As the ELECTRON study points out... treating hep c without interferon is extremely challenging!! Now I have to wait another six months to see if GILD's new data holds any weight because if you go on previous results their SVR 12 is going to fall like a rock! Really its just a guess which is funny because SVR 24 is the only number that matters and we are a long long way from getting that answer!!
True... EOT does not translate to SVR4... and SVR4 is still too early but starts to be a good indicator. SVR12, however... that you may want to hang your hat on these days. Here is a bit of info on drug pharmacokinetics. Peg has a pretty long half-life (not to mention ribavirin...why do you think the ribavirin label tells you to practice safe you-know-what for a long time AFTER you finish taking the drug?)... anyway you need to get to SVR12 with Peg/Riba just to see if there will be a lot of relapse due to this half-life (I didn't make this up... there is good data in the public domain from companies and the FDA to show this). If you are giving oral therapies with a short half-life, the drug pressure is gone rapidly. HCV also grows very fast (just ask a liver transplant patient) once the drug pressure is removed. I would have strong doubts you will see much relapse if any after SVR12. Probably you will see some patients in the study lost to follow-up between 12 and 24 (that is a long time to expect someone to come back for a blood draw) that may be counted conservatively as a "failure"... but that is really just a failure to obtain a blood draw!
I always find it so funny when people try to say things on these boards to get folks all crazy. I don't even have holding in these companies... I just know the science and it annoys me when people start shouting that the earth is flat and herbs and berries will cure you of all your woes.
A sustained virologic response (SVR) in patients with chronic hepatitis C receiving pegylated interferon (PEG-IFN) plus ribavirin is defined as undetectable serum HCV-RNA at 24 weeks (W+24) posttreatment follow-up. Viral load outcome in patients with virological relapse (VR) has not been explored. This study evaluated whether the assessment of serum HCV-RNA 12 weeks (W+12) after the end of treatment was as relevant as W+24 to evaluate SVR in 573 patients who received combination PEG-IFN and ribavirin and had a virological response at the end of treatment. Serum HCV-RNA was measured, using a new assay based on transcription-mediated amplification (TMA) with a lowest detection limit of 5-10 IU/mL, at W+12 and W+24 after the end of treatment. VR was defined as reappearance of detectable HCV-RNA at W+24 posttreatment follow-up. The positive predictive value (PPV) of undetectable serum HCV-RNA at W+12 was evaluated to identify patients with SVR, and the viral load outcome was measured in relapse patients. At the W+24 posttreatment follow-up, 408 (71%) patients had an SVR, 181 (71.2%) were treated with PEG-IFNalpha-2a and ribavirin, and 227 (71.1%) were treated with PEG-IFNalpha-2b and ribavirin. At W+12, serum HCV-RNA was undetectable in 409 patients, and 408 patients were SVR (PPV 99.7%, 95% confidence interval 99.1-100). In relapse patients, serum HCV-RNA levels were 5.623 +/- 0.748, 4.979 +/- 0.870, and 5.216 +/- 0.758 log(10) IU/mL at baseline, W+12, and W+24, respectively.
Conclusion: Our results show that the assessment of serum HCV-RNA 12 weeks after the end of treatment, using the highly sensitive TMA assay (PPV 99.7%), is as relevant as after 24 weeks to predict SVR and make decisions on the management of treated patients, suggesting a new definition for SVR.