Abstract
Hepatitis C virus (HCV) follows quasispecies dynamics in infected hosts and this influences its biology, how the virus diversifies into several genotypes and many subtypes, and how viral populations respond to antiviral therapies. Despite current antiviral combinations being able to cure a great percentage of HCV-infected patients, the presence of resistance-associated substitutions (RASs) diminishes the success of antiviral therapies, which is a main concern in the re-treatment of patients treated with direct-acting antiviral agents. Current methodologies such as ultra deep sequencing are ideal tools to obtain a detailed representation of the mutant spectrum composition circulating in infected patients. Such knowledge should allow optimisation of rescue treatments. A new mechanism of antiviral resistance not based on the selection of RASs but on high viral fitness is discussed.
Published Version
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