Structural and Energetic Analyses of the Effects of the K103N Mutation of HIV-1 Reverse Transcriptase on Efavirenz Analogues

Abstract
The effect of the K103N mutation of HIV-1 reverse transcriptase (RT) on the activity of efavirenz analogues was studied via Monte Carlo/free energy perturbation calculations. The relative fold resistance energies indicate that efavirenz binds to K103N RT in a manner similar to the wild-type enzyme. The improved performance of the quinazolinones against the mutant enzyme is attributed to formation of a more optimal hydrogen-bonding network with bridging water molecules between the ligands and Glu138.