Dioxolane guanosine 5'-triphosphate, an alternative substrate inhibitor of wild-type and mutant HIV-1 reverse transcriptase. Steady state and pre-steady state kinetic analyses.
PMID: 12651859
2003
The Journal of biological chemistry
Abstract: HIV-1 with the reverse transcriptase mutations K65R, L74V, and/or Q151M were less sensitive to DXG, whereas the mutation K103N re-sensitized the virus to the inhibitory effect of DXG.
A novel genetic pathway of human immunodeficiency virus type 1 resistance to stavudine mediated by the K65R mutation.
Abstract: K65R was selected in seven viruses and was associated with a high level of enzymatic resistance to d4T-triphosphate (median, 16-fold; range, 5- to 48-fold).
Abstract: Four of the six viruses that had 215C/D mutations at baseline acquired the 215Y mutation alone or in association with K65R.
Abstract: Mutants having K65R and T215Y replicated less efficiently than viruses that had T215Y only, suggesting that selection of T215Y in patients treated with d4T may be favored.
Abstract: Our results demonstrate that K65R plays a role in d4T resistance and indicate that resistance pathways for d4T and AZT may not be identical.
Abstract: Phenotypic assays based on recombinant single-cycle replication or a whole-virus multiple r
K65R with and without S68: a new resistance profile in vivo detected in most patients failing abacavir, didanosine and stavudine.
Abstract: All five patients with wild-type virus developed K65R and four of these patients also acquired the S68G mutation.
Abstract: Failure of a triple NRTI regimen is possible and frequent with only the K65R mutation.
Abstract: The unexpected high incidence of S68G suggests a functional role of this mutation in viruses harbouring K65R.
Abstract: Under adequate selection pressure K65R can easily emerge in vivo and may compromise several future treatment options including newer NRTIs.
Relationship between 3'-azido-3'-deoxythymidine resistance and primer unblocking activity in foscarnet-resistant mutants of human immunodeficiency virus type 1 reverse transcriptase.
Abstract: We have compared the primer-unblocking activity for HIV-1 RT containing various foscarnet resistance mutations (K65R, W88G, W88S, E89K, S117T, Q161L, M164I, and the double mutant Q161L/H208Y) alone or in combination with AZT resistance mutations.
HIV-1 resistance profile of the novel nucleoside reverse transcriptase inhibitor beta-D-2',3'-dideoxy-2',3'-didehydro-5-fluorocytidine (Reverset).
Abstract: Finally, in vitro selections for HIV-1 mutants capable of replicating in the presence of D-d4FC yielded a mutant carrying the RT K65R mutation.
Extended treatment with tenofovir disoproxil fumarate in treatment-experienced HIV-1-infected patients: genotypic, phenotypic, and rebound analyses.
PMID: 12792350
2003
Journal of acquired immune deficiency syndromes (1999)
Abstract: These 96-week results were analogous to the 48-week results, in which 33% (n = 63) and 2.1% (n = 4) of patients developed thymidine analog-associated mutations or the K65R mutation, respectively.
Abstract: Through 96 weeks of tenofovir DF therapy, 48 weeks of which included suboptimal doses of tenofovir DF, there was infrequent development of RT mutations associated with tenofovir DF therapy (K65R mutation, 3%), consistent with the durability of the observed HIV-1 RNA responses.
Abstract: Two patients (1.5%) developed the K65R RT mutation (selected by tenofovir in vitro) but maintained HIV-1 suppression (-0.39 log(10)).
Abstract: Four of these five patients had either the K65R mutation, the M184V/I mutation, or both.
A review of HIV-1 resistance to the nucleoside and nucleotide inhibitors.
PMID: 14754429
2003
Current drug targets. Infectious disorders
Abstract: There are several major genetic mutational patterns of resistance and cross-resistance that evolve with the NRTIs including the thymidine analog mutations M41L, D67N, K70R, L210W, T215Y, and K219Q/E/W, the non-thymidine mutations M184V, L74V, and K65R, and the multidrug resistant Q151M complex, as well as others.
HIV mutation literature information.
PMID: 
2003
The Journal of biological chemistry
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