Locked nucleic acid containing antisense oligonucleotides enhance inhibition of HIV-1 genome dimerization and inhibit virus replication.
Identifieur interne : 000324 ( Ncbi/Merge ); précédent : 000323; suivant : 000325Locked nucleic acid containing antisense oligonucleotides enhance inhibition of HIV-1 genome dimerization and inhibit virus replication.
Auteurs : Joacim Elmén [Suède] ; Hong-Yan Zhang ; Bartek Zuber ; Karl Ljungberg ; Britta Wahren ; Claes Wahlestedt ; Zicai LiangSource :
- FEBS letters [ 0014-5793 ] ; 2004.
Descripteurs français
- KwdFr :
- Activation enzymatique, Cellules Jurkat, Dimérisation, Génome viral, Humains, Lymphocytes T (), Lymphocytes T (métabolisme), Oligonucléotides antisens (), Oligonucléotides antisens (pharmacologie), Ribonuclease H (métabolisme), Réplication virale (), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (génétique), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (isolement et purification).
- MESH :
- génétique : VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- isolement et purification : VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- métabolisme : Lymphocytes T, Ribonuclease H.
- pharmacologie : Oligonucléotides antisens.
- Activation enzymatique, Cellules Jurkat, Dimérisation, Génome viral, Humains, Lymphocytes T, Oligonucléotides antisens, Réplication virale, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
English descriptors
- KwdEn :
- Dimerization, Enzyme Activation, Genome, Viral, HIV-1 (drug effects), HIV-1 (genetics), HIV-1 (isolation & purification), Humans, Jurkat Cells, Oligonucleotides, Antisense (chemistry), Oligonucleotides, Antisense (pharmacology), Ribonuclease H (metabolism), T-Lymphocytes (drug effects), T-Lymphocytes (metabolism), Virus Replication (drug effects).
- MESH :
- chemical , chemistry : Oligonucleotides, Antisense.
- drug effects : HIV-1, T-Lymphocytes, Virus Replication.
- genetics : HIV-1.
- isolation & purification : HIV-1.
- chemical , metabolism : Ribonuclease H, T-Lymphocytes.
- chemical , pharmacology : Oligonucleotides, Antisense.
- Dimerization, Enzyme Activation, Genome, Viral, Humans, Jurkat Cells.
Abstract
We have evaluated antisense design and efficacy of locked nucleic acid (LNA) and DNA oligonucleotide (ON) mix-mers targeting the conserved HIV-1 dimerization initiation site (DIS). LNA is a high affinity nucleotide analog, nuclease resistant and elicits minimal toxicity. We show that inclusion of LNA bases in antisense ONs augments the interference of HIV-1 genome dimerization. We also demonstrate the concomitant RNase H activation by six consecutive DNA bases in an LNA/DNA mix-mer. We show ON uptake via receptor-mediated transfection of a human T-cell line in which the mix-mers subsequently inhibit replication of a clinical HIV-1 isolate. Thus, the technique of LNA/DNA mix-mer antisense ONs targeting the conserved HIV-1 DIS region may provide a strategy to prevent HIV-1 assembly in the clinic.
DOI: 10.1016/j.febslet.2004.11.015
PubMed: 15589834
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- to stream PubMed, to step Corpus: 002353
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pubmed:15589834Le document en format XML
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<author><name sortKey="Zhang, Hong Yan" sort="Zhang, Hong Yan" uniqKey="Zhang H" first="Hong-Yan" last="Zhang">Hong-Yan Zhang</name>
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<term>Enzyme Activation</term>
<term>Genome, Viral</term>
<term>HIV-1 (drug effects)</term>
<term>HIV-1 (genetics)</term>
<term>HIV-1 (isolation & purification)</term>
<term>Humans</term>
<term>Jurkat Cells</term>
<term>Oligonucleotides, Antisense (chemistry)</term>
<term>Oligonucleotides, Antisense (pharmacology)</term>
<term>Ribonuclease H (metabolism)</term>
<term>T-Lymphocytes (drug effects)</term>
<term>T-Lymphocytes (metabolism)</term>
<term>Virus Replication (drug effects)</term>
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<term>Dimérisation</term>
<term>Génome viral</term>
<term>Humains</term>
<term>Lymphocytes T ()</term>
<term>Lymphocytes T (métabolisme)</term>
<term>Oligonucléotides antisens ()</term>
<term>Oligonucléotides antisens (pharmacologie)</term>
<term>Ribonuclease H (métabolisme)</term>
<term>Réplication virale ()</term>
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) ()</term>
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<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (isolement et purification)</term>
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<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Oligonucleotides, Antisense</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>HIV-1</term>
<term>T-Lymphocytes</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>HIV-1</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Ribonuclease H</term>
<term>T-Lymphocytes</term>
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<term>Enzyme Activation</term>
<term>Genome, Viral</term>
<term>Humans</term>
<term>Jurkat Cells</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term>
<term>Cellules Jurkat</term>
<term>Dimérisation</term>
<term>Génome viral</term>
<term>Humains</term>
<term>Lymphocytes T</term>
<term>Oligonucléotides antisens</term>
<term>Réplication virale</term>
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<front><div type="abstract" xml:lang="en">We have evaluated antisense design and efficacy of locked nucleic acid (LNA) and DNA oligonucleotide (ON) mix-mers targeting the conserved HIV-1 dimerization initiation site (DIS). LNA is a high affinity nucleotide analog, nuclease resistant and elicits minimal toxicity. We show that inclusion of LNA bases in antisense ONs augments the interference of HIV-1 genome dimerization. We also demonstrate the concomitant RNase H activation by six consecutive DNA bases in an LNA/DNA mix-mer. We show ON uptake via receptor-mediated transfection of a human T-cell line in which the mix-mers subsequently inhibit replication of a clinical HIV-1 isolate. Thus, the technique of LNA/DNA mix-mer antisense ONs targeting the conserved HIV-1 DIS region may provide a strategy to prevent HIV-1 assembly in the clinic.</div>
</front>
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<Abstract><AbstractText>We have evaluated antisense design and efficacy of locked nucleic acid (LNA) and DNA oligonucleotide (ON) mix-mers targeting the conserved HIV-1 dimerization initiation site (DIS). LNA is a high affinity nucleotide analog, nuclease resistant and elicits minimal toxicity. We show that inclusion of LNA bases in antisense ONs augments the interference of HIV-1 genome dimerization. We also demonstrate the concomitant RNase H activation by six consecutive DNA bases in an LNA/DNA mix-mer. We show ON uptake via receptor-mediated transfection of a human T-cell line in which the mix-mers subsequently inhibit replication of a clinical HIV-1 isolate. Thus, the technique of LNA/DNA mix-mer antisense ONs targeting the conserved HIV-1 DIS region may provide a strategy to prevent HIV-1 assembly in the clinic.</AbstractText>
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<name sortKey="Wahlestedt, Claes" sort="Wahlestedt, Claes" uniqKey="Wahlestedt C" first="Claes" last="Wahlestedt">Claes Wahlestedt</name>
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<name sortKey="Zhang, Hong Yan" sort="Zhang, Hong Yan" uniqKey="Zhang H" first="Hong-Yan" last="Zhang">Hong-Yan Zhang</name>
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