E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings
Identifieur interne : 001488 ( Pmc/Corpus ); précédent : 001487; suivant : 001489E138A 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.
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.
Url:
DOI: 10.1016/j.antiviral.2014.04.001
PubMed: 24746459
PubMed Central: 4089891
Links to Exploration step
PMC:4089891Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings</title><author><name sortKey="Sluis Cremer, Nicolas" sort="Sluis Cremer, Nicolas" uniqKey="Sluis Cremer N" first="Nicolas" last="Sluis-Cremer">Nicolas Sluis-Cremer</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Jordan, Michael R" sort="Jordan, Michael R" uniqKey="Jordan M" first="Michael R." last="Jordan">Michael R. Jordan</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Division of Geographic Medicine and Infectious Disease, Tufts Medical Center, Boston, USA</nlm:aff></affiliation></author><author><name sortKey="Huber, Kelly" sort="Huber, Kelly" uniqKey="Huber K" first="Kelly" last="Huber">Kelly Huber</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Wallis, Carole L" sort="Wallis, Carole L" uniqKey="Wallis C" first="Carole L." last="Wallis">Carole L. Wallis</name><affiliation><nlm:aff id="A4">Lancet Laboratories, Johannesburg, South Africa</nlm:aff></affiliation></author><author><name sortKey="Bertagnolio, Silvia" sort="Bertagnolio, Silvia" uniqKey="Bertagnolio S" first="Silvia" last="Bertagnolio">Silvia Bertagnolio</name><affiliation><nlm:aff id="A5">HIV Department, World Health Organization, Geneva, Switzerland</nlm:aff></affiliation></author><author><name sortKey="Mellors, John W" sort="Mellors, John W" uniqKey="Mellors J" first="John W." last="Mellors">John W. Mellors</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Parkin, Neil T" sort="Parkin, Neil T" uniqKey="Parkin N" first="Neil T." last="Parkin">Neil T. Parkin</name><affiliation><nlm:aff id="A6">Data First Consulting, Belmont, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Harrigan, P Richard" sort="Harrigan, P Richard" uniqKey="Harrigan P" first="P. Richard" last="Harrigan">P. Richard Harrigan</name><affiliation><nlm:aff id="A7">BC Centre for Excellence in HIV/AIDS, Vancouver, Canada</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24746459</idno><idno type="pmc">4089891</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4089891</idno><idno type="RBID">PMC:4089891</idno><idno type="doi">10.1016/j.antiviral.2014.04.001</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">001488</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001488</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings</title><author><name sortKey="Sluis Cremer, Nicolas" sort="Sluis Cremer, Nicolas" uniqKey="Sluis Cremer N" first="Nicolas" last="Sluis-Cremer">Nicolas Sluis-Cremer</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Jordan, Michael R" sort="Jordan, Michael R" uniqKey="Jordan M" first="Michael R." last="Jordan">Michael R. Jordan</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Division of Geographic Medicine and Infectious Disease, Tufts Medical Center, Boston, USA</nlm:aff></affiliation></author><author><name sortKey="Huber, Kelly" sort="Huber, Kelly" uniqKey="Huber K" first="Kelly" last="Huber">Kelly Huber</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Wallis, Carole L" sort="Wallis, Carole L" uniqKey="Wallis C" first="Carole L." last="Wallis">Carole L. Wallis</name><affiliation><nlm:aff id="A4">Lancet Laboratories, Johannesburg, South Africa</nlm:aff></affiliation></author><author><name sortKey="Bertagnolio, Silvia" sort="Bertagnolio, Silvia" uniqKey="Bertagnolio S" first="Silvia" last="Bertagnolio">Silvia Bertagnolio</name><affiliation><nlm:aff id="A5">HIV Department, World Health Organization, Geneva, Switzerland</nlm:aff></affiliation></author><author><name sortKey="Mellors, John W" sort="Mellors, John W" uniqKey="Mellors J" first="John W." last="Mellors">John W. Mellors</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Parkin, Neil T" sort="Parkin, Neil T" uniqKey="Parkin N" first="Neil T." last="Parkin">Neil T. Parkin</name><affiliation><nlm:aff id="A6">Data First Consulting, Belmont, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Harrigan, P Richard" sort="Harrigan, P Richard" uniqKey="Harrigan P" first="P. Richard" last="Harrigan">P. Richard Harrigan</name><affiliation><nlm:aff id="A7">BC Centre for Excellence in HIV/AIDS, Vancouver, Canada</nlm:aff></affiliation></author></analytic><series><title level="j">Antiviral research</title><idno type="ISSN">0166-3542</idno><idno type="eISSN">1872-9096</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P2">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.