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.
Abstract: The K65R RT mutant virus was more resistant to the bisPOC prodrugs of 7 and 8 than bisPOC PMPA (tenofovir DF) 1.
Mutations at 65 and 70 within the context of a Q151M cluster in human immunodeficiency virus type 1 reverse transcriptase impact the susceptibility to the different nucleoside reverse transcriptase inhibitors in distinct ways.
PMID: 17567542
2007
Infection, genetics and evolution
Abstract: In vitro culturing in the presence of tenofovir resulted in further enhancement of phenotypic resistance levels towards tenofovir and nucleoside reverse transcriptase inhibitors due to the development of K65R.
Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase.
Abstract: CONCLUSION: K65R antagonizes the NRTI monophosphate excision activity of RT containing TAMs.
Abstract: METHODS: Steady-state and pre-steady-state kinetic analyses of NRTI triphosphate incorporation and NRTI monophosphate excision by RT containing K65R or TAMs were conducted and complemented by molecular modeling.
Abstract: OBJECTIVES: The K65R mutation in HIV-1 reverse transcriptase (RT) decreases susceptibility to all approved nucleoside reverse transcriptase inhibitors (NRTI) except zidovudine by selectively decreasing the incorporation of the
Didanosine enteric-coated capsule: current role in patients with HIV-1 infection.
Abstract: Didanosine may select for resistance mutations that may render the drug inactive against the virus; L74V and K65R remain as the main didanosine-related mutations.
Low-level K65R mutation in HIV-1 reverse transcriptase of treatment-experienced patients exposed to abacavir or didanosine.
PMID: 17667333
2007
Journal of acquired immune deficiency syndromes (1999)
Abstract: Among baseline samples from 154 treatment-experienced patients, 8 had K65R and 44 had L74V/I by population sequencing.
Abstract: BACKGROUND: Prior abacavir (ABC) or didanosine (ddI) therapy can result in the L74V/I or K65R mutation in HIV-1 reverse transcriptase.
Abstract: Baseline K65R correlated with absence of thymidine analog mutations (TAMs; P = 0.003) and use of ABC or ddI (P = 0.004).
Abstract: CONCLUSIONS: Prior therapy with ABC or ddI can result in a population genotype that shows K65R or L74V/I but does not reveal low-level K65R present in some patients.
Abstract: Low-level K65R was detecte
Changing rates and patterns of drug resistance mutations in antiretroviral-experienced HIV-infected patients.
PMID: 17678470
2007
AIDS research and human retroviruses
Abstract: K65R significantly increased since 1999 (0.8%) to 2003 (7.3%) but declined up to 3.3% in 2005.
Genotype testing and antiretroviral resistance profiles from HIV-1 patients experiencing therapeutic failure in northeast Brazil.
PMID: 17873990
2007
The Brazilian journal of infectious diseases
Abstract: K65R was detected in 5.9% of the isolates.
Presence of M184I/V in minor HIV-1 populations of patients with lamivudine and/or didanosine treatment failure.
Abstract: Although M184I/V may reduce the genetic barrier of ddI for mutations such as K65R and L74V, the lack of re-emergence of M184I/V in the minor quasispecies of most patients who failed ddI suggests that M184I/V was not a preferred route to ddI resistance in our patient population.
HIV mutation literature information.
PMID: 
2007
Antiviral chemistry & chemotherapy
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