYN="Y">NFE2L2</Keyword>
<Keyword MajorTopicYN="Y">ROS</Keyword>
<Keyword MajorTopicYN="Y">SQSTM1/p62</Keyword>
<Keyword MajorTopicYN="Y">STAT3</Keyword>
<Keyword MajorTopicYN="Y">autophagy</Keyword>
<Keyword MajorTopicYN="Y">dendritic cells</Keyword>
<Keyword MajorTopicYN="Y">monocytes</Keyword>
</KeywordList>
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<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>10</Month>
<Day>17</Day>
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation.

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation.

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