Serum HCV RNA was measured using the COBAS TaqMan HCV Test v2·0 (Roche Molecular Systems; lower limit of quantitation (LLOQ) of 25 IU/ml) at baseline, at all subsequent study visits during treatment, and post-treatment weeks 4 and 12. Patients with confirmed HCV RNA one log IU/ml increase in HCV RNA from nadir while on-treatment; or non-response, i.e., HCV RNA persistently ≥LLOQ through 8 weeks of treatment. Relapse was defined as confirmed HCV RNA ≥LLOQ during the post-treatment period having achieved HCV RNA
Cobas taqman hcv test v2
Manufactured by Roche
Sourced in United States, Germany, Switzerland, Japan
The Cobas TaqMan HCV Test v2.0 is an in vitro diagnostic test used for the quantitative detection of Hepatitis C Virus (HCV) RNA in human serum or plasma samples. The test utilizes real-time PCR technology to measure the viral load of HCV.
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39 protocols using cobas taqman hcv test v2
1
Quantification of HCV RNA in Treatment
2
Comprehensive Monitoring of HCV Treatment with Substance Use Assessment
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Laboratory monitoring, including quantitative HCV RNA (COBAS TaqMan HCV Test v2.0; Roche Molecular Systems Inc., Branchburg, New Jersey), was performed at treatment weeks 0, 4, 8, 12, and post-treatment weeks 6 and 12. Adverse effects and medication adherence were assessed at each visit. CD4 cell count and HIV RNA levels were measured at screening and as clinically indicated. Liver elastography (FibroScan 502 Touch, Echosens North America, Waltham, Massachusetts) was performed before HCV treatment and at post-treatment week 12. Drug and alcohol use was assessed at each study visit by questionnaires, including the 10-question Alcohol Use Disorders Identification Test (AUDIT) [19 (link)]. At study entry and treatment week 6, drug use was measured by urine toxicology and alcohol use was measured by whole blood levels of phosphatidylethanol (PEth) (United States Drug Testing Laboratories, Des Plaines, Illinois) [20 (link)].
3
Liver Stiffness and Portal Flow in Hemodialysis Patients with Chronic Hepatitis C
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We conducted a retrospective, cross-sectional study to include hemodialysis patients with chronic HCV infection at the National Taiwan University Hospital (NTUH) and NTUH Yun-Lin Branch who underwent a liver stiffness measurement (LSM) with TE (FibroScan®, Echosens, Paris, France) and SAPI with duplex Doppler ultrasonography (Aplio 500®, Canon Medical Systems Incorporation, Tokyo, Japan) between January 2010 and June 2022. Hemodialysis patients were defined as those who had an estimated glomerular filtration (eGFR) rate <15 mL/min/1.73 m2 using the chronic kidney disease–epidemiology collaboration (CKD–EPI) equation and were on maintenance dialysis through vascular routes [33 (link),34 (link),35 (link)]. Chronic HCV infection was defined as patients who presented detectable HCV antibodies (anti-HCV; Abbott HCV EIA 2.0, Abbott Laboratories, Abbott Park, IL, USA) and quantifiable serum HCV RNA (Cobas TaqMan HCV Test v2.0, Roche Diagnostics GmbH, Mannheim, Germany, lower limit of quantification [LLOQ]: 15 IU/mL) for 6 months or more. Patients were excluded from the study if they had hepatitis B virus (HBV) or human immunodeficiency virus (HIV) coinfection, decompensated cirrhosis (Child-Pugh B or C), a history of hepatocellular carcinoma (HCC), a failed or unreliable LSM with TE, or a failed SAPI assessment due to splenectomy.
4
Comprehensive HCV Evaluation and Treatment
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We collected demographic and clinical characteristics at baseline, including HCV viral load and GT, stage of hepatic fibrosis, prior HCV treatment experience, past injection substance use, HIV, and hepatitis B virus (HBV) infection, for risk factor analysis. Human immunodeficiency virus-positive patients were referred to infection subspecialist for further medical care.
Serum HCV RNA level was determined by Cobas TaqMan HCV Test v2.0 (Roche Molecular Diagnostics, Pleasanton, CA) with a lower limit of quantification (LLOQ) of 15 IU/mL. Hepatitis C virus GT was determined by Cobas HCV GT (Roche Molecular Diagnostics). Advanced hepatic fibrosis (fibrosis stage F3) was assessed using fibrosis index based on 4 factors (FIB-4) test ≥3.25. Abdominal ultrasonography was performed to detect the presence of liver cirrhosis and for hepatocellular carcinoma surveillance. Baseline laboratory tests were performed within 3 months before the initiation of GLE/PIB treatment. Patients were followed every 4 weeks until the end of treatment (EOT) and at week 12 after treatment completion. Treatment-emergent adverse events (AEs) were recorded at every follow-up appointment. Safety data and laboratory abnormalities were graded using the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE).
Serum HCV RNA level was determined by Cobas TaqMan HCV Test v2.0 (Roche Molecular Diagnostics, Pleasanton, CA) with a lower limit of quantification (LLOQ) of 15 IU/mL. Hepatitis C virus GT was determined by Cobas HCV GT (Roche Molecular Diagnostics). Advanced hepatic fibrosis (fibrosis stage F3) was assessed using fibrosis index based on 4 factors (FIB-4) test ≥3.25. Abdominal ultrasonography was performed to detect the presence of liver cirrhosis and for hepatocellular carcinoma surveillance. Baseline laboratory tests were performed within 3 months before the initiation of GLE/PIB treatment. Patients were followed every 4 weeks until the end of treatment (EOT) and at week 12 after treatment completion. Treatment-emergent adverse events (AEs) were recorded at every follow-up appointment. Safety data and laboratory abnormalities were graded using the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE).
