RapamycinFungusV1, Main, Exploration, bibRecord, 000294

Long non-coding RNAs and latent HIV - A search for novel targets for latency reversal.

Identifieur interne : 000294 ( Main/Exploration ); précédent : 000293; suivant : 000295

Long non-coding RNAs and latent HIV - A search for novel targets for latency reversal.

Auteurs : Wim Trypsteen [Belgique] ; Cory H. White [Royaume-Uni] ; Amey Mukim [États-Unis] ; Celsa A. Spina [États-Unis] ; Ward De Spiegelaere [Belgique] ; Steve Lefever [Belgique] ; Vicente Planelles [États-Unis] ; Alberto Bosque [États-Unis] ; Christopher H. Woelk [Royaume-Uni] ; Linos Vandekerckhove [Belgique] ; Nadejda Beliakova-Bethell [États-Unis]

Source :

PloS one [ 1932-6203 ] ; 2019.

RBID : pubmed:31710657

Descripteurs français

KwdFr :
- ARN long non codant (génétique), ARN long non codant (métabolisme), ARN messager (génétique), ARN messager (métabolisme), Depsipeptides (pharmacologie), Humains (MeSH), Latence virale (effets des médicaments et des substances chimiques), Latence virale (génétique), Lymphocytes T (immunologie), Mémoire immunologique (MeSH), Reproductibilité des résultats (MeSH), Régulation négative (effets des médicaments et des substances chimiques), Transduction du signal (effets des médicaments et des substances chimiques), Transduction du signal (génétique), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (effets des médicaments et des substances chimiques), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (génétique), Vorinostat (pharmacologie).
MESH :
- effets des médicaments et des substances chimiques : Latence virale, Régulation négative, Transduction du signal, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- génétique : ARN long non codant, ARN messager, Latence virale, Transduction du signal, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- immunologie : Lymphocytes T.
- métabolisme : ARN long non codant, ARN messager.
- pharmacologie : Depsipeptides, Vorinostat.
- Humains, Mémoire immunologique, Reproductibilité des résultats.

English descriptors

KwdEn :
- Depsipeptides (pharmacology), Down-Regulation (drug effects), HIV-1 (drug effects), HIV-1 (genetics), Humans (MeSH), Immunologic Memory (MeSH), RNA, Long Noncoding (genetics), RNA, Long Noncoding (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), Reproducibility of Results (MeSH), Signal Transduction (drug effects), Signal Transduction (genetics), T-Lymphocytes (immunology), Virus Latency (drug effects), Virus Latency (genetics), Vorinostat (pharmacology).
MESH :
- chemical , genetics : RNA, Long Noncoding, RNA, Messenger.
- chemical , metabolism : RNA, Long Noncoding, RNA, Messenger.
- chemical , pharmacology : Depsipeptides, Vorinostat.
- drug effects : Down-Regulation, HIV-1, Signal Transduction, Virus Latency.
- genetics : HIV-1, Signal Transduction, Virus Latency.
- immunology : T-Lymphocytes.
- Humans, Immunologic Memory, Reproducibility of Results.

Abstract

The latent cellular reservoir of HIV is recognized as the major barrier to cure from HIV infection. Long non-coding RNAs (lncRNAs) are more tissue and cell type-specific than protein coding genes, and may represent targets of choice for HIV latency reversal. Using two in vitro primary T-cell models, we identified lncRNAs dysregulated in latency. PVT1 and RP11-347C18.3 were up-regulated in common between the two models, and RP11-539L10.2 was down-regulated. The major component of the latent HIV reservoir, memory CD4+ T-cells, had higher expression of these lncRNAs, compared to naïve T-cells. Guilt-by-association analysis demonstrated that lncRNAs dysregulated in latency were associated with several cellular pathways implicated in HIV latency establishment and maintenance: proteasome, spliceosome, p53 signaling, and mammalian target of rapamycin (MTOR). PVT1, RP11-347C18.3, and RP11-539L10.2 were down-regulated by latency reversing agents, suberoylanilide hydroxamic acid and Romidepsin, suggesting that modulation of lncRNAs is a possible secondary mechanism of action of these compounds. These results will facilitate prioritization of lncRNAs for evaluation as targets for HIV latency reversal. Importantly, our study provides insights into regulatory function of lncRNA during latent HIV infection.

DOI: 10.1371/journal.pone.0224879
PubMed: 31710657
PubMed Central: PMC6844474

Affiliations:

