Abstract
of HCV-PI resistance in liver but not in plasma compartment of 3 pts: 2 of these 3 pts harbored D168E amino acid (aa) substitution associated with macrocyclic PI resistance and one harbored V55A aa change associated with boceprevir resistance. The remaining 2 pts exhibited a wild-type sequence in both compartments. Conclusions: The detection of discordant G1 subtypes in liver and plasma may be consequent to a mixed infection and selection of a specific subtype with greater adaptability to different environmental condition. The presence of natural mutations associated with HCV-PI resistance in liver tissue may explain the early emergence of these strains during triple therapy including HCV-PI.
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