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.
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.
Abstract: BACKGROUND: We reported previously on the emergence and clinical implications of simian immunodeficiency virus (SIVmac251) mutants with a K65R mutation in reverse transcriptase (RT), and the role of CD8+ cell-mediated immune responses in suppressing viremia during tenofovir therapy.
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.
Abstract: One animal eventually suppressed K65R viremia to undetectable levels for more than 4 years; sequential experiments using CD8+ cell depletion and tenofovir interruption demonstrated that both CD8+ cells and continued tenofovir therapy were
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.
Molecular basis of antagonism between K70E and K65R tenofovir-associated mutations in HIV-1 reverse transcriptase.
Method: NRTI-selected mutations included T39A, M41L,
Result: A62V, K65R, and Y115F are mutations that cluster with Q151M but may also occur with Type II (but not Type I) TAMs.
Result: The mutations included in this analysis were the 23 positively associated mutations in Table 2 and 11 additional clinically relevant NRTI-resistance mutations (K65R, A62V, T69ins, L74I/V, V75M, Y115F, M184V, and K219R/E/N).
Mechanism of action of (-)-(2R,4R)-1-(2-hydroxymethyl-1,3-dioxolan-4-yl) thymine as an anti-HIV agent.
Abstract: However, K65R did not affect rates of primer unblocking for apricitabine-TP.
Abstract: The results showed that the K65R mutation in RT caused reductions in the efficiency of chain-termination of apricitabine-TP by increasing its Ki.
Abstract: Thus, the mechanism of reduced susceptibility to apricitabine of viruses containing K65R in RT seems to be mediated exclusively through a reduction in binding or incorporation of apricitabine-TP.
Synthesis, anti-HIV activity, and resistance profile of thymidine phosphonomethoxy nucleosides and their bis-isopropyloxymethylcarbonyl (bisPOC) prodrugs.
HIV mutation literature information.
PMID: 
2007
AIDS (London, England)
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