5
Direct-acting Antiviral Therapy for HCV
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The DAA regimen, indication for treatment, dose and duration of therapy were determined by the transplant hepatologist as standard of care independent of this study. All patients received a combination of non-interferon based DAAs available during the study time frame, with or without the addition of ribavirin. Successful treatment was determined by achievement of SVR, defined as undetectable HCV RNA by COBAS® TAQMAN® HCV TEST v2.0, Roche Diagnostics, Indianapolis, Indiana, USA at 12 weeks after end of treatment (SVR12) and one year after SVR12 in all patients.
6
Quantitative HCV RNA Detection and Genotyping
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HCV-RNA was extracted from plasma samples using High Pure System Viral Nucleic Acid kit (Roche Diagnostics, Manheim, Germany) following the manufacturer’s instructions and HCV RNA was amplified by Real-time PCR using COBAS Taq-Man HCV Test v2.0 (Roche Diagnostics) (range 25–3,91*108 IU/ml) and COBAS TaqMan 48 Analyzer for automated amplification and detection. HCV genotype was determined by INNO-LipA HCV II kit (Innogenetics, Ghent, Belgium). Were indicated HCV-RNA was analyzed using COBAS Amplicor HCV Monitor test v.2.0 and COBAS Amplicor Analyzer (Roche Diagnostics) following the manufacturer’s instructions.
7
HCV Resistance Assay Protocol
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Blood samples for resistance assays were collected from all participants at the baseline visit, at the time of virologic failure or at the end-of-treatment visit and at follow-up visits at weeks 4, 12 and 24. Plasma HCV RNA levels were measured using the Roche COBAS® Taqman® HCV Test v2.0, which has a lower limit of quantitation of 25 IU/mL. To assess the presence of polymorphisms at baseline or time of virologic failure, the HCV NS3/4A gene was amplified using the reverse transcriptase-polymerase chain reaction (PCR) followed by consensus Sanger and selective clonal sequencing. Due to the sensitivity of the consensus sequencing assay, resistance analysis was performed only on samples from participants with HCV viral loads >1000 IU/mL. The limit of variant detection using consensus Sanger sequencing was >25% of viral quasispecies. For clonal sequencing, PCR amplification was performed only on the NS3 protease region (amino acids 1–181) and the resultant amplicons cloned into a TOPO TA vector (Thermo Fisher Scientific, Waltham, MA, USA). Approximately 40 clones were sequenced at each time point and resultant amino acid sequences were compared with wild-type (WT) HCV GT1a (H77) or GT1b (Con1) reference sequences.
8
Sofosbuvir-Ledipasvir Therapy for HCV-1
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Between April 2015 and August 2017, HCV-1 infected patients who received SOF/LDV for 8, 12 or 24 weeks with or without ribavirin (RBV) were retrospectively enrolled at the National Taiwan University Hospital (NTUH) and NTUH Yun-Lin Branch. All patients were aged ≥ 20 years and had chronic HCV infection, defined as detectable HCV antibody (anti-HCV; Abbott HCV EIA 2.0, Abbott Laboratories, Abbott Park, Illinois, USA) and quantifiable serum HCV RNA (Cobas TaqMan HCV Test v2.0, Roche Diagnostics GmbH, Mannheim, Germany, lower limit of detection [LLOD]: 15 IU/mL) for ≥ 6 months. Patients who had non-HCV-1 infection, had prior DAA exposure, had active HCC, had estimated glomerular filtration rate (eGFR) < 30 mL/min/1.73m2, received treatment regimens outside the guideline recommendation, or refused to provide written informed consent were excluded from the study [27 (link)–29 (link)]. The study was approved by the NTUH Research Ethics Committee (201205058RIC) and was conducted in accordance with the principles of Declaration of Helsinki and the International Conference on Harmonization for Good Clinical Practice. All patients provided written informed consent before the study.
9
Automated Serum RNA Extraction and HCV Detection
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Total RNA in serum samples was extracted by an automated process performed in BioRobot 9604 (Qiagen, Hilden, Germany) and viral loads were determined by means of the COBAS Taqman HCV Test v.2.0 (Roche Molecular Systems, Indianapolis, IN).
10
Quantifying HCV RNA Viral Load
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Serum HCV RNA was measured using the COBAS TaqMan HCV Test v2.0 (Roche Molecular Systems, Pleasanton, CA, USA; lower limit of quantitation (LLOQ) of 15 IU/ml) at baseline, all subsequent study visits during treatment, and posttreatment at weeks 4, 12, and 24. Patients with confirmed HCV RNA < LLOQ at the end of the treatment and posttreatment visits continued until the subsequent posttreatment visits, unless there was a confirmed virologic relapse. On-treatment virologic failure was defined as follows: breakthrough, i.e., confirmed by HCV RNA > LLOQ after having previously had HCV RNA < LLOQ while on treatment; rebound, i.e., confirmed > 1-log10 IU/ml increase in HCV RNA while on treatment; or nonresponse, i.e., HCV RNA persistently > LLOQ through 8 weeks of treatment. Relapse was defined as confirmed HCV RNA > LLOQ during the posttreatment period having achieved HCV RNA < LLOQ at the end of the treatment.
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