Protease Inhibitors Drug Resistance Mutations in Turkish Patients with Chronic Hepatitis C
Autor: | Aynur Aynioglu, Gülden Ersöz, Dilara Inan, Sıla Akhan, Sukran Kose, Saadet Yazici, Suda Tekin Koruk, Celal Ayaz, Onur Ural, Reşit Mistik, Bilgehan Aygen, Nazan Tuna, Safiye Koculu, Fatime Korkmaz, Murat Sayan, Neşe Demirtürk, Faruk Karakeçili, Taner Yildirmak, Elif Sargin Altunok, Derya Keten, Orhan Yildiz |
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Přispěvatelé: | Zonguldak Bülent Ecevit Üniversitesi, Uludağ Üniversitesi/Tıp Fakültesi/Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Anabilim Dalı., Mıstık, Reşit, Giresun Üniversitesi, Selçuk Üniversitesi |
Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Simeprevir Male hepatitis C virus Amino acid substitution Turkey Hepacivirus Clinical assessment Drug resistance Antiviral therapy Antagonists and inhibitors Viral Nonstructural Proteins medicine.disease_cause Chronic hepatitis C Treatment response Telaprevir chemistry.chemical_compound 0302 clinical medicine Virus resistance Faldaprevir Antiviral activity Aged 80 and over Boceprevir Analogs and derivatives biology NS3 protein hepatitis C virus Genetic analysis Antiviral resistance General Medicine Hepatitis C Middle Aged Genotype 1 Hepatitis C virus genotype 1 Turkish citizen Amino acid Infectious Diseases Retreatment Oligopeptide Medical examination 030211 gastroenterology & hepatology Female Infection Oligopeptides Pegylated interferon medicine.drug Human Microbiology (medical) Adult Genotype Proline Hepatitis C virus protease inhibitors Major clinical study Unspecified side effect Antiviral Agents Article lcsh:Infectious and parasitic diseases N-(3-amino-1-(cyclobutylmethyl)-2 3-dioxopropyl)-3-(2-((((1 1-dimethylethyl)amino)carbonyl)amino)-3 3-dimethyl-1-oxobutyl)-6 6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 03 medical and health sciences Young Adult Virology Ribavirin Drug Resistance Viral medicine Genetics Humans lcsh:RC109-216 Gene mutation Antivirus agent Aged Genetic polymorphism Drug effects Baseline resistance Interleukin 28B Very elderly Hepatitis C Chronic medicine.disease biology.organism_classification Virus genotypes Chronic Hepatitis C 030104 developmental biology Metabolism chemistry Isolation and purification Enzymology Proteinase inhibitor mutation Polymorphisms |
Zdroj: | International Journal of Infectious Diseases, Vol 50, Iss C, Pp 1-5 (2016) |
ISSN: | 1878-3511 1201-9712 |
Popis: | WOS: 000388326300001 PubMed: 27401586 Background: Drug resistance development is an expected problem during treatment with protease inhibitors (PIs), this is largely due to the fact that Pls are low-genetic barrier drugs. Resistance-associated variants (RAVs) however may also occur naturally, and prior to treatment with Pls, the clinical impact of this basal resistance remains unknown. In Turkey, there is yet to be an investigation into the hepatitis C (HCV) drug associated resistance to oral antivirals. Materials and methods: 178 antiviral-naive patients infected with HCV genotype 1 were selected from 27 clinical centers of various geographical regions in Turkey and included in the current study. The basal NS3 Pls resistance mutations of these patients were analyzed. Results: In 33 (18.5%) of the patients included in the study, at least one mutation pattern that can cause drug resistance was identified. The most frequently detected mutation pattern was T54S while R109K was the second most frequently detected. Following a more general examination of the patients studied, telaprevir (TVR) resistance in 27 patients (15.2%), boceprevir (BOC) resistance in 26 (14.6%) patients, simeprevir (SMV) resistance in 11 (6.2%) patients and faldaprevir resistance in 13 (7.3%) patients were detected. Our investigation also revealed that rebound developed in the presence of a Q80K mutation and amongst two V55A mutations following treatment with TVR, while no response to treatment was detected in a patient with a R55K mutation. Conclusion: We are of the opinion that drug resistance analyses can be beneficial and necessary in revealing which variants are responsible for pre-treatment natural resistance and which mutations are responsible for the viral breakthrough that may develop during the treatment. (C) 2016 The Authors. Published by Elsevier Ltd on behalf of International Society for Infectious Diseases. Department of Scientific Research Project of Kocaeli University; Turkish Society of Clinic Microbiology and Infectious Diseases This study was funded by Department of Scientific Research Project of Kocaeli University and Turkish Society of Clinic Microbiology and Infectious Diseases. |
Databáze: | OpenAIRE |
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