In short, I don’t see how the research you cited advances the thesis that a normal, healthy immune system cannot avert relapse when the level of HCV virus has been rendered de minimis.
You appear to be assuming that the way that HCV becomes chronic is by overwhelming the immune system with numbers. When this paper says numbers have nothing to do with it - instead it is the fact that the immune system can't see any of the virus particles very effectively. In the former case knocking down the numbers by any technique whatsoever is equally effective. But in the latter case a drug cocktail is like giving the man a fish while ifn, when it is successful, is like teaching a man to fish.
The paper you cited describes the genetic changes to the HCV virus before it turns into a chronic infection. In other words, these changes will already have occurred by the time anyone seeks treatment, regardless of the treatment regimen employed.
Yes, thereby becoming chronic. But if you are making a point I am not getting it. ? A genetic arms race is a balance between being resistant to the other guy and being an efficient reproducer. Over time in such a race the organism learns how to get the best of both worlds to the extent possible - then the other guy comes in and wipes out the best hybrids leaving those that are the best resistors, but stink at reproducing. Takes time to reoptimize. Maybe they never can because they don't have the 10 weeks of happy time to make boat loads of offspring with a ton of genetic variation.
I am now leaning towards (note the tentative nature of the word 'leaning' - I would be the last person to take a stand based upon MOA) the camp of assuming that the relapse rate will be significantly higher in drug cocktail than in ifn. But this being hcv (with its decades to develop) it still might take years to really climb up (but note that given the rapid recovery of viral load after drug treatment I wouldn't put money on the table).
I suspect an optimum treatment would be ifn - and then in those who don't respond a drug cocktail, perhaps in perpetuity. (Note - you probably woulnd't want to do the drug cocktail at the same time as ifn because you'd be removing the educational material.)
as though the only issue were whether the HCV virus is present or is not present. Such a viewpoint is justified for HBV and HIV, which integrate into the host genome, but it not justified for HCV, which does not.
??Who cares whether it is integrated into the genome or not???? The point is that if any virus remains after a drug cocktail it is likely to be a virus that is genetically adapted to be somewhat invisible to the immune system while still being able to reproduce moderately quickly (because that was what 99.9% of the virus was at the start of treatment). However this is probably not true in a successfully treated ifn patient. The virus left in that individual is undoubtedly largely invisible - but given that it was obviously a rare genotype it probably wasn't a rapid reproducer.
PS Thanks for the foil.
PPS Note that even though I suspect that the relapse rate will be much higher for drug cocktails that doesn't remove the risk for ifn-lambda. Unless the FDA demands a multiyear relapse rate check it may not be immediately understood drug cocktails don't have the same long term benefit. (Note that one early look will be the first trials on the antivirals with ifn - my bet is that they have meaningfully higher relapse rates)
PPPS It is possible that a multidrug therapy knocks out so much virus that it literally can't build back up again to measurable levels even with the normal doubling time seen in chronic hcv. Possible. But given the doubling time of hcv after a anti viral this seems unlikely. Well, this will be an interesting thing to watch.
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