The are no studies on the use of Telaprevir or Boceprevir in genotype 4 (HCV4) patients. The concentration of the western nations pharma industry is on genotype 1 which had been the most difficult to cure genotype until recently and is the vast majority of HCV patients in the United States and Europe. (70-80%) This is where the money is. HCV4 represents 1–3% of the hepatitis C infections in Western countries.HCV4 is the predominant HCV genotype in Saudi Arabia and Kuwait and small studies in Africa suggest that HCV4 is the predominant genotype on that continent.
There are other approaches besides protease inhibitors that are being tried to increase the SVR rates for genotype 4. (See below).
"The future for the treatment of genotype 4 chronic hepatitis C" - Jan, 4 2012
"New types of interferon (Consensus Interferon, Y-shaped, Albinterferon…) and new direct action antiviral drugs (Nitazoxanide, Vit.D, other) may improve the treatment of patients with HCV-4. The IL28B CC polymorphism may be associated with sustained virological response.
The development of new drugs and off-label use of other drugs is still of interest to improve the treatment of chronic HCV, especially in patients with genotype 4. Many promising molecules must still be evaluated to determine their potency, efficacy and safety."
The standard regimen of therapy
Combined treatment with pegylated interferon (PEG-IFN) -2a or -2b plus ribavirin (RBV) is now the standard therapy for chronic HCV infection .The addition of the synthetic guanosine analogue RBV to IFN was a major breakthrough in the treatment of HCV infection. Diago et al. reported preliminary results in which 49 HCV4 patients from North America and Europe were treated in one of four groups: PEG-IFN-2a plus 800 mg of RBV or 1000–1200 mg of RBV for 24 weeks or 48 weeks. Seventy nine per cent of patients who were treated with PEG-IFN plus 1000–1200 mg of RBV achieved a sustained virological response (SVR), while the SR was lower in other groups .
Shobokshi et al. treated 180 HCV4 patients in a randomized open label multicenter trial. The first group received PEG-IFN-2a 180 μg weekly plus RBV 800 mg/day for 48 weeks, the second group received PEG-IFN monotherapy and the third group was treated with standard IFN--2a 4.5 MU TIW plus RBV 800 mg/day. The end of treatment viral response (ETVR) was 67%, 59% and 37% respectively. The SVR was obtained in 50%, 28% and 30% respectively .
Al Faleh et al. randomized 96 patients for treatment with either 100 μg of PEG-IFN--2b plus 800 mg/day of RBV or standard IFN plus RBV combination therapy. The ETVR was 70% in the PEG-IFN arm and 52% in the standard IFN arm. A SVR was achieved in 43.8% of patients in the PEG-IFN arm and in 29.2% of patients in the standard IFN arm. These results were probably not statistically significant because of the relatively small sample size .
We reported results from a randomized trial involving 200 patients, 90% of whom had HCV4. One hundred patients were randomized to receive PEG-IFN--2b 100 μg/week plus 800–1000 mg of RBV based on body weight or standard IFN plus RBV for 48 weeks. A SVR was achieved in 45% of those receiving PEG-IFN compared with 38% in the IFN group .
In a prospective open label study from Kuwait using PEG-IFN--2b, Hasan et al. enrolled 66 patients to receive a higher (currently standard) dose of RBV (1000–1200 mg/day) resulting in a higher ETVR and SVR (77% and 68%, respectively) than in other studies .
An early virological response (EVR) helps predicts patients who will probably not respond to combination therapy. Patients who are HCV-RNA negative after 4 weeks of treatment are defined as having a rapid virological response (RVR). In contrast to EVR, RVR is predictive of patients who will probably respond to combination therapy . Treatment of HCV-4 non-responders, injection drug users, patients coinfected with the HIV, thalassaemic patients, patients on haemodialysis and patients with HCV-4 recurrence after LTx is still a significant therapeutic challenge .
Identifying new IFN molecules and other combination therapies, especially direct acting antiviral drugs is an important mission for all clinical researchers whose goal is to improve the current treatment response.
There is a new member called chainsawmaggie who is Geno 4 and starting Triple Therapy. Other than that you are the only two Genotype 4's I have ever encountered:
zako7 is a geno 4 using bociprevir here is the link to his personal page, you can go and read through his post or PM him if you have any questions
I'm a Geno 4 also, as HPguy said Zako7 is treating with 1 of the PI's which was okayed with his insurance( Big surprise to me) and doing well with it. I know the new drug 7977 has also been tested with type 4's which is what i'm waiting for. I was inviting into a trial with 7977 and rib + interveron which I declined. I'm waiting for another all oral for us G4's, it's coming soon i'm told.As Hector stated here in the US of A there's really no money in clinical testing Geno 4's.
thanks very much for your helpful comment. do you have a reference to the study you mentioned? I am now at a point where i have to decide whether to try existing drugs or to wait.
Who is to say you are not going to respond well to SOC ?
I would run the IL28b , get an idea about your fibrosis stage,
make sure you are not insulin resistant , check Vit D , B12 ect....
If nothing else indicates poor response other than being geno4
I would give SOC+NTZ a shot and see your actual response.
If not UND by sensitive PCR by wk12 stop tx and wait for new meds.
It is possible you achieve RVR by sensitive PCR than you could consider shortening tx to 36wks.
thanks very much for your thoughts and experience. I had fibroscan which suggested early phase 3. since i've had the virus for 25 years, my doctor says the process is slow. i tried the alpha interferon plus riibavirin in 1995 and did not benefit from treatment. therefore i am reluctant about peginterferon based treatment, especially since after first treatment my liver functions went up and stabilized on higher levels.
I am a combination of genotypes 4 and type 1 as well. I am an American born, and never traveled out of the USA so its still a mystery how I even got type 4. I have had HCV since 1989-90 and it wasnt until 2 years after I did my first clinical study in 1999-2000 that i even found out that I carried 2 genotypes. I am concerned as to how this linits my treatment ops. I have been through 1.5 rounds of interferon/ribavirin, and 6 months of a triple combo but my virus keeps coming back active.....if its not the type 1 then its the type 4. I cant seem to win. So for the person who had never heard of more than 2 people who have type 4...i do, and type 1 as well.