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8109699</journal-id><journal-id journal-id-type="pubmed-jr-id">688</journal-id><journal-id journal-id-type="nlm-ta">Antiviral Res</journal-id><journal-id journal-id-type="iso-abbrev">Antiviral Res.</journal-id><journal-title-group><journal-title>Antiviral research</journal-title></journal-title-group><issn pub-type="ppub">0166-3542</issn><issn pub-type="epub">1872-9096</issn></journal-meta><article-meta><article-id pub-id-type="pmid">24746459</article-id><article-id pub-id-type="pmc">4089891</article-id><article-id pub-id-type="doi">10.1016/j.antiviral.2014.04.001</article-id><article-id pub-id-type="manuscript">NIHMS587191</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Sluis-Cremer</surname><given-names>Nicolas</given-names></name><xref ref-type="aff" rid="A1">a</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib><contrib contrib-type="author"><name><surname>Jordan</surname><given-names>Michael R.</given-names></name><xref ref-type="aff" rid="A1">a</xref><xref ref-type="aff" rid="A2">b</xref></contrib><contrib contrib-type="author"><name><surname>Huber</surname><given-names>Kelly</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Wallis</surname><given-names>Carole L.</given-names></name><xref ref-type="aff" rid="A4">d</xref></contrib><contrib contrib-type="author"><name><surname>Bertagnolio</surname><given-names>Silvia</given-names></name><xref ref-type="aff" rid="A5">e</xref></contrib><contrib contrib-type="author"><name><surname>Mellors</surname><given-names>John W.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Parkin</surname><given-names>Neil T.</given-names></name><xref ref-type="aff" rid="A6">f</xref></contrib><contrib contrib-type="author"><name><surname>Harrigan</surname><given-names>P. Richard</given-names></name><xref ref-type="aff" rid="A7">g</xref></contrib></contrib-group><aff id="A1"><label>a</label>University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, Pittsburgh, PA, USA</aff><aff id="A2"><label>b</label>Division of Geographic Medicine and Infectious Disease, Tufts Medical Center, Boston, USA</aff><aff id="A3"><label>c</label>Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA, USA</aff><aff id="A4"><label>d</label>Lancet Laboratories, Johannesburg, South Africa</aff><aff id="A5"><label>e</label>HIV Department, World Health Organization, Geneva, Switzerland</aff><aff id="A6"><label>f</label>Data First Consulting, Belmont, CA, USA</aff><aff id="A7"><label>g</label>BC Centre for Excellence in HIV/AIDS, Vancouver, Canada</aff><author-notes><corresp id="FN1"><label>*</label>Corresponding author: Nicolas Sluis-Cremer, University of Pittsburgh School of Medicine, Department of Medicine, Division of Infectious Diseases, S817 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA, 15261, USA; Tel: 1-412-648-8457; Fax: 1-412-648-8521; <email>nps2@pitt.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>22</day><month>5</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>16</day><month>4</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>7</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>7</month><year>2015</year></pub-date><volume>107</volume><fpage>31</fpage><lpage>34</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.antiviral.2014.04.001</pmc-comment>
<permissions><copyright-statement>© 2014 Elsevier B.V. All rights reserved.</copyright-statement><copyright-year>2014</copyright-year></permissions><abstract><p id="P2">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.</p></abstract><kwd-group><kwd>HIV-1</kwd><kwd>reverse transcriptase</kwd><kwd>NNRTI</kwd><kwd>rilpivirine</kwd><kwd>E138A</kwd><kwd>resistance</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Amérique/explor/PittsburghV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001488 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 001488 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Amérique
|area= PittsburghV1
|flux= Pmc
|étape= Corpus
|type= RBID
|clé= PMC:4089891
|texte= E138A in HIV-1 reverse transcriptase is more common in subtype C than B: Implications for rilpivirine use in resource-limited settings
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/RBID.i -Sk "pubmed:24746459" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a PittsburghV1
| This area was generated with Dilib version V0.6.38. |  |