First, I need to correct a typo, it should be - "Unless they compensate." What I was suggesting is an explanation to the shift in variants population from baseline to breakthrough and relapse. What drives the relapse in that case imo, is incomplete suppression of viral replication under the selection stress of the drug. High level resistant strains of HCV do not mutate to be low level resistance strains once the treatment stops, they are replaced by strains with higher fitness i.e better replication efficiency.
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