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Role of NS5A-L31/Y93 Double Wild-type in Failure of Glecaprevir/Pibrentasvir Double Therapy in Two Patients with a History of Direct-acting Antiviral Agent Failure: An Ultra-deep Sequencing Analysis.


ABSTRACT: We experienced two cases of hepatitis C virus (HCV) eradication failure in patients with a history of non-responsiveness to previous treatments with direct-acting antiviral agents (DAAs) who were subsequently treated with the combination of glecaprevir and pibrentasvir (GLE/PIB). Direct sequencing at commencement of GLE/PIB therapy showed non-structural protein (NS) 5A-P32 deletion in the first patient and NS5A-R30E/Q54H/A92K in the second patient (both genotype 1b). The common point was that L31/Y93 was double wild-type, and the IL28B polymorphism was non-TT type. Even when L31/Y93 is double wild-type, other NS5A mutations may affect the DAA re-treatment outcome. We analyzed the transition of amino acid mutations at NS5A by ultra-deep sequencing.

SUBMITTER: Sano T 

PROVIDER: S-EPMC6794189 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Role of NS5A-L31/Y93 Double Wild-type in Failure of Glecaprevir/Pibrentasvir Double Therapy in Two Patients with a History of Direct-acting Antiviral Agent Failure: An Ultra-deep Sequencing Analysis.

Sano Tomoya T   Akuta Norio N   Suzuki Fumitaka F   Kasuya Kayoko K   Fujiyama Shunichiro S   Kawamura Yusuke Y   Sezaki Hitomi H   Hosaka Tetsuya T   Saitoh Satoshi S   Kobayashi Masahiro M   Suzuki Yoshiyuki Y   Kobayashi Mariko M   Arase Yasuji Y   Ikeda Kenji K   Kumada Hiromitsu H  

Internal medicine (Tokyo, Japan) 20190607 18


We experienced two cases of hepatitis C virus (HCV) eradication failure in patients with a history of non-responsiveness to previous treatments with direct-acting antiviral agents (DAAs) who were subsequently treated with the combination of glecaprevir and pibrentasvir (GLE/PIB). Direct sequencing at commencement of GLE/PIB therapy showed non-structural protein (NS) 5A-P32 deletion in the first patient and NS5A-R30E/Q54H/A92K in the second patient (both genotype 1b). The common point was that L3  ...[more]

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