E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings
Identifieur interne : 000923 ( PascalFrancis/Corpus ); précédent : 000922; suivant : 000924E138A 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 ; Michael R. Jordan ; Kelly Huber ; Carole L. Wallis ; Silvia Bertagnolio ; John W. Mellors ; Neil T. Parkin ; P. Richard HarriganSource :
- Antiviral research [ 0166-3542 ] ; 2014.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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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Format Inist (serveur)
NO : | PASCAL 14-0168537 INIST |
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ET : | E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings |
AU : | SLUIS-CREMER (Nicolas); JORDAN (Michael R.); HUBER (Kelly); WALLIS (Carole L.); BERTAGNOLIO (Silvia); MELLORS (John W.); PARKIN (Neil T.); HARRIGAN (P. Richard) |
AF : | University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases/Pittsburgh, PA/Etats-Unis (1 aut., 3 aut., 6 aut.); Division of Geographic Medicine and Infectious Disease, Tufts Medical Center/Boston/Etats-Unis (2 aut.); Department of Public Health and Community Medicine, Tufts University School of Medicine/Boston, MA/Etats-Unis (2 aut.); Lancet Laboratories/Johannesburg/Afrique du Sud (4 aut.); HIV Department, World Health Organization/Geneva/Suisse (5 aut.); Data First Consulting/Belmont, CA/Etats-Unis (7 aut.); BC Centre for Excellence in HIV/AIDS/Vancouver/Canada (8 aut.) |
DT : | Publication en série; Courte communication, note brève; Niveau analytique |
SO : | Antiviral research; ISSN 0166-3542; Coden ARSRDR; Royaume-Uni; Da. 2014; Vol. 107; Pp. 31-34; Bibl. 1/4 p. |
LA : | Anglais |
EA : | 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. |
CC : | 002B02S05; 002B05C02D; 002B06D01 |
FD : | Virus HIV1; SIDA; RNA-directed DNA polymerase; Rilpivirine; Ressource; Inhibiteur reverse transcriptase; Composé non nucléoside; Résistance; Antiviral; Reverse transcriptase; Soustype C |
FG : | Virus immunodéficience humaine; Lentivirus; Retroviridae; Virus; Virose; Infection; Nucleotidyltransferases; Transferases; Enzyme; Immunodéficit; Immunopathologie |
ED : | HIV-1 virus; AIDS; RNA-directed DNA polymerase; Rilpivirine; Resource; Reverse transcriptase inhibitor; Non nucleoside compound; Resistance; Antiviral |
EG : | Human immunodeficiency virus; Lentivirus; Retroviridae; Virus; Viral disease; Infection; Nucleotidyltransferases; Transferases; Enzyme; Immune deficiency; Immunopathology |
SD : | HIV-1 virus; SIDA; RNA-directed DNA polymerase; Rilpivirina; Recurso; Inhibitor reverse transcriptase; Compuesto no nucleósido; Resistencia; Antiviral |
LO : | INIST-18839.354000502765430050 |
ID : | 14-0168537 |
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Pascal:14-0168537Le document en format XML
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</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Non nucleoside compound</s0>
<s5>07</s5>
</fC03>
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<s5>07</s5>
</fC03>
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<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>
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<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>
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<s4>INC</s4>
<s5>86</s5>
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<s4>INC</s4>
<s5>87</s5>
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<s2>NW</s2>
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<s2>NW</s2>
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<fC07 i1="02" i2="X" l="FRE"><s0>Lentivirus</s0>
<s2>NW</s2>
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<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Lentivirus</s0>
<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Retroviridae</s0>
<s2>NW</s2>
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<s2>NW</s2>
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<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>
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<fC07 i1="05" i2="X" l="FRE"><s0>Virose</s0>
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<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
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<s2>FE</s2>
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<s2>FE</s2>
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<s2>FE</s2>
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<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>
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<s2>FE</s2>
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<s5>37</s5>
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<fC07 i1="10" i2="X" l="ENG"><s0>Immune deficiency</s0>
<s5>37</s5>
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<fC07 i1="10" i2="X" l="SPA"><s0>Inmunodeficiencia</s0>
<s5>37</s5>
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<fC07 i1="11" i2="X" l="FRE"><s0>Immunopathologie</s0>
<s5>39</s5>
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<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>
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<server><NO>PASCAL 14-0168537 INIST</NO>
<ET>E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings</ET>
<AU>SLUIS-CREMER (Nicolas); JORDAN (Michael R.); HUBER (Kelly); WALLIS (Carole L.); BERTAGNOLIO (Silvia); MELLORS (John W.); PARKIN (Neil T.); HARRIGAN (P. Richard)</AU>
<AF>University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases/Pittsburgh, PA/Etats-Unis (1 aut., 3 aut., 6 aut.); Division of Geographic Medicine and Infectious Disease, Tufts Medical Center/Boston/Etats-Unis (2 aut.); Department of Public Health and Community Medicine, Tufts University School of Medicine/Boston, MA/Etats-Unis (2 aut.); Lancet Laboratories/Johannesburg/Afrique du Sud (4 aut.); HIV Department, World Health Organization/Geneva/Suisse (5 aut.); Data First Consulting/Belmont, CA/Etats-Unis (7 aut.); BC Centre for Excellence in HIV/AIDS/Vancouver/Canada (8 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Antiviral research; ISSN 0166-3542; Coden ARSRDR; Royaume-Uni; Da. 2014; Vol. 107; Pp. 31-34; Bibl. 1/4 p.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B02S05; 002B05C02D; 002B06D01</CC>
<FD>Virus HIV1; SIDA; RNA-directed DNA polymerase; Rilpivirine; Ressource; Inhibiteur reverse transcriptase; Composé non nucléoside; Résistance; Antiviral; Reverse transcriptase; Soustype C</FD>
<FG>Virus immunodéficience humaine; Lentivirus; Retroviridae; Virus; Virose; Infection; Nucleotidyltransferases; Transferases; Enzyme; Immunodéficit; Immunopathologie</FG>
<ED>HIV-1 virus; AIDS; RNA-directed DNA polymerase; Rilpivirine; Resource; Reverse transcriptase inhibitor; Non nucleoside compound; Resistance; Antiviral</ED>
<EG>Human immunodeficiency virus; Lentivirus; Retroviridae; Virus; Viral disease; Infection; Nucleotidyltransferases; Transferases; Enzyme; Immune deficiency; Immunopathology</EG>
<SD>HIV-1 virus; SIDA; RNA-directed DNA polymerase; Rilpivirina; Recurso; Inhibitor reverse transcriptase; Compuesto no nucleósido; Resistencia; Antiviral</SD>
<LO>INIST-18839.354000502765430050</LO>
<ID>14-0168537</ID>
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