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The effectiveness of interferon in blocking the replication of hepatitis C virus (HCV) in infected cells is enhanced in patients with genotypes 2 and 3 as compared to genotype 1.1 2 The clinical counterpart of these experimental observations is the higher rate of viral clearance in easy-to-cure genotypes, as reported in registration trials on Peg-Interferon (Peg-IFN) and ribavirin therapy.3 4 5 Consequently, so far, HCV genotyping has represented the common approach to tailoring drug dosage and length of therapy. Recently, an innovative concept has emerged which might also govern treatment schedules besides HCV genotypes: in response to a single interferon injection, viral decline in blood differs not only among individual genotypes but also from patient to patient infected by the same viral strain.6 7 8 This evidence has led to the claim that patients with prompt response could benefit from a shorter duration of treatment compared to that which is currently recommended, whereas for slower responders a prolonged course of treatment might be needed to maximise virological response.
How to categorise rapid, slow or null responders according to current antiviral therapy is a matter of intensive investigation.9 10 Past experience has corroborated the usefulness of evaluating serum HCV-RNA at treatment weeks 4, 12 and 24: rapid responders are patients who are non-viraemic at week 4, and non-responders are those still viraemic at week 24; all other patients falling between these two extremes are defined as slow responders.11 12 As the timing and magnitude of virological response are highly variable from one patient to another, slow responders might include several subgroups of patients with differing chances of achieving a sustained virological response (SVR). Indeed, if a subset of patients defined as complete early virological responders shows an absence of HCV-RNA at treatment week 12, it is …
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