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Nucleotide Polymerase Inhibitor So fos bu vir plus Ribavirin for Hepatitis C

TLDR
Sofosbuvir plus ribavirin for 12 weeks may be effective in previously untreated patients with HCV genotype 1, 2, or 3 infection, and the rate of sustained virologic response 24 weeks after therapy is reported.
Abstract
BACKGROUND The standard treatment for hepatitis C virus (HCV) infection is interferon, which is administered subcutaneously and can have troublesome side effects. We evaluated so fos bu vir, an oral nucleotide inhibitor of HCV polymerase, in interferon-sparing and interferon-free regimens for the treatment of HCV infection. METHODS

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Efficacy and safety of a fixed dose combination tablet of asunaprevir + beclabuvir + daclatasvir for the treatment of Hepatitis C

TL;DR: This review focuses on the pharmacokinetics, efficacy, tolerability and safety profile of DCV-TRIO, a twice-daily fixed-dose combination of daclatasvir, asunaprevir and beclabuvir approved in Japan for the treatment of genotype 1 HCV infection.
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Asunaprevir-containing regimens for the treatment of hepatitis C virus infection

TL;DR: A recently developed NS3 protease inhibitor, asunaprevir (ASV), in combination with other DAAs as IFN/RBV-containing or -free regimen, has shown promising results with fewer adverse effects.
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Cost-effectiveness of pretransplant sofosbuvir for preventing recurrent hepatitis C virus infection after liver transplantation

TL;DR: A dynamic model is proposed based on real‐life data from northern Italy for adjusting the costs of pre‐LT direct‐acting antiviral therapies to the actual sustained virological response reached after LT, proving cost‐effective in this particular Italian scenario.
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Polymorphisms at IL28B gene as predictors of viral relapse in genotype 4 Egyptian hepatitis C patients

TL;DR: SNPs at IL‐28/60 and IL-28/75 are possible predictors of relapse in patients receiving dual treatment in patients with chronic HCV and no statistical significant difference was observed between the TT patients compared with GG/GT patients on the basis of the IL‐ 28/17 genotype.
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Advances in the Diagnosis and Monitoring of Hepatitis C Virus Infection.

TL;DR: This review summarizes the most recent advances in the diagnosis and monitoring of HCV chronic infection.
References
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Journal ArticleDOI

Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance.

TL;DR: It is reported that a genetic polymorphism near the IL28B gene, encoding interferon-λ-3 (IFN-α-2a) is associated with an approximately twofold change in response to treatment, both among patients of European ancestry and African-Americans.
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Diagnosis, management, and treatment of hepatitis C: An update

TL;DR: This document has been approved by the AASLD, the Infectious Diseases Society of America, and the American College of Gastroenterology.
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Discovery of a β-d-2'-deoxy-2'-α-fluoro-2'-β-C-methyluridine nucleotide prodrug (PSI-7977) for the treatment of hepatitis C virus.

TL;DR: Phosphoramidate prodrugs of the 5'-phosphate derivative of the β-d- 2'-deoxy-2'-α-fluoro-2-β-C-methyluridine nucleoside showed significant potency in the HCV subgenomic replicon assay and produced high levels of triphosphates 6 in primary hepatocytes and in the livers of rats, dogs, and monkeys when administered in vivo.
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Preliminary Study of Two Antiviral Agents for Hepatitis C Genotype 1

TL;DR: This preliminary study involving patients with chronic HCV genotype 1 infection who had not had a response to prior therapy showed that a sustained virologic response can be achieved with two direct-acting antiviral agents only.
Journal ArticleDOI

Naturally occurring dominant resistance mutations to hepatitis c virus protease and polymerase inhibitors in treatment-naive patients

TL;DR: Naturally occurring dominant STAT‐C resistance mutations are common in treatment‐naïve patients infected with HCV genotype 1, and their influence on treatment outcome should be characterized to evaluate possible benefits of drug resistance testing for individual tailoring of drug combinations when treatment options are limited due to previous nonresponse to peginterferon and ribavirin.
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