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.
45 yo male; UK; HCV since 1996; G4; F2-3 (fibroscan score 9.1);
Null responder interferon/ribavirin 2008;
4/16 Harvoni 8 weeks; Pre-tx VL 2.1 million; week 4 VL 269; EOT UND; but...
6/16 Tx extended w/ generic sof/dac x 12 weeks due to concerns around my slow response to Harvoni. UND at end of 2nd round of treatment and EOT+4.