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
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
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.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
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.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
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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