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논문 기본 정보

자료유형
학술저널
저자정보
Kyung-Ah Kim (Department of Internal Medicine Inje University Ilsan Paik Hospital) Sejoon Lee (Department of Precision Medicine Center/Department of Pathology and Translational Medicine Seoul National University Bundang Hospital) Hye Jung Park (Department of Internal Medicine Institute of Gastroenterology Yonsei University College of Medicine) Eun Sun Jang (Department of Internal Medicine Seoul National University Bundang Hospital) Youn Jae Lee (Department of Internal Medicine Inje University Busan Paik Hospital) Sung Bum Cho (Department of Internal Medicine Chonnam National University Hwasun Hospital) Young Suk Kim (Department of Internal Medicine Soonchunhyang University Bucheon Hospital) In Hee Kim (Department of Internal Medicine Jeonbuk National University Hospital) Byung Seok Lee (Department of Internal Medicine Chungnam National University Hospital) Woo Jin Chung (Department of Internal Medicine Keimyung University School of Medicine) Sang Hoon Ahn (Department of Internal MedicineInstitute of Gastroenterology Yonsei University College of Medicine) Seungtaek Kim (Zoonotic Virus Laboratory Institut Pasteur Korea) Sook Hyang Jeong (Department of Internal Medicine Seoul National University Bundang Hospital)
저널정보
대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology 제29권 제2호
발행연도
2023.4
수록면
496 - 509 (14page)

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Background/Aims: We used next-generation sequencing (NGS) to analyze resistance-associated substitutions (RASs) and retreatment outcomes in patients with chronic hepatitis C virus (HCV) infection who failed direct-acting antiviral agent (DAA) treatment in South Korea. Methods: Using prospectively collected data from the Korean HCV cohort study, we recruited 36 patients who failed DAA treatment in 10 centers between 2007 and 2020; 29 blood samples were available from 24 patients. RASs were analyzed using NGS. Results: RASs were analyzed for 13 patients with genotype 1b, 10 with genotype 2, and one with genotype 3a. The unsuccessful DAA regimens were daclatasvir+asunaprevir (n=11), sofosbuvir+ribavirin (n=9), ledipasvir/sofosbuvir (n=3), and glecaprevir/pibrentasvir (n=1). In the patients with genotype 1b, NS3, NS5A, and NS5B RASs were detected in eight, seven, and seven of 10 patients at baseline and in four, six, and two of six patients after DAA failure, respectively. Among the 10 patients with genotype 2, the only baseline RAS was NS3 Y56F, which was detected in one patient. NS5A F28C was detected after DAA failure in a patient with genotype 2 infection who was erroneously treated with daclatasvir+asunaprevir. After retreatment, 16 patients had a 100% sustained virological response rate. Conclusions: NS3 and NS5A RASs were commonly present at baseline, and there was an increasing trend of NS5A RASs after failed DAA treatment in genotype 1b. However, RASs were rarely present in patients with genotype 2 who were treated with sofosbuvir+ribavirin. Despite baseline or treatment-emergent RASs, retreatment with pan-genotypic DAA was highly successful in Korea, so we encourage active retreatment after unsuccessful DAA treatment.

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