Is the other possibility that the patient profile through here (from what I can see) tends to be baby boomers who were effectively riding the crest of the initial wave of the epidemic within their region so less opportunity for co-infection. But if a more representative sampling by infection date was taken then the incidence would indeed be higher given the now greater spread of GTs between continents?

That’s interesting. I was wondering about this overnight and whether it may explain some non-responders and supposed re infections where the patient swears they haven’t put themselves at further risk.

Whichever way you look at it though, it does seem to indicate that the way forward for new HCV drugs development should be pangenotypic where possible.

Thanks. As you say, very interesting.

I don’t think mine was rechecked so just glad I’m on Dac which is pangenotypic.

Indeed, it is very interesting that so few dual or multiple genotypic infections occur. If you think of the primary cause of HCV infection and the multiple opportunities that arise for transmission, in the course of active addiction, it’s quite astonishing really that the vast majority of people only have one genotype.

I hear the analysis bias argument, but there must be more to it. If one thinks of the incidence of co-infection with HIV then wouldn’t it be logical that rates of multiple HCV genotypic infection would be higher than they (apparently) are, especially so given that it’s much easier to contract HCV than HIV through IVDU.

Anyway, it’s a bit academic.

There are now 2 people on this forum with G4. It’s a real drag that so few data exist around G4 and that treatment decisions need to be extrapolated from G1 studies. That said, there seems to be more and more G4s included in studies these days.

Dr Freeman was onto it back in October last year … SOF + DCV as the pangenotypic cure for HCV … you wouldn’t even need a genotype test done… if you had GT1 – GT6, or any combination, the Darvoni would be the cure all. See:

http://fixhepc.com/forum/media-news/1053-darvoni-story.html#17255

From my understanding, the only reason a patented version has not been developed is Gilead refused BMS’s offer to work together on this … and has been developing its own pangenotypic NS5A inhibitor called Velpatasvir (VEL). SOF + VEL has been reported as having very high cure rates for all genotypes, but seems to have more side effects than SOF + DCV.

It’s all about money. Gilead simply wants to corner the market with a one pill cure all. However, there’s already a generic one pill cure all called Darvoni.