Abstract
Hepatitis C infection is the leading cause of liver diseases worldwide and a major health concern that affects an estimated 3% of the global population. Novel therapies available since 2014 and 2017 are very efficient and the WHO considers HCV eradication possible by the year 2030. These treatments are based on the so-called direct acting antivirals (DAAs) that have been developed through research efforts by academia and industry since the 1990s. After a brief overview of the HCV life cycle, we describe here the functions of the different targets of current DAAs, the mode of action of these DAAs and potential future inhibitors.
Highlights
Hepatitis C Virus (HCV), the leading cause of chronic liver disease worldwide, is a positive-sense single-strand RNA virus classified in the Flaviviridae family in the Hepacivirus genus [1]
NS5A has long been considered as a potential antiviral target, since it was known early to be essential for viral RNA replication [114] and later for viral assembly
host-targeting antivirals (HTA) are less specific than highly efficient direct-acting antivirals (DAAs) that were faster into the clinic, but this is one of their advantages
Summary
Hepatitis C Virus (HCV), the leading cause of chronic liver disease worldwide, is a positive-sense single-strand RNA virus classified in the Flaviviridae family in the Hepacivirus genus [1]. In the 2010s, the health authorities approved a succession of new medicines called direct-acting antivirals (DAAs) These molecules opened a new era in the treatment of HCV, achieving higher rates of SVR for most viral genotypes, with shorter treatment durations and fewer side effects. The two main challenges when using DAAs, as experienced in the fight against HIV, are to treat all genotypes and to fight the appearance of resistance It is true for HCV, for which genetic variability is illustrated by the existence of seven genotypes and more than 80 different confirmed subtypes worldwide [1]. RAVs can develop during treatment or may pre-exist as naturally occurring variants, albeit at low but sometimes clinically relevant levels, as reviewed in [12]. The use of a combination of antivirals with different targets, each of them with high potency and high genetic barrier, allows a high success of IFN-free oral regimens HCV treatment
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