Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case
Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated hig...
Ausführliche Beschreibung
Autor*in: |
Schildgen, Verena [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
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2010 |
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Anmerkung: |
© Schildgen et al; licensee BioMed Central Ltd. 2010 |
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Übergeordnetes Werk: |
Enthalten in: Virology journal - London : BioMed Central, 2004, 7(2010), 1 vom: 21. Juli |
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Übergeordnetes Werk: |
volume:7 ; year:2010 ; number:1 ; day:21 ; month:07 |
Links: |
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DOI / URN: |
10.1186/1743-422X-7-167 |
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Katalog-ID: |
SPR029242533 |
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245 | 1 | 0 | |a Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case |
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520 | |a Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. | ||
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700 | 1 | |a Ziegler, Susanne |4 aut | |
700 | 1 | |a Tillmann, Ramona L |4 aut | |
700 | 1 | |a Schildgen, Oliver |4 aut | |
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10.1186/1743-422X-7-167 doi (DE-627)SPR029242533 (SPR)1743-422X-7-167-e DE-627 ger DE-627 rakwb eng Schildgen, Verena verfasserin aut Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Schildgen et al; licensee BioMed Central Ltd. 2010 Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. Lamivudine (dpeaa)DE-He213 Adefovir (dpeaa)DE-He213 Adefovir Dipivoxil (dpeaa)DE-He213 Lamivudine Resistance (dpeaa)DE-He213 Position Rt188 (dpeaa)DE-He213 Ziegler, Susanne aut Tillmann, Ramona L aut Schildgen, Oliver aut Enthalten in Virology journal London : BioMed Central, 2004 7(2010), 1 vom: 21. Juli (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:7 year:2010 number:1 day:21 month:07 https://dx.doi.org/10.1186/1743-422X-7-167 kostenfrei 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_31 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 7 2010 1 21 07 |
spelling |
10.1186/1743-422X-7-167 doi (DE-627)SPR029242533 (SPR)1743-422X-7-167-e DE-627 ger DE-627 rakwb eng Schildgen, Verena verfasserin aut Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Schildgen et al; licensee BioMed Central Ltd. 2010 Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. Lamivudine (dpeaa)DE-He213 Adefovir (dpeaa)DE-He213 Adefovir Dipivoxil (dpeaa)DE-He213 Lamivudine Resistance (dpeaa)DE-He213 Position Rt188 (dpeaa)DE-He213 Ziegler, Susanne aut Tillmann, Ramona L aut Schildgen, Oliver aut Enthalten in Virology journal London : BioMed Central, 2004 7(2010), 1 vom: 21. Juli (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:7 year:2010 number:1 day:21 month:07 https://dx.doi.org/10.1186/1743-422X-7-167 kostenfrei 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_31 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 7 2010 1 21 07 |
allfields_unstemmed |
10.1186/1743-422X-7-167 doi (DE-627)SPR029242533 (SPR)1743-422X-7-167-e DE-627 ger DE-627 rakwb eng Schildgen, Verena verfasserin aut Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Schildgen et al; licensee BioMed Central Ltd. 2010 Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. Lamivudine (dpeaa)DE-He213 Adefovir (dpeaa)DE-He213 Adefovir Dipivoxil (dpeaa)DE-He213 Lamivudine Resistance (dpeaa)DE-He213 Position Rt188 (dpeaa)DE-He213 Ziegler, Susanne aut Tillmann, Ramona L aut Schildgen, Oliver aut Enthalten in Virology journal London : BioMed Central, 2004 7(2010), 1 vom: 21. Juli (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:7 year:2010 number:1 day:21 month:07 https://dx.doi.org/10.1186/1743-422X-7-167 kostenfrei 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_31 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 7 2010 1 21 07 |
allfieldsGer |
10.1186/1743-422X-7-167 doi (DE-627)SPR029242533 (SPR)1743-422X-7-167-e DE-627 ger DE-627 rakwb eng Schildgen, Verena verfasserin aut Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Schildgen et al; licensee BioMed Central Ltd. 2010 Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. Lamivudine (dpeaa)DE-He213 Adefovir (dpeaa)DE-He213 Adefovir Dipivoxil (dpeaa)DE-He213 Lamivudine Resistance (dpeaa)DE-He213 Position Rt188 (dpeaa)DE-He213 Ziegler, Susanne aut Tillmann, Ramona L aut Schildgen, Oliver aut Enthalten in Virology journal London : BioMed Central, 2004 7(2010), 1 vom: 21. Juli (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:7 year:2010 number:1 day:21 month:07 https://dx.doi.org/10.1186/1743-422X-7-167 kostenfrei 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_31 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 7 2010 1 21 07 |
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10.1186/1743-422X-7-167 doi (DE-627)SPR029242533 (SPR)1743-422X-7-167-e DE-627 ger DE-627 rakwb eng Schildgen, Verena verfasserin aut Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Schildgen et al; licensee BioMed Central Ltd. 2010 Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. Lamivudine (dpeaa)DE-He213 Adefovir (dpeaa)DE-He213 Adefovir Dipivoxil (dpeaa)DE-He213 Lamivudine Resistance (dpeaa)DE-He213 Position Rt188 (dpeaa)DE-He213 Ziegler, Susanne aut Tillmann, Ramona L aut Schildgen, Oliver aut Enthalten in Virology journal London : BioMed Central, 2004 7(2010), 1 vom: 21. Juli (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:7 year:2010 number:1 day:21 month:07 https://dx.doi.org/10.1186/1743-422X-7-167 kostenfrei 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_31 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 7 2010 1 21 07 |
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Schildgen, Verena Ziegler, Susanne Tillmann, Ramona L Schildgen, Oliver |
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Schildgen, Verena |
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novel mutation in ymdd motif and direct neighbourhood in a child with chronic hbv-infection and clinical lamivudine and adefovir resistance - a scholarly case |
title_auth |
Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case |
abstract |
Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. © Schildgen et al; licensee BioMed Central Ltd. 2010 |
abstractGer |
Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. © Schildgen et al; licensee BioMed Central Ltd. 2010 |
abstract_unstemmed |
Context Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the $ 5^{th} $ most reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity. Objective, Design, Setting, and Patient The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described. Interventions and Main Outcome Measure(s) Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment. Results and Conclusions Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV. © Schildgen et al; licensee BioMed Central Ltd. 2010 |
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title_short |
Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case |
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