scholarly journals Prediction of Sustained Virological Response to Telaprevir/Simeprevir-Based Triple Therapy in Patients with Genotype 1 Hepatitis C Virus Using Super-Early Viral Response within 2 Weeks

2017 ◽  
Vol 06 (03) ◽  
Author(s):  
Yoshinori Ozono ◽  
Yuka Takaishi ◽  
Mai Tsuchimochi ◽  
Kenichi Nakamura ◽  
Hiroo Abe ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Triple Therapy ◽  
Sustained Virological Response ◽  
Virological Response ◽  
Genotype 1 ◽  
Viral Response ◽  
Early Viral Response

Effects of Smoking on Pegylated Interferon alpha 2a and First Generation Protease Inhibitor-based Antiviral Therapy in Naïve Patients Infected with Hepatitis C Virus Genotype 1

2016 ◽  
Vol 25 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Tim Zimmermann ◽  
Dietrich Hueppe ◽  
Stefan Mauss ◽  
Peter Buggisch ◽  
Heike Pfeiffer-Vornkahl ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Antiviral Therapy ◽  
Interferon Alpha ◽  
Virological Response ◽  
Sustained Viral Response ◽  
Pegylated Interferon ◽  
Genotype 1 ◽  
Pegylated Interferon Alpha ◽  
Viral Response

Background & Aims: Smoking has multiple effects on factors influencing hepatitis C and antiviral therapy, including lipid metabolism, fibrosis, platelet count and adherence aspects. The aim of this analysis was to determine the impact of smoking on hepatitis C virus antiviral therapy. Methods: Data of two cohorts of an observational multicenter study including therapy-naïve patients infected with genotype 1 hepatitis C virus (HCV) treated with dual antiviral therapy (n=7,796) with pegylated interferon alpha 2a in combination with ribavirin, or triple antiviral therapy (n=1,122) containing telaprevir or boceprevir, were analysed. Results: In the univariate matched pair analysis of dual antiviral therapy patients (n=584), smoking was significantly associated with lower sustained viral response rates (p=0.026, OR 0.69 CI: 0.50 – 0.96). The effect of smoking on sustained viral response remained significant (p=0.028, OR 0.67 CI: 0.47 – 0.96) in the multivariate analysis when adjusting for all other baseline parameters with a significant association in the univariate analysis, i.e. diabetes, fibrosis, body mass index, transaminases and baseline viral load. Under protease inhibitors the influence of smoking on virological response did not arise. Conclusions: Smoking has a negative impact on antiviral therapy in naïve patients infected with HCV genotype 1 independently of age, gender, history of drug use or alcoholic liver disease. The effects of smoking might be overcome by the new antiviral agents.Abbreviations: APRI: AST to platelet ratio index; DAA: direct antiviral agent; DT: dual antiviral therapy; EoTR: end of treatment response; RVR: rapid virological response; EVR: early virological response; HCV: hepatitis C virus; IFN: interferon alpha; MPA: Matched Pair Analysis; NS: non-smokers; PEG-IFN: pegylated interferon alpha 2a; PI: protease inhibitor; RBV: ribavirin; SAE: serious adverse event; SOC: standard of care; S: smokers; SVR: sustained viral response.    

IL-28B - Predictor of Sustained Virological Response for IFN-based Regimens in Chronic Hepatitis C and Criteria for Optimizing DAAs Indication

2019 ◽  
Vol 70 (11) ◽  
pp. 3964-3966
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Treatment Response ◽  
Sustained Virological Response ◽  
Chronic Hepatitis C ◽  
Virological Response ◽  
Response Rates ◽  
Beta Subunit ◽  
Viral Response

Chronic viral infections affecting the liver represents a global burden for medical comunities. More than 170 million individuals are infected chronically with hepatitis C virus (HCV), this accounting about 2-3% of the world’s population. Despite numerous progresses aquired in viral pahogenesis and treatment, chronic hepatitis C management is influenced by a multitude of factors. Interleukin IL-28 beta subunit (IL28B) demonstrated to be involved in both sustained virological response (SVR) to treatment, but even with spontaneous viral clearance without any therapy. In the era of direct antiviral agents (DAAs) we aimed to find out what was the real influence of IL28B phenotypes over the response to Peg-IFN and Ribavirin treatment in patients with chronic hepatitis C, many of theses being non-responders or relapsers, and as consequence, to optimize the referal of patients to more expensive and efficient treatments. In a retrospectively manner, we analyzed the IL28B phenotype and its influence over the rapid viral response (RVR), early viral response (EVR) and sustained viral response (SVR), in 250 patients HCV treated patients. We made correlations between the treatment response rates and the IL28B polymorphism.TT phenotype was correlated negatively with all parameters studied, while CC phenotype was correlated with the best response rates. We concluded that IL28B phenotypes interfere with the EVR and SVR rates, IL28B phenotype being an independent prognostic factor for antiviral treatment response in our patient groups, and according to this characteristics, we created the premise to optimize the patients referal to expensive therapies as DAAs. Keywords: hepatitis C virus, IL-28 beta subunit,viral treatment

scholarly journals Hepatitis C Drugs: The End of the Pegylated Interferon Era and the Emergence of All-Oral, Interferon-Free Antiviral Regimens: A Concise Review

2014 ◽  
Vol 28 (8) ◽  
pp. 445-451 ◽  
Author(s):  
Alan Hoi Lun Yau ◽  
Eric M Yoshida
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protease Inhibitor ◽  
Sustained Virological Response ◽  
Virological Response ◽  
Second Generation ◽  
Pegylated Interferon ◽  
Genotype 1 ◽  
Replication Complex ◽  
Polymerase Inhibitor

Between 2001 and 2011, the standard of care for chronic hepatitis C virus (HCV) infection was a combination of pegylated interferon (PEGIFN) and ribavirin (RBV). In May 2011, boceprevir and telaprevir, two first-generation NS3/4A protease inhibitors, were approved in combination with PEG-IFN and RBV for 24 to 48 weeks in hepatitis C virus genotype 1 infections. In December 2013, simeprevir, a second-generation NS3/4A protease inhibitor, was approved for use with PEG-IFN and RBV for 12 weeks in genotype 1, while sofosbuvir, a NS5B nucleotide polymerase inhibitor, was approved for use with PEG-IFN and RBV for 12 weeks in genotypes 1 and 4, as well as with RBV alone for 12 weeks in genotype 2 and for 24 weeks in genotype 3. Sofosbuvir combined with simeprevir or an NS5A replication complex inhibitor (ledipasvir or daclatasvir) with or without RBV for 12 weeks in genotype 1 resulted in a sustained virological response >90%, irrespective of previous treatment history or presence of cirrhosis. Similarly impressive sustained virological response rates have been shown with ABT-450/r (ritonavir-boosted NS3/4A protease inhibitor)-based regimens in combination with other direct-acting antiviral agent(s) with or without RBV for 12 weeks in genotype 1. The optimal all-oral interferon-free antiviral regimen likely entails a combination of an NS5B nucleotide polymerase inhibitor with either a second-generation NS3/4A protease inhibitor or an NS5A replication complex inhibitor with or without RBV. Further research is needed to determine the role of resistance testing, clarify the optimal follow-up duration post-treatment, and evaluate the antiviral efficacy and safety in difficult-to-cure patient populations.

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