Optimal therapy in hepatitis C virus genotypes 2 and 3 patients
Article first published online: 4 JAN 2011
© 2011 John Wiley & Sons A/S
Special Issue: Proceedings of the 4th Paris Hepatitis Conference. The publication of this supplement was supported by an unrestricted educational grant from F. Hoffmann-Laroche Ltd.
Volume 31, Issue Supplement s1, pages 36–44, January 2011
How to Cite
Petta, S. and Craxì, A. (2011), Optimal therapy in hepatitis C virus genotypes 2 and 3 patients. Liver International, 31: 36–44. doi: 10.1111/j.1478-3231.2010.02382.x
- Issue published online: 4 JAN 2011
- Article first published online: 4 JAN 2011
- Received 10 November 2010Accepted 25 November 2010
- genotype 2;
- genotype 3;
- response-guided therapy;
Current guidelines recommend that patients with genotype 2 (G2) and 3 (G3) chronic hepatitis C be treated with pegylated interferon (PEG-IFN) plus low doses of ribavirin (800 mg/day) for 24 weeks, resulting in a sustained virological response (SVR) rate of approximately 80%. Considering these high response rates, several recent randomized trials have assessed whether shorter treatment (12–16 weeks) could be cost-effective in these patients. The results of these studies vary but suggest better responsiveness in G2 patients, and overall, do not strongly support reducing treatment to <24 weeks in all patients. On the other hand, the presence of a rapid virological response (RVR) (defined as an undetectable hepatitis C virus-RNA at 4 weeks of treatment) was always reported to be the best positive predictor of achieving SVR in both G2 and G3 patients. These results suggest that in a subgroup of subjects with RVR (G2>G3, viral load <400 000 IU, low fibrosis, no metabolic cofactors), shorter treatment is as effective as standard regimens, and that it can be proposed mainly if problems of poor tolerance or adherence are foreseen. It is possible that the SVR rate in non-RVR patients and non-responder patients could also be improved by prolonging therapy, but this must be specifically investigated in other studies along with the role of IL28B polymorphisms.