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. 2007 Oct 15;52(1):110–120. doi: 10.1128/AAC.00863-07

TABLE 5.

Susceptibilities of HCV NS3 protease variants to other anti-HCV agents in replicon cellsa

Variant IFN-α
Ribavirin
EC50 (U/ml) Fold change EC50 (μM) Fold change
Wild type 11.6 ± 1.1 1.0 ± 0.1 58 ± 18 1.0 ± 0.3
V36M 11.3 ± 5.9 1.0 ± 0.5 33 ± 18 0.6 ± 0.3
V36A 10.3 ± 6.0 0.9 ± 0.5 43 ± 21 0.8 ± 0.4
T54A 3.9 ± 0.5 0.3 ± 0.04 22 ± 11 0.4 ± 0.2
V36M + R155K 10.1 ± 5.9 0.9 ± 0.5 41 ± 6 0.7 ± 0.1
V36A + R155K 6.8 ± 0.5 0.6 ± 0.04 36 ± 2 0.6 ± 0.04
V36M + R155T 3.1 ± 0.2 0.3 ± 0.02 36 ± 1 0.6 ± 0.02
V36A + R155T 3.9 ± 2.1 0.3 ± 0.2 42 ± 22 0.7 ± 0.4
a

Stable cell lines containing wild-type and variant HCV subgenomic replicons were generated by using the T7 RNA runoff transcripts from the corresponding high-efficiency Con1 replicon plasmids. The average replicon EC50 values of IFN-α and ribavirin ± SDs were determined for the HCV replicon cell lines in the 48-h assay in three independent experiments. The fold change was determined by dividing the replicon EC50 of a given variant by that of the wild-type HCV replicon.