First, although pre-treatment PCR-direct sequencing and cloning for the N-terminal in the NS3 region showed a protease inhibitor-resistant variant (T54A) in 1 of 32 independent clones, the T54A substitution has only a low-level resistance to protease inhibitors and his viral load was low. Second, when compared to a consequence
sequence of 35 treatment-naïve patients with HCV genotype
1b, R130K and Q195K substitutions were unique to the present case.