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Emergence of hepatitis C virus NS5A L31V plus Y93H variant upon treatment failure of daclatasvir and asunaprevir is relatively resistant to ledipasvir and NS5B polymerase nucleotide inhibitor GS-558093 in human hepatocyte chimeric mice

Background Resistance-associated variants (RAVs) emerge at multiple positions spanning hepatitis C virus (HCV) NS3/4A and NS5A regions upon failure of asunaprevir/daclatasvir combination therapy. It has not been determined whether the emergence of such RAVs have an impact on re-treatment by a combin... Full description

Journal Title: Journal of gastroenterology 2015-07-25, Vol.50 (11), p.1145-1151
Main Author: Kai, Yugo
Other Authors: Hikita, Hayato , Tatsumi, Tomohide , Nakabori, Tasuku , Saito, Yoshinobu , Morishita, Naoki , Tanaka, Satoshi , Nawa, Takatoshi , Oze, Tsugiko , Sakamori, Ryotaro , Yakushijin, Takayuki , Hiramatsu, Naoki , Suemizu, Hiroshi , Takehara, Tetsuo
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Tokyo: Springer Japan
ID: ISSN: 0944-1174
Link: https://www.ncbi.nlm.nih.gov/pubmed/26208695
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title: Emergence of hepatitis C virus NS5A L31V plus Y93H variant upon treatment failure of daclatasvir and asunaprevir is relatively resistant to ledipasvir and NS5B polymerase nucleotide inhibitor GS-558093 in human hepatocyte chimeric mice
format: Article
creator:
  • Kai, Yugo
  • Hikita, Hayato
  • Tatsumi, Tomohide
  • Nakabori, Tasuku
  • Saito, Yoshinobu
  • Morishita, Naoki
  • Tanaka, Satoshi
  • Nawa, Takatoshi
  • Oze, Tsugiko
  • Sakamori, Ryotaro
  • Yakushijin, Takayuki
  • Hiramatsu, Naoki
  • Suemizu, Hiroshi
  • Takehara, Tetsuo
subjects:
  • Abdominal Surgery
  • Animals
  • Antiviral Agents - therapeutic use
  • Benzimidazoles - therapeutic use
  • Colorectal Surgery
  • Drug Combinations
  • Drug Resistance, Multiple, Viral - genetics
  • Female
  • Fluorenes - therapeutic use
  • Gastroenterology
  • Health aspects
  • Hepacivirus - drug effects
  • Hepacivirus - genetics
  • Hepatitis C virus
  • Hepatitis C, Chronic - drug therapy
  • Hepatitis C, Chronic - virology
  • Hepatitis, Viral, Animal - drug therapy
  • Hepatitis, Viral, Animal - virology
  • Hepatocytes - virology
  • Hepatology
  • Humans
  • Imidazoles - therapeutic use
  • Isoquinolines - therapeutic use
  • Male
  • Medicine
  • Medicine & Public Health
  • Middle Aged
  • Rapid Communication
  • Sofosbuvir - therapeutic use
  • Sulfonamides - therapeutic use
  • Surgical Oncology
  • Transplantation Chimera
  • Treatment Failure
  • Virus diseases
ispartof: Journal of gastroenterology, 2015-07-25, Vol.50 (11), p.1145-1151
description: Background Resistance-associated variants (RAVs) emerge at multiple positions spanning hepatitis C virus (HCV) NS3/4A and NS5A regions upon failure of asunaprevir/daclatasvir combination therapy. It has not been determined whether the emergence of such RAVs have an impact on re-treatment by a combination of ledipasvir and sofosbuvir, a potent regimen for HCV genotype 1 infection. Methods TK-NOG human hepatocyte chimeric mice were inoculated with sera from a patient with treatment failure of asunaprevir/daclatasvir therapy. Results They developed persistent HCV infection with triple variants of NS3/4A D168V, NS5A L31V plus Y93H. Administration of ledipasvir/GS-558093 (a NS5B nucleotide analog) in these mice failed to achieve end-of-treatment response or sustained virologic response, which was in sharp contrast to the results in mice with wild-type virus infection. The administration of telaprevir/GS-558093 successfully achieved it in those mice. Conclusions Treatment failure with asunaprevir/daclatasvir may limit further treatment options. This population may represent a growing unmet medical need.
