Abstract
In less than a decade, antiviral therapy for chronic hepatitis C (HCV) has undergone dramatic change. The sustained virologic response rate (SVR), defined as HCV RNA undetectability 12 weeks post-therapy, is recognized as being a virologic “cure” and has increased from 40–50%, with peginterferon and ribavirin, to 95–99% with the newest direct acting antiviral agents (DAA) (1). Unlike the non-specific antiviral and immunostimulatory effects of interferon, DAAs specifically target the HCV replicative machinery and include protease inhibitors, NS5a inhibitors and NS5b RNA dependent polymerase inhibitors.
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