4%; 95% CI: −9.8% to + 1%). In G2/G3 rapid responders, SVR was more common for standard 24-week duration than for shortened durations (+4.1%; 95% CI: +0.1% to + 8.5), but this benefit was not significant when ribavirin was weight-adjusted and the short duration was 16 weeks (−1.7%; 95% CI: −6.1% to + 2.7%) and for G2 patients (+1.6%; 95% CI:

−0.2% to + 5.5%). Conclusion: Long durations of P/R therapy improve SVR, regardless of genotype. This effect is nonetheless negligible in rapid responders, with the most favorable conditions for SVR (G2, G1 with low viral load, and G3 with weight-adjusted ribavirin regimen). (HEPATOLOGY 2011;) The standard of care for chronic hepatitis C is the combination of peg-interferon plus ribavirin that leads to hepatitis C virus (HCV) eradication in 60% of cases, with variations depending on the EPZ-6438 mw characteristics of host and virus and, in particular, viral genotype.1,2 Patients infected with genotype 1 (G1) are the most difficult to cure: they achieve sustained virologic response (SVR) in under 50% of cases in pivotal studies.1, 2 This PD-332991 explains the considerable recent efforts to develop new antiviral molecules specific

to G1 strains, including boceprevir3 and telaprevir.4 However, despite their virologic efficacy, concerns are raised regarding the induction of viral cross-resistance,5 which could impede long-term viral elimination. This leaves the systematic use of these molecules as first-line treatments in naïve G1 patients open to debate, particularly in patients with genetic susceptibility for SVR with standard treatment, such as the CC polymorphism Silibinin of the interleukin-28B (IL-28B) gene.6 Moreover, no similar therapeutic advances have been made for

HCV genotype 2 (G2) and 3 (G3) strains, which are reputed to be the most sensitive to standard treatment, with SVR rates of 80%-90%. With standard pegylated interferon (peg-IFN) plus ribavirin therapy, the concept of response-guided duration therapy (i.e., adjusting treatment duration according to the outcome of HCV viral load under treatment) has been widely investigated, particularly in two situations. In the 70% of G2/G3 patients and the 15% of G1 patients who develop a rapid virological response (RVR), as defined by undetectable HCV viral load at week 4, the aim was to reduce treatment duration to lower the risk of adverse events and cost of treatment. G2 and G3 patients were thus tested for receiving a 12-16-week treatment duration versus the standard 24-week therapeutic regimen, whereas G1 patients were tested for receiving a 24-week duration versus the standard 48-week regimen. The second situation involved G1 patients who develop slow virologic response, as defined by a decrease in viral load of over 2 log between baseline and week 12, followed by subsequent HCV RNA loss before week 24. In these patients, the aim was to extend treatment duration beyond the standard 48 weeks to increase the probability of SVR.