language: eng
source:
identifier: ISSN: 0944-1174
fulltext: no_fulltext
issn:
  • 0944-1174
  • 1435-5922
url: Link


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titleEmergence of hepatitis C virus NS5A L31V plus Y93H variant upon treatment failure of daclatasvir and asunaprevir is relatively resistant to ledipasvir and NS5B polymerase nucleotide inhibitor GS-558093 in human hepatocyte chimeric mice
creatorKai, Yugo ; Hikita, Hayato ; Tatsumi, Tomohide ; Nakabori, Tasuku ; Saito, Yoshinobu ; Morishita, Naoki ; Tanaka, Satoshi ; Nawa, Takatoshi ; Oze, Tsugiko ; Sakamori, Ryotaro ; Yakushijin, Takayuki ; Hiramatsu, Naoki ; Suemizu, Hiroshi ; Takehara, Tetsuo
creatorcontribKai, Yugo ; Hikita, Hayato ; Tatsumi, Tomohide ; Nakabori, Tasuku ; Saito, Yoshinobu ; Morishita, Naoki ; Tanaka, Satoshi ; Nawa, Takatoshi ; Oze, Tsugiko ; Sakamori, Ryotaro ; Yakushijin, Takayuki ; Hiramatsu, Naoki ; Suemizu, Hiroshi ; Takehara, Tetsuo
descriptionBackground Resistance-associated variants (RAVs) emerge at multiple positions spanning hepatitis C virus (HCV) NS3/4A and NS5A regions upon failure of asunaprevir/daclatasvir combination therapy. It has not been determined whether the emergence of such RAVs have an impact on re-treatment by a combination of ledipasvir and sofosbuvir, a potent regimen for HCV genotype 1 infection. Methods TK-NOG human hepatocyte chimeric mice were inoculated with sera from a patient with treatment failure of asunaprevir/daclatasvir therapy. Results They developed persistent HCV infection with triple variants of NS3/4A D168V, NS5A L31V plus Y93H. Administration of ledipasvir/GS-558093 (a NS5B nucleotide analog) in these mice failed to achieve end-of-treatment response or sustained virologic response, which was in sharp contrast to the results in mice with wild-type virus infection. The administration of telaprevir/GS-558093 successfully achieved it in those mice. Conclusions Treatment failure with asunaprevir/daclatasvir may limit further treatment options. This population may represent a growing unmet medical need.
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subjectAbdominal Surgery ; Animals ; Antiviral Agents - therapeutic use ; Benzimidazoles - therapeutic use ; Colorectal Surgery ; Drug Combinations ; Drug Resistance, Multiple, Viral - genetics ; Female ; Fluorenes - therapeutic use ; Gastroenterology ; Health aspects ; Hepacivirus - drug effects ; Hepacivirus - genetics ; Hepatitis C virus ; Hepatitis C, Chronic - drug therapy ; Hepatitis C, Chronic - virology ; Hepatitis, Viral, Animal - drug therapy ; Hepatitis, Viral, Animal - virology ; Hepatocytes - virology ; Hepatology ; Humans ; Imidazoles - therapeutic use ; Isoquinolines - therapeutic use ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Rapid Communication ; Sofosbuvir - therapeutic use ; Sulfonamides - therapeutic use ; Surgical Oncology ; Transplantation Chimera ; Treatment Failure ; Virus diseases
ispartofJournal of gastroenterology, 2015-07-25, Vol.50 (11), p.1145-1151
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7Nawa, Takatoshi
8Oze, Tsugiko
9Sakamori, Ryotaro
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12Suemizu, Hiroshi
13Takehara, Tetsuo
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0Emergence of hepatitis C virus NS5A L31V plus Y93H variant upon treatment failure of daclatasvir and asunaprevir is relatively resistant to ledipasvir and NS5B polymerase nucleotide inhibitor GS-558093 in human hepatocyte chimeric mice
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descriptionBackground Resistance-associated variants (RAVs) emerge at multiple positions spanning hepatitis C virus (HCV) NS3/4A and NS5A regions upon failure of asunaprevir/daclatasvir combination therapy. It has not been determined whether the emergence of such RAVs have an impact on re-treatment by a combination of ledipasvir and sofosbuvir, a potent regimen for HCV genotype 1 infection. Methods TK-NOG human hepatocyte chimeric mice were inoculated with sera from a patient with treatment failure of asunaprevir/daclatasvir therapy. Results They developed persistent HCV infection with triple variants of NS3/4A D168V, NS5A L31V plus Y93H. Administration of ledipasvir/GS-558093 (a NS5B nucleotide analog) in these mice failed to achieve end-of-treatment response or sustained virologic response, which was in sharp contrast to the results in mice with wild-type virus infection. The administration of telaprevir/GS-558093 successfully achieved it in those mice. Conclusions Treatment failure with asunaprevir/daclatasvir may limit further treatment options. This population may represent a growing unmet medical need.
