Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase

Abstract

K65R antagonizes the NRTI monophosphate excision activity of RT containing TAMs. TAMs antagonize the ability of K65R RT to discriminate against the nucleotide analog. Therapies including NRTI that select for both TAMs and K65R may prolong treatment response through the mutually antagonistic interactions between these resistance mutations.