E138A in HIV-1 reverse transcriptase is more common in subtype C than B: implications for rilpivirine use in resource-limited settings.
Identifieur interne : 003143 ( PubMed/Checkpoint ); précédent : 003142; suivant : 003144E138A 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 [ 1872-9096 ] ; 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.
- Humains, Mutation faux-sens, Rilpivirine, Résistance virale aux médicaments, Substitution d'acide aminé, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
English descriptors
- KwdEn :
- Amino Acid Substitution, Anti-HIV Agents (pharmacology), 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), Humans, Mutation, Missense, Nitriles (pharmacology), Pyrimidines (pharmacology), 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.
DOI: 10.1016/j.antiviral.2014.04.001
PubMed: 24746459
Affiliations:
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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>
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<Abstract><AbstractText>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.</AbstractText>
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<CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>AIDS. 2003 Jan 3;17(1):F1-5</RefSource>
<PMID Version="1">12478089</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>AIDS. 2006 Mar 21;20(5):643-51</RefSource>
<PMID Version="1">16514293</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Eur J Pharm Biopharm. 2009 Aug;72(3):502-8</RefSource>
<PMID Version="1">19328850</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Clin Infect Dis. 2010 Jan 1;50(1):98-105</RefSource>
<PMID Version="1">19951169</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Antimicrob Agents Chemother. 2010 Feb;54(2):718-27</RefSource>
<PMID Version="1">19933797</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>AIDS. 2013 Jan 2;27(1):81-5</RefSource>
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</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Acquir Immune Defic Syndr. 2011 Sep 1;58(1):18-22</RefSource>
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<CommentsCorrections RefType="Cites"><RefSource>AIDS Rev. 2012 Apr-Jun;14(2):83-100</RefSource>
<PMID Version="1">22627605</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Clin Infect Dis. 2012 Sep;55(5):737-45</RefSource>
<PMID Version="1">22618567</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Lancet. 2012 Oct 6;380(9849):1250-8</RefSource>
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</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>AIDS Res Hum Retroviruses. 2011 Jan;27(1):5-12</RefSource>
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