E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings
Identifieur interne : 005611 ( Main/Exploration ); précédent : 005610; suivant : 005612E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings
Auteurs : Nicolas Sluis-Cremer [États-Unis] ; Michael R. Jordan [États-Unis] ; Kelly Huber [États-Unis] ; Carole L. Wallis [Afrique du Sud] ; Silvia Bertagnolio [Suisse] ; John W. Mellors [États-Unis] ; Neil T. Parkin [États-Unis] ; P. Richard Harrigan [Canada]Source :
- Antiviral research [ 0166-3542 ] ; 2014.
Descripteurs français
- KwdFr :
- Agents antiVIH (pharmacologie), Humains, Infections à VIH (traitement médicamenteux), Infections à VIH (virologie), Mutation faux-sens, Nitriles (pharmacologie), Pyrimidines (pharmacologie), Rilpivirine, Résistance virale aux médicaments, Substitution d'acide aminé, Transcriptase inverse du VIH (génétique), Transcriptase inverse du VIH (métabolisme), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (enzymologie), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (génétique).
- MESH :
- enzymologie : VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- génétique : Transcriptase inverse du VIH, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- métabolisme : Transcriptase inverse du VIH.
- pharmacologie : Agents antiVIH, Nitriles, Pyrimidines.
- traitement médicamenteux : Infections à VIH.
- virologie : Infections à VIH.
- Pascal (Inist)
- Humains, Mutation faux-sens, Rilpivirine, Résistance virale aux médicaments, Substitution d'acide aminé, VIH-1 (Virus de l'Immunodéficience Humaine de type 1), Virus HIV1, SIDA, RNA-directed DNA polymerase, Rilpivirine, Ressource, Inhibiteur reverse transcriptase, Composé non nucléoside, Résistance, Antiviral, Reverse transcriptase, Soustype C.
English descriptors
- KwdEn :
- AIDS, Amino Acid Substitution, Anti-HIV Agents (pharmacology), Antiviral, Drug Resistance, Viral, HIV Infections (drug therapy), HIV Infections (virology), HIV Reverse Transcriptase (genetics), HIV Reverse Transcriptase (metabolism), HIV-1 (classification), HIV-1 (enzymology), HIV-1 (genetics), HIV-1 virus, Humans, Mutation, Missense, Nitriles (pharmacology), Non nucleoside compound, Pyrimidines (pharmacology), RNA-directed DNA polymerase, Resistance, Resource, Reverse transcriptase inhibitor, Rilpivirine.
- MESH :
- chemical , genetics : HIV Reverse Transcriptase.
- chemical , metabolism : HIV Reverse Transcriptase.
- chemical , pharmacology : Anti-HIV Agents, Nitriles, Pyrimidines.
- classification : HIV-1.
- drug therapy : HIV Infections.
- enzymology : HIV-1.
- genetics : HIV-1.
- virology : HIV Infections.
- Amino Acid Substitution, Drug Resistance, Viral, Humans, Mutation, Missense, Rilpivirine.
Abstract
The nonnucleoside reverse transcriptase (RT) inhibitor rilpivirine (RPV) has been co-formulated with emtricitabine and tenofovir disoproxil fumarate for initial therapy of HIV-1-infected individuals. RPV, formulated as a long-acting nanosuspension, will also be assessed for its ability to prevent HIV-1 infection in resource limited settings. In this study, we determined whether any pre-existing genetic differences occurred among different HIV-1 subtypes at residues in RT associated with decreased virologic response to RPV. We found that the E138A substitution occurs more frequently in subtype C (range: 5.9-7.5%) than B (range: 0-2.3%) sequences from both treatment-naïve and -experienced individuals (p < 0.01) in 4 independent genotype databases. In one of the databases (Stanford University), E138K and E138Q were also more common in RTI-experienced subtype C sequences (1.0% and 1.1%, respectively) than in subtype B sequences (0.3% and 0.6%, respectively). E138A/K/Q in subtype C decreased RPV susceptibility 2.9-, 5.8-, and 5.4-fold, respectively. Taken together, these data suggest that E138A could impact treatment or prevention strategies that include RPV in geographic areas where subtype C infection is prevalent.
