Suppression of virus load by highly active antiretroviral therapy in rhesus macaques infected with a recombinant simian immunodeficiency virus containing reverse transcriptase from human immunodeficiency virus type 1.
Abstract: The virus load in one of these two animals rebounded; virus from this animal was initially free of drug-resistance mutations but acquired the K65R mutation in reverse transcriptase at 11 weeks after efavirenz treatment was withdrawn.
Anti-HIV activity of (-)-(2R,4R)-1- (2-hydroxymethyl-1,3-dioxolan-4-yl)-thymine against drug-resistant HIV-1 mutants and studies of its molecular mechanism.
PMID: 15943470
2005
Journal of medicinal chemistry
Abstract: (-)-(2R,4R)-1-(2-Hydroxymethyl-1,3-dioxolan-4-yl)thymine (DOT) is the first thymidine kinase-activated nucleoside that is significantly active against all of the clinically significant NRTI-resistant HIV-1 mutants, including AZT (D67N/K70R/T215Y/K219Q), Tenofovir (K65R), and Lamivudine (M184V).
[Efficacy of anti-HIV treatment and drug-resistance mutations in some parts of China].
Abstract: In addition, intermediate level and low level resistance against NRTIs caused by K65R and L74V can also be found, but less commonly.
Comparative selection of the K65R and M184V/I mutations in human immunodeficiency virus type 1-infected patients enrolled in a trial of first-line triple-nucleoside analog therapy (Tonus IMEA 021).
Abstract: All three nucleoside analogs are known to select the K65R and/or M184V/I mutation.
Abstract: At W12, M184V/I was found in 18/20 patient, together with the K65R in 13 patients.
Abstract: At W12, the K65R mutation was found in 30 to 100% of clones.
Abstract: At W4, M184V/I was detected in 12/19 patients and K65K/R in 2 patients by bulk sequencing.
Abstract: At W4, clonal analysis revealed the K65R mutation in 0.6 to 48% of clones in the five patients studied.
Abstract: However, K65R was also detected early using a clone-sensitive genotyping method.
Quantifying mixed populations of drug-resistant human immunodeficiency virus type 1.
PMID: 16048944
2005
Antimicrobial agents and chemotherapy
Abstract: For cDNA, nucleotide polymorphisms for codon M184V (ATG to GTG) and K65R (AAA to AGA) could be differentiated and quantified even when the population mixture varied as much as 1 to 10,000.
Anti-human immunodeficiency virus type 1 activity and resistance profile of 2',3'-didehydro-3'-deoxy-4'-ethynylthymidine in vitro.
PMID: 16048947
2005
Antimicrobial agents and chemotherapy
Abstract: In contrast, the susceptibility of the virus carrying the K65R mutation or the multidrug-resistant mutation with the Q151M complex (A62V, V75I, F77L, F116Y, and Q151M) was not altered.
In vitro selection and analysis of human immunodeficiency virus type 1 resistant to derivatives of beta-2',3'-didehydro-2',3'-dideoxy-5-fluorocytidine.
PMID: 16127074
2005
Antimicrobial agents and chemotherapy
Abstract: Serial passage of human immunodeficiency virus type 1 in MT-2 cells in increasing concentrations of the d- and l-enantiomers of beta-2',3'-didehydro-2',3'-dideoxy-5-fluorocytidine (d4FC) resulted in the selection of viral variants with reverse transcriptase substitutions M184I or M184V for l-d4FC and I63L, K65R, K70N, K70E, or R172K for d-d4FC.
High rate of virological failure in maintenance antiretroviral therapy with didanosine and tenofovir.
Abstract: At virological failure 'de novo' selected mutations were identified in 11 of the 12 failing patients, including the K65R mutation in seven patients.
HIV-1 reverse transcriptase mutations that confer decreased in vitro susceptibility to anti-RT DNA aptamer RT1t49 confer cross resistance to other anti-RT aptamers but not to standard RT inhibitors.
Abstract: This result was tempered by the observation that NRTI-resistance mutations such as K65R can confer resistance to some anti-RT aptamers.
Result: K65R is known to cause resistance to all clinically approved
Result: However, in vitro biochemical experiments do show some resistance to AZTTP and it has been suggested this is due to K65R decreasing the rate of AZTMP excision.
Result: In contrast, mutations shown to confer resistance to multiple NRTIs, including E89G, K65R and M184V displayed low levels of resistance to RT1t49 (2-5 fold), with K65R displaying the highest level of resistance (5-fold).
A combination of decreased NRTI incorporation and decreased excision determines the resistance profile of HIV-1 K65R RT.
Abstract: For K65R, the combination of these opposing mechanisms results in decreased susceptibility to most NRTI but increased susceptibility to ZDV.
Abstract: For ABC, tenofovir, and d4T, despite having decreased excision, decreased binding or incorporation resulted in reduced susceptibilities to K65R.
Abstract: For ddI, ddC, 3TC, and FTC, decreased binding or incorporation by K65R appeared responsible for the decreased susceptibilities in cell culture.
Abstract: However, K65R also showed decreased excision of all NRTI compared to wild-type, indicating greater stability once incorporated.
Abstract: Ki/Km values were increased 2- to 13-fold for K65R compared to wild-type RT for all
HIV mutation literature information.
PMID: 
2005
Journal of virology
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