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Quantitative Structure-Activity Relationship, Activity Prediction, and Molecular Dynamics of Non-nucleotide Reverse Transcriptase Inhibitors
Published on: May 9, 2025
HIV-1 reverse transcriptase (RT) genotypic patterns and treatment characteristics associated with the K65R RT
S Boucher1, P Recordon-Pinson, J M Ragnaud
1Département de Virologie et d'Immunologie Biologique, CHU de Bordeaux, and EA 2968 Université Victor Segalen Bordeaux, France.
HIV Medicine
|September 2, 2006
Summary
The K65R mutation in HIV-1 reverse transcriptase (RT) is found in 1.9% of patients. This multidrug resistance mutation is linked to specific antiretroviral drugs and rarely co-occurs with thymidine analogue mutations (TAMs).
Area of Science:
- Virology
- Infectious Diseases
- Pharmacogenomics
Background:
- The K65R mutation in HIV-1 reverse transcriptase (RT) confers multidrug resistance.
- Its emergence may be influenced by specific antiretroviral drug combinations and the presence of other RT resistance mutations.
Purpose of the Study:
- To determine the prevalence of the K65R mutation in a cohort of HIV-1 patients receiving antiretroviral therapy.
- To analyze genotypic patterns and treatment characteristics associated with the K65R mutation.
Main Methods:
- Retrospective analysis of HIV-1 genotypic resistance data from antiretroviral-experienced patients.
- Inclusion of patients from Bordeaux University Hospital between 2003-2004.
- Investigation of K65R prevalence and examination of genotypic patterns and treatment data at mutation detection.
Main Results:
- The K65R mutation was present in 1.9% (26/1404) of patients.
- K65R was associated with nucleoside RT inhibitor-based regimens and specific drugs including tenofovir disoproxil fumarate, lamivudine, didanosine, and abacavir.
- M184V and Q151M were common co-selected mutations, while thymidine analogue mutations (TAMs) were rarely co-selected and inversely associated with K65R.
Conclusions:
- The K65R mutation may preferentially emerge in the absence of zidovudine and TAMs.
- This suggests a potential antagonistic interaction between K65R and TAMs in HIV-1 treatment resistance.
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