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.
Nucleoside and nucleotide analogue reverse transcriptase inhibitors: a clinical review of antiretroviral resistance.
Abstract: Resistance to multiple nucleoside reverse transcriptase inhibitors (NRTIs) may result from several genotypically distinct pathways, including the Q151M (151 complex), the 69 insertion complex, two distinct thymidine analogue mutational pathways and the K65R mutation.
Dioxolane guanosine, the active form of the prodrug diaminopurine dioxolane, is a potent inhibitor of drug-resistant HIV-1 isolates from patients for whom standard nucleoside therapy fails.
PMID: 11782585
2002
Journal of acquired immune deficiency syndromes (1999)
Abstract: The L74V mutant remained susceptible to inhibition by DXG, and the K65R mutant demonstrated moderate resistance to DXG.
Abstract: We also examined site-directed mutants containing only L74V or K65R, the characteristic resistance mutations for DXG.
HIV mutation literature information.
PMID: 
2003
Antiviral therapy
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