Asians have mainly the CC genotype which means they respond better to PEG-IFN than say Africans. If one looks at HCV trial data, results out of Asia and Europe always look better than those out of the US - the African population in the US and obesity mean they get 10-15% less response.
Geno 1 is the target for all the new drugs because the SVR rates for geno 2 and 3 are already 80-90% with PEG-IFN/riba so to demonstrate a statistically significant effect in these patients you'd need sample sizes at least twice as large.
The one month dosing business says more about the compound's pharmacodynamics than anything else. Hopefully it doesn't cause cumulative toxicity, as this would limit its use in the current management of HIV which is being simplified all the time towards single (3-4 drug combination) pill a day dosing. The inability to be incorporated into this ultrasimple dosing is what sank Avexa's apricitabine, which was otherwise a better agent on its own than other nucleosides currently in use.
HIV treatment is pretty much an exercise in getting the viral load to zero - when there is no circulating virus then resistance cannot develop and the patient will never develop immune compromise/AIDS. If a combination of reasonably-priced and reasonably safe drugs is able to do this, then there is actually little incentive to develop newer drugs because they will almost certainly be more expensive, and can't be more effective (you can't go lower than zero viral load). The only way to break such a hegemony would be if the strategy changed to CURING the infection. This is just beginning to occur with HBV, with a combination of tenofovir and PEG-IFN likely to be the method. HIV is probably a bit further afield, but if BIT225 is able to clear privileged sites of virus then it could presumably be a useful part of the formula.
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