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The latent cellular reservoir of HIV is recognized as the major barrier to cure from HIV infection. Long non-coding RNAs (lncRNAs) are more tissue and cell type-specific than protein coding genes, and may represent targets of choice for HIV latency reversal. Using two in vitro primary T-cell models, we identified lncRNAs dysregulated in latency. PVT1 and RP11-347C18.3 were up-regulated in common between the two models, and RP11-539L10.2 was down-regulated. The major component of the latent HIV reservoir, memory CD4+ T-cells, had higher expression of these lncRNAs, compared to naïve T-cells. Guilt-by-association analysis demonstrated that lncRNAs dysregulated in latency were associated with several cellular pathways implicated in HIV latency establishment and maintenance: proteasome, spliceosome, p53 signaling, and mammalian target of rapamycin (MTOR). PVT1, RP11-347C18.3, and RP11-539L10.2 were down-regulated by latency reversing agents, suberoylanilide hydroxamic acid and Romidepsin, suggesting that modulation of lncRNAs is a possible secondary mechanism of action of these compounds. These results will facilitate prioritization of lncRNAs for evaluation as targets for HIV latency reversal. Importantly, our study provides insights into regulatory function of lncRNA during latent HIV infection.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31710657</PMID>
<DateCompleted><Year>2020</Year>
<Month>03</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>10</Month>
<Day>28</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>14</Volume>
<Issue>11</Issue>
<PubDate><Year>2019</Year>
</PubDate>
</JournalIssue>
<Title>PloS one</Title>
<ISOAbbreviation>PLoS One</ISOAbbreviation>
</Journal>
<ArticleTitle>Long non-coding RNAs and latent HIV - A search for novel targets for latency reversal.</ArticleTitle>
<Pagination><MedlinePgn>e0224879</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0224879</ELocationID>
<Abstract><AbstractText>The latent cellular reservoir of HIV is recognized as the major barrier to cure from HIV infection. Long non-coding RNAs (lncRNAs) are more tissue and cell type-specific than protein coding genes, and may represent targets of choice for HIV latency reversal. Using two in vitro primary T-cell models, we identified lncRNAs dysregulated in latency. PVT1 and RP11-347C18.3 were up-regulated in common between the two models, and RP11-539L10.2 was down-regulated. The major component of the latent HIV reservoir, memory CD4+ T-cells, had higher expression of these lncRNAs, compared to naïve T-cells. Guilt-by-association analysis demonstrated that lncRNAs dysregulated in latency were associated with several cellular pathways implicated in HIV latency establishment and maintenance: proteasome, spliceosome, p53 signaling, and mammalian target of rapamycin (MTOR). PVT1, RP11-347C18.3, and RP11-539L10.2 were down-regulated by latency reversing agents, suberoylanilide hydroxamic acid and Romidepsin, suggesting that modulation of lncRNAs is a possible secondary mechanism of action of these compounds. These results will facilitate prioritization of lncRNAs for evaluation as targets for HIV latency reversal. Importantly, our study provides insights into regulatory function of lncRNA during latent HIV infection.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Trypsteen</LastName>
<ForeName>Wim</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>HIV Cure Research Center, Department of Internal Medicine, Ghent University and Ghent University Hospital, Ghent, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>White</LastName>
<ForeName>Cory H</ForeName>
<Initials>CH</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, University of Southampton, Southampton, Hants, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mukim</LastName>
<ForeName>Amey</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>San Diego VA Medical Center and Veterans Medical Research Foundation, San Diego, CA, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Spina</LastName>
<ForeName>Celsa A</ForeName>
<Initials>CA</Initials>
<AffiliationInfo><Affiliation>San Diego VA Medical Center and Veterans Medical Research Foundation, San Diego, CA, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pathology, University of California San Diego, La Jolla, CA, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>De Spiegelaere</LastName>
<ForeName>Ward</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Morphology, Faculty of Veterinary Sciences, Ghent University, Ghent, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lefever</LastName>
<ForeName>Steve</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Center for Medical Genetics, Ghent University, Ghent, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Planelles</LastName>
<ForeName>Vicente</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bosque</LastName>
<ForeName>Alberto</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, Immunology and Tropical Medicine, The George Washington University, Washington, DC, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Woelk</LastName>
<ForeName>Christopher H</ForeName>
<Initials>CH</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, University of Southampton, Southampton, Hants, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Vandekerckhove</LastName>
<ForeName>Linos</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>HIV Cure Research Center, Department of Internal Medicine, Ghent University and Ghent University Hospital, Ghent, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Beliakova-Bethell</LastName>
<ForeName>Nadejda</ForeName>
<Initials>N</Initials>
<Identifier Source="ORCID">0000-0001-9765-7786</Identifier>
<AffiliationInfo><Affiliation>San Diego VA Medical Center and Veterans Medical Research Foundation, San Diego, CA, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Medicine, University of California San Diego, La Jolla, CA, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>IK2 BX002731</GrantID>
<Acronym>BX</Acronym>
<Agency>BLRD VA</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 AI036214</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R33 AI104282</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>11</Month>
<Day>11</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS One</MedlineTA>
<NlmUniqueID>101285081</NlmUniqueID>
<ISSNLinking>1932-6203</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047630">Depsipeptides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D062085">RNA, Long Noncoding</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>58IFB293JI</RegistryNumber>
<NameOfSubstance UI="D000077337">Vorinostat</NameOfSubstance>
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<Chemical><RegistryNumber>CX3T89XQBK</RegistryNumber>
<NameOfSubstance UI="C087123">romidepsin</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D047630" MajorTopicYN="N">Depsipeptides</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015497" MajorTopicYN="N">HIV-1</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007156" MajorTopicYN="N">Immunologic Memory</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D062085" MajorTopicYN="N">RNA, Long Noncoding</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015203" MajorTopicYN="N">Reproducibility of Results</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017735" MajorTopicYN="N">Virus Latency</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077337" MajorTopicYN="N">Vorinostat</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<CoiStatement>The authors have declared that no competing interests exist.</CoiStatement>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>07</Month>
<Day>26</Day>
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<Day>23</Day>
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Long non-coding RNAs and latent HIV - A search for novel targets for latency reversal.

Long non-coding RNAs and latent HIV - A search for novel targets for latency reversal.

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