my guess is that patients with high viral load - simply by virtue of the high replicative activity and mutations that occur during replication - tend to have more HCV quasi-species if you will, and so have higher chance of having wild type virus that is naturally DAA resistant. conversely, those in whom resistance is selected due to drug exposure have variants with lower replicative efficiency (as expected) due to the fact that predominant isolates are selected not based on replicative efficiency but rather drug resistance