Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications?
Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutation...
Ausführliche Beschreibung
Autor*in: |
Anadol, E. [verfasserIn] Kaiser, R. [verfasserIn] Verheyen, J. [verfasserIn] Schülter, E. [verfasserIn] Emmelkamp, J. [verfasserIn] Schwarze-Zander, C. [verfasserIn] Kupfer, B. [verfasserIn] Wasmuth, J. C. [verfasserIn] Rockstroh, J. K. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2010 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: European journal of medical research - London : BioMed Central, 2000, 15(2010), 5 vom: 18. Mai |
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Übergeordnetes Werk: |
volume:15 ; year:2010 ; number:5 ; day:18 ; month:05 |
Links: |
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DOI / URN: |
10.1186/2047-783X-15-5-225 |
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Katalog-ID: |
SPR032591667 |
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10.1186/2047-783X-15-5-225 doi (DE-627)SPR032591667 (SPR)2047-783X-15-5-225-e DE-627 ger DE-627 rakwb eng 610 ASE Anadol, E. verfasserin aut Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications? 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. transmitted resistance (dpeaa)DE-He213 Drug Resistance (dpeaa)DE-He213 Human immunodeficiency virus I (dpeaa)DE-He213 T215 D (dpeaa)DE-He213 Kaiser, R. verfasserin aut Verheyen, J. verfasserin aut Schülter, E. verfasserin aut Emmelkamp, J. verfasserin aut Schwarze-Zander, C. verfasserin aut Kupfer, B. verfasserin aut Wasmuth, J. C. verfasserin aut Rockstroh, J. K. verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 15(2010), 5 vom: 18. Mai (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:15 year:2010 number:5 day:18 month:05 https://dx.doi.org/10.1186/2047-783X-15-5-225 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2010 5 18 05 |
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10.1186/2047-783X-15-5-225 doi (DE-627)SPR032591667 (SPR)2047-783X-15-5-225-e DE-627 ger DE-627 rakwb eng 610 ASE Anadol, E. verfasserin aut Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications? 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. transmitted resistance (dpeaa)DE-He213 Drug Resistance (dpeaa)DE-He213 Human immunodeficiency virus I (dpeaa)DE-He213 T215 D (dpeaa)DE-He213 Kaiser, R. verfasserin aut Verheyen, J. verfasserin aut Schülter, E. verfasserin aut Emmelkamp, J. verfasserin aut Schwarze-Zander, C. verfasserin aut Kupfer, B. verfasserin aut Wasmuth, J. C. verfasserin aut Rockstroh, J. K. verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 15(2010), 5 vom: 18. Mai (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:15 year:2010 number:5 day:18 month:05 https://dx.doi.org/10.1186/2047-783X-15-5-225 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2010 5 18 05 |
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10.1186/2047-783X-15-5-225 doi (DE-627)SPR032591667 (SPR)2047-783X-15-5-225-e DE-627 ger DE-627 rakwb eng 610 ASE Anadol, E. verfasserin aut Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications? 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. transmitted resistance (dpeaa)DE-He213 Drug Resistance (dpeaa)DE-He213 Human immunodeficiency virus I (dpeaa)DE-He213 T215 D (dpeaa)DE-He213 Kaiser, R. verfasserin aut Verheyen, J. verfasserin aut Schülter, E. verfasserin aut Emmelkamp, J. verfasserin aut Schwarze-Zander, C. verfasserin aut Kupfer, B. verfasserin aut Wasmuth, J. C. verfasserin aut Rockstroh, J. K. verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 15(2010), 5 vom: 18. Mai (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:15 year:2010 number:5 day:18 month:05 https://dx.doi.org/10.1186/2047-783X-15-5-225 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2010 5 18 05 |
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10.1186/2047-783X-15-5-225 doi (DE-627)SPR032591667 (SPR)2047-783X-15-5-225-e DE-627 ger DE-627 rakwb eng 610 ASE Anadol, E. verfasserin aut Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications? 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. transmitted resistance (dpeaa)DE-He213 Drug Resistance (dpeaa)DE-He213 Human immunodeficiency virus I (dpeaa)DE-He213 T215 D (dpeaa)DE-He213 Kaiser, R. verfasserin aut Verheyen, J. verfasserin aut Schülter, E. verfasserin aut Emmelkamp, J. verfasserin aut Schwarze-Zander, C. verfasserin aut Kupfer, B. verfasserin aut Wasmuth, J. C. verfasserin aut Rockstroh, J. K. verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 15(2010), 5 vom: 18. Mai (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:15 year:2010 number:5 day:18 month:05 https://dx.doi.org/10.1186/2047-783X-15-5-225 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2010 5 18 05 |
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Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications? |
abstract |
Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. |
abstractGer |
Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. |
abstract_unstemmed |
Abstract The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used. |
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score |
7.40172 |