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Affiliations:
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Le document en format XML
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<term>Drug Resistance, Viral</term>
<term>HIV Infections (drug therapy)</term>
<term>HIV Infections (virology)</term>
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<term>HIV Reverse Transcriptase (metabolism)</term>
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<term>Nitriles (pharmacology)</term>
<term>Non nucleoside compound</term>
<term>Pyrimidines (pharmacology)</term>
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<term>Resistance</term>
<term>Resource</term>
<term>Reverse transcriptase inhibitor</term>
<term>Rilpivirine</term>
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<term>Infections à VIH (traitement médicamenteux)</term>
<term>Infections à VIH (virologie)</term>
<term>Mutation faux-sens</term>
<term>Nitriles (pharmacologie)</term>
<term>Pyrimidines (pharmacologie)</term>
<term>Rilpivirine</term>
<term>Résistance virale aux médicaments</term>
<term>Substitution d'acide aminé</term>
<term>Transcriptase inverse du VIH (génétique)</term>
<term>Transcriptase inverse du VIH (métabolisme)</term>
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) ()</term>
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (enzymologie)</term>
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<front><div type="abstract" xml:lang="en">The nonnucleoside reverse transcriptase (RT) inhibitor rilpivirine (RPV) has been co-formulated with emtricitabine and tenofovir disoproxil fumarate for initial therapy of HIV-1-infected individuals. RPV, formulated as a long-acting nanosuspension, will also be assessed for its ability to prevent HIV-1 infection in resource limited settings. In this study, we determined whether any pre-existing genetic differences occurred among different HIV-1 subtypes at residues in RT associated with decreased virologic response to RPV. We found that the E138A substitution occurs more frequently in subtype C (range: 5.9-7.5%) than B (range: 0-2.3%) sequences from both treatment-naïve and -experienced individuals (p < 0.01) in 4 independent genotype databases. In one of the databases (Stanford University), E138K and E138Q were also more common in RTI-experienced subtype C sequences (1.0% and 1.1%, respectively) than in subtype B sequences (0.3% and 0.6%, respectively). E138A/K/Q in subtype C decreased RPV susceptibility 2.9-, 5.8-, and 5.4-fold, respectively. Taken together, these data suggest that E138A could impact treatment or prevention strategies that include RPV in geographic areas where subtype C infection is prevalent.</div>
</front>
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<affiliations><list><country><li>Afrique du Sud</li>
<li>Canada</li>
<li>Suisse</li>
<li>États-Unis</li>
</country>
<region><li>Massachusetts</li>
</region>
<settlement><li>Boston</li>
</settlement>
</list>
<tree><country name="États-Unis"><noRegion><name sortKey="Sluis Cremer, Nicolas" sort="Sluis Cremer, Nicolas" uniqKey="Sluis Cremer N" first="Nicolas" last="Sluis-Cremer">Nicolas Sluis-Cremer</name>
</noRegion>
<name sortKey="Huber, Kelly" sort="Huber, Kelly" uniqKey="Huber K" first="Kelly" last="Huber">Kelly Huber</name>
<name sortKey="Jordan, Michael R" sort="Jordan, Michael R" uniqKey="Jordan M" first="Michael R." last="Jordan">Michael R. Jordan</name>
<name sortKey="Jordan, Michael R" sort="Jordan, Michael R" uniqKey="Jordan M" first="Michael R." last="Jordan">Michael R. Jordan</name>
<name sortKey="Mellors, John W" sort="Mellors, John W" uniqKey="Mellors J" first="John W." last="Mellors">John W. Mellors</name>
<name sortKey="Parkin, Neil T" sort="Parkin, Neil T" uniqKey="Parkin N" first="Neil T." last="Parkin">Neil T. Parkin</name>
</country>
<country name="Afrique du Sud"><noRegion><name sortKey="Wallis, Carole L" sort="Wallis, Carole L" uniqKey="Wallis C" first="Carole L." last="Wallis">Carole L. Wallis</name>
</noRegion>
</country>
<country name="Suisse"><noRegion><name sortKey="Bertagnolio, Silvia" sort="Bertagnolio, Silvia" uniqKey="Bertagnolio S" first="Silvia" last="Bertagnolio">Silvia Bertagnolio</name>
</noRegion>
</country>
<country name="Canada"><noRegion><name sortKey="Harrigan, P Richard" sort="Harrigan, P Richard" uniqKey="Harrigan P" first="P. Richard" last="Harrigan">P. Richard Harrigan</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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