Abstract: In contrast, mutant viruses exhibited strongly impaired RC relative to the wild type (WT) in macrophages, with the following RC order: WT > two TAMs > four TAMs = M184V > K65R.
Abstract: Mutant viruses bearing thymidine analogue mutations (TAMs) or the K65R mutation had similar resistance levels in the two cell types.
Biochemical studies on the mechanism of human immunodeficiency virus type 1 reverse transcriptase resistance to 1-(beta-D-dioxolane)thymine triphosphate.
PMID: 17403997
2007
Antimicrobial agents and chemotherapy
Abstract: A lower degree of resistance to DOT-TP than to tenofovir diphosphate or carbovir-TP was found for RT containing the K65R mutation.
Abstract: The results suggest that DOT, compared with other approved nucleoside analogs, is overall more resilient to mutations such as TAM, M184V, and K65R, which are commonly found in viruses derived from subjects failing multinucleoside therapy.
Diminished efficiency of HIV-1 reverse transcriptase containing the K65R and M184V drug resistance mutations.
Abstract: CONCLUSIONS: The simultaneous presence of K65R and M184V in reverse transcriptase has a negative impact with regard to the efficiency of initiation of (-)ssDNA synthesis and RNA usage, that exceeds the effect of either mutation on its own.
Abstract: OBJECTIVES: To determine the underlying biochemical mechanisms responsible for the diminished viral replicative capacity associated with K65R/M184V-containing viruses.
Abstract: RESULTS: We observed that the K65R/M184V mutations in reverse transcriptase caused reductions in the efficiency of initiation of (-)ssDNA synthesis by increasing pausing at positions +3 and +5 as well as diminished RNA usage.
Abstract: These mechanisms, among others, a
Long-term follow-up of patients taking tenofovir DF with low-level HIV-1 viremia and the K65R substitution in HIV-1 RT.
Abstract: K65R became undetectable in two patients, and the development of additional resistance mutations was minimal.
Abstract: K65R was observed in 10 out of 536 treatment-experienced patients entering the study.
Abstract: Patients with on-going HIV-1 replication and a K65R mutation in HIV-1 RT were assessed for further development of RT mutations while taking tenofovir disoproxil fumarate and other antiretroviral drugs.
National survey of the prevalence and conditions of selection of HIV-1 reverse transcriptase K70E mutation.
Abstract: For all animals, sensitive real-time PCR assays detected the transient emergence of K70E RT mutants within 4 weeks of therapy, which were then replaced by K65R mutants within 12 weeks of therapy.
Figure: At the onset of tenofovir therapy (i.e, baseline, BL), no K65R and K70E virus could be detected.
Figure: Despite an initial rebound associated with emergence of K70E followed by K65R viral mutants (table 1.
Figure: Kinetics of K70E and K65R RT mutants during tenofovir therapy.
Figure: Plasma viral RNA samples in which real-time PCR assays detected both K65R and
Sequential emergence and clinical implications of viral mutants with K70E and K65R mutation in reverse transcriptase during prolonged tenofovir monotherapy in rhesus macaques with chronic RT-SHIV infection.
Result: Five weeks later, virus could be isolated again from PBMC, and this virus had the K65R and the same other RT mutations (including S68N) that were also detected during the viral rebound of the CD8+ depletion experiment (table 1).
Result: For all 12 animals, the K65R mutation became detectable in plasma viral RNA within 2 to 12 weeks of treatment (median time, 4 weeks).
Result: Similarly to our previous studies in tenofovir-treated SIVmac251-infected macaques, we investigated if this suppressed viremia of K65R virus in animal 30577 during prolonged tenofovir treatment was due to (i) a replication-impaired phenotype of the K65R mutant in this animal, (ii) strong CD8+ cell-mediated antiviral immune responses, and/or (iii) residual antiviral activity of the tenofovir regimen.|
Mutations in human immunodeficiency virus type 1 RNase H primer grip enhance 3'-azido-3'-deoxythymidine resistance.
Abstract: To test the hypothesis that connection domain mutations enhanced AZT resistance by influencing the RNase H primer grip, we determined the effects of alanine substitutions in RNase H primer grip residues on nucleoside RT inhibitor resistance in the context of a WT, TAM-containing, or K65R-containing polymerase domain.
National survey of the prevalence and conditions of selection of HIV-1 reverse transcriptase K70E mutation.
ViMRT
HIV mutation literature information.
PMID: 
2007
Journal of virology