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2Antiviral Agents - therapeutic use
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5Drug Combinations
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30Surgical Oncology
31Transplantation Chimera
32Treatment Failure
33Virus diseases
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titleEmergence of hepatitis C virus NS5A L31V plus Y93H variant upon treatment failure of daclatasvir and asunaprevir is relatively resistant to ledipasvir and NS5B polymerase nucleotide inhibitor GS-558093 in human hepatocyte chimeric mice
authorKai, Yugo ; Hikita, Hayato ; Tatsumi, Tomohide ; Nakabori, Tasuku ; Saito, Yoshinobu ; Morishita, Naoki ; Tanaka, Satoshi ; Nawa, Takatoshi ; Oze, Tsugiko ; Sakamori, Ryotaro ; Yakushijin, Takayuki ; Hiramatsu, Naoki ; Suemizu, Hiroshi ; Takehara, Tetsuo
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0Abdominal Surgery
1Animals
2Antiviral Agents - therapeutic use
3Benzimidazoles - therapeutic use
4Colorectal Surgery
5Drug Combinations
6Drug Resistance, Multiple, Viral - genetics
7Female
8Fluorenes - therapeutic use
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11Hepacivirus - drug effects
12Hepacivirus - genetics
13Hepatitis C virus
14Hepatitis C, Chronic - drug therapy
15Hepatitis C, Chronic - virology
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31Transplantation Chimera
32Treatment Failure
33Virus diseases
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1Hikita, Hayato
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3Nakabori, Tasuku
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atitleEmergence of hepatitis C virus NS5A L31V plus Y93H variant upon treatment failure of daclatasvir and asunaprevir is relatively resistant to ledipasvir and NS5B polymerase nucleotide inhibitor GS-558093 in human hepatocyte chimeric mice
jtitleJournal of gastroenterology
stitleJ Gastroenterol
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date2015-07-25
risdate2015
volume50
issue11
spage1145
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pages1145-1151
issn0944-1174
eissn1435-5922
abstractBackground Resistance-associated variants (RAVs) emerge at multiple positions spanning hepatitis C virus (HCV) NS3/4A and NS5A regions upon failure of asunaprevir/daclatasvir combination therapy. It has not been determined whether the emergence of such RAVs have an impact on re-treatment by a combination of ledipasvir and sofosbuvir, a potent regimen for HCV genotype 1 infection. Methods TK-NOG human hepatocyte chimeric mice were inoculated with sera from a patient with treatment failure of asunaprevir/daclatasvir therapy. Results They developed persistent HCV infection with triple variants of NS3/4A D168V, NS5A L31V plus Y93H. Administration of ledipasvir/GS-558093 (a NS5B nucleotide analog) in these mice failed to achieve end-of-treatment response or sustained virologic response, which was in sharp contrast to the results in mice with wild-type virus infection. The administration of telaprevir/GS-558093 successfully achieved it in those mice. Conclusions Treatment failure with asunaprevir/daclatasvir may limit further treatment options. This population may represent a growing unmet medical need.
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pubSpringer Japan
pmid26208695
doi10.1007/s00535-015-1108-6