Triple therapy for HCV genotype 1 infection: telaprevir or boceprevir?
Article first published online: 29 DEC 2011
© 2012 John Wiley & Sons A/S
Special Issue: Proceedings of the 5th Paris Hepatitis Conference. International Conference of the Management of Patients with Viral Hepatitis: Special Edition Hepatitis C
Volume 32, Issue Supplement s1, pages 54–60, February 2012
How to Cite
Shiffman, M. L. and Esteban, R. (2012), Triple therapy for HCV genotype 1 infection: telaprevir or boceprevir?. Liver International, 32: 54–60. doi: 10.1111/j.1478-3231.2011.02718.x
- Issue published online: 29 DEC 2011
- Article first published online: 29 DEC 2011
- Manuscript Accepted: 7 OCT 2011
- Manuscript Received: 27 SEP 2011
- direct acting antivirals;
- protease inhibitors;
- sustained virological response
Boceprevir and telaprevir are the first two protease inhibitors available for the treatment of patients infected with hepatitis C virus (HCV) genotype 1. A sustained virological response (SVR) of 70–80% is observed when either of these protease inhibitors is utilized with pegylated interferon (PEG-IFN) and ribavirin (RBV) in treatment naïve patients. Both agents are also highly effective in patients who failed to achieve a SVR during previous treatment with PEG-IFN/RBV. A rapid virological response (RVR) is observed in 56–60% of treatment naïve patients. Patients who achieve a RVR can be treated with a shorter course of therapy (24–28 weeks) and still achieve a SVR rate of 90% or higher. Patients who do not achieve a RVR, those with cirrhosis and certain prior non-responders should be treated for 48 weeks. Although the SVR rates observed with boceprevir and telaprevir are quite similar both globally and within sub-populations, the treatment algorithms for the two agents are unique. The decision of which protease inhibitor to use should assess several factors including the treatment scheme, duration of therapy, adverse event profile, cost and the likelihood of achieving a RVR. The latter is highly dependent upon IFN sensitivity and the IL28B genotype.