HIV mutation literature information.


  Relationship between 3'-azido-3'-deoxythymidine resistance and primer unblocking activity in foscarnet-resistant mutants of human immunodeficiency virus type 1 reverse transcriptase.
 PMID: 12743270       2003       Journal of virology
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).
 PMID: 12790516       2003       Antiviral chemistry & chemotherapy
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)).


  Tenofovir disoproxil fumarate.
 PMID: 12887265       2003       Drugs
Abstract: Isolates of HIV infrequently developed the K65R mutation during 96 weeks of tenofovir DF therapy.


  Tenofovir disoproxil fumarate.
 PMID: 13130407       2003       Clinical infectious diseases
Abstract: The signature mutation is the K65R mutation, which causes variable loss in susceptibility to tenofovir DF, didanosine, and abacavir.


  Change to abacavir-lamivudine-tenofovir combination treatment in patients with HIV-1 who had complete virological suppression.
 PMID: 14683659       2003       Lancet (London, England)
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.
 PMID: 14760883       2003       Antiviral therapy
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.


  T69D/N pol mutation, human immunodeficiency virus type 1 RNA levels, and syncytium-inducing phenotype are associated with CD4 cell depletion during didanosine therapy.
 PMID: 11865396       2002       The Journal of infectious diseases
Abstract: Disease progression was not associated with mutations in the reverse-transcriptase gene previously associated with resistance to ddI (L74V, K65R, or M184V).



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