ArticleInternal medicine (Tokyo, Japan)2019
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.
Article in Internal medicine (Tokyo, Japan), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Japanese Man with HCV Genotype 4 Infection and Cirrhosis Who Was Successfully Treated by the Combination of Glecaprevir and Pibrentasvir.Internal medicine (Tokyo, Japan) · 2021Article
- Real-word efficacy of sofosbuvir, velpatasvir plus ribavirin therapy for chronic hepatitis patients who failed to prior DAA therapy with NS5A-P32 deletion mutated HCV infection.Clinical journal of gastroenterology · 2020Article
- Computational analysis of naturally occurring resistance-associated substitutions in genesInfection and drug resistance · 2019Article
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Authors and funding
15 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
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.
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