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Treatment of wild-type human immunodeficiency virus [HIV-1(IIIB)]-infected cell cultures with the thiocarboxanilide UC-781 under low selective pressure (i.e., 0.01 microg/ml) resulted in the emergence of V106A RT mutant virus. On increasing drug concentrations (stepwise up to 30 microg/ml) the virus retained the V106A RT mutation but acquired the novel F227L mutation in the RT genome in addition to the L100I, K1O1I, and Y181C mutations. This multiple-mutant virus proved highly resistant to virtually all nonnucleoside RT inhibitors (NNRTIs) (e.g., nevirapine, delavirdine, and loviride), but retained full sensitivity to nucleoside analogs such as AZT, ddI, (-)FTC, and 3TC. The F227 amino acid is highly conserved in HIV-1 strains and forms part of the NNRTI-binding pocket. Our model suggests a hydrophobic interaction between F227 and the chloro atom of UC-781.

Original publication




Journal article


AIDS research and human retroviruses

Publication Date





255 - 260


Rega Institute for Medical Research, Katholieke Universiteit Leuven, Belgium.


Tumor Cells, Cultured, Humans, HIV-1, Anilides, Furans, Reverse Transcriptase Inhibitors, Anti-HIV Agents, Microbial Sensitivity Tests, Evolution, Molecular, Drug Resistance, Microbial, Dose-Response Relationship, Drug, Mutation, Genes, Viral, HIV Reverse Transcriptase