FIG. 3.

Resistance to DKAs conferred by T66I and T66I/S153Y mutations in HIV-1 IN. Inhibition of integration was determined in the single-replication-cycle assay in the presence of 50 μM DKAs. Luciferase activities for control infections (No drug) were set at 100% for each experiment. The mean of three independent experiments and standard error of the mean (error bars) are indicated. To achieve similar luciferase activity in infected target cells, infections were performed at different dilutions for wild-type (WT) and mutant viruses (WT virus was diluted 100-fold; T66I virus was diluted 10-fold; T66I/S153Y mutant virus was diluted 2-fold). In these experiments, the average luminometer signal for WT virus infection in the absence of drug was 21,654 relative light units (RLU); the average luminometer signal for T66I virus infection in the absence of drug was 84,791 RLU; the average luminometer signal for T66I/S153Y virus infection in the absence of drug was 12,719 RLU. A negative control (uninfected cells) resulted in luminometer signals lower than 100 RLU.