PittsburghV1, PascalFrancis, Curation, bibRecord, 003D07

E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings

Identifieur interne : 003D07 ( PascalFrancis/Curation ); précédent : 003D06; suivant : 003D08

E138A 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.

RBID : Pascal:14-0168537

Descripteurs français

Pascal (Inist)
- 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, Antiviral, HIV-1 virus, Non nucleoside compound, RNA-directed DNA polymerase, Resistance, Resource, Reverse transcriptase inhibitor, 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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Pascal:14-0168537

Le document en format XML

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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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<fA11 i1="04" i2="1"><s1>WALLIS (Carole L.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>BERTAGNOLIO (Silvia)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>MELLORS (John W.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>PARKIN (Neil T.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>HARRIGAN (P. Richard)</s1>
</fA11>
<fA14 i1="01"><s1>University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Division of Geographic Medicine and Infectious Disease, Tufts Medical Center</s1>
<s2>Boston</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Public Health and Community Medicine, Tufts University School of Medicine</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Lancet Laboratories</s1>
<s2>Johannesburg</s2>
<s3>ZAF</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>HIV Department, World Health Organization</s1>
<s2>Geneva</s2>
<s3>CHE</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Data First Consulting</s1>
<s2>Belmont, CA</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>BC Centre for Excellence in HIV/AIDS</s1>
<s2>Vancouver</s2>
<s3>CAN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA20><s1>31-34</s1>
</fA20>
<fA21><s1>2014</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>18839</s2>
<s5>354000502765430050</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2014 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>1/4 p.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>14-0168537</s0>
</fA47>
<fA60><s1>P</s1>
<s3>CC</s3>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Antiviral research</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B02S05</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05C02D</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B06D01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Virus HIV1</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>HIV-1 virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>HIV-1 virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>SIDA</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>AIDS</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>SIDA</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>RNA-directed DNA polymerase</s0>
<s2>FE</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>RNA-directed DNA polymerase</s0>
<s2>FE</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>RNA-directed DNA polymerase</s0>
<s2>FE</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Rilpivirine</s0>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Rilpivirine</s0>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Rilpivirina</s0>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Ressource</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Resource</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Recurso</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Inhibiteur reverse transcriptase</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Reverse transcriptase inhibitor</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Inhibitor reverse transcriptase</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Composé non nucléoside</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Non nucleoside compound</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Compuesto no nucleósido</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Résistance</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Resistance</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Resistencia</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Antiviral</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Antiviral</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Antiviral</s0>
<s5>23</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Reverse transcriptase</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Soustype C</s0>
<s4>INC</s4>
<s5>87</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Virus immunodéficience humaine</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Nucleotidyltransferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Nucleotidyltransferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Nucleotidyltransferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Immunodéficit</s0>
<s5>37</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Immune deficiency</s0>
<s5>37</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Inmunodeficiencia</s0>
<s5>37</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Immunopathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Immunopathology</s0>
<s5>39</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Inmunopatología</s0>
<s5>39</s5>
</fC07>
<fN21><s1>209</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings

E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings

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