Nucleoside reverse transcriptase inhibitor resistance mutations in subtype F1 strains isolated from heavily treated adolescents in Romania.
PMID: 18632295
2009
International journal of infectious diseases
Abstract: Although the combination of K65R mutation with TAMs has rarely been reported because of their antagonistic effects on NRTI resistance, its presence was confirmed by clonal analysis of one strain.
Abstract: The RT gene carrying the K65R mutation and thymidine analog mutations (TAMs) was cloned into pGEM-T vector (Promega), followed by sequencing.
Sensitivity of phenotypic susceptibility analyses for nonthymidine nucleoside analogues conferred by K65R or M184V in mixtures with wild-type HIV-1.
PMID: 19032103
2009
The Journal of infectious diseases
Abstract: Phenotypic resistance masking by wild-type virus may explain this discrepancy.Consistent with this notion were (1) the presence of low level nucleoside reverse-transcriptase inhibitor-resistant human immunodeficiency virus in subjects receiving failing first-line regimens consisting of tenofovir (TDF), abacavir (ABC), and lamivudine (3TC); (2) lower fold resistance associated with mixtures versus mutants in a clinical-isolate database; and (3) dose dependent changes in susceptibility to ABC, 3TC, TDF, and didanosine on titration of K65R and/or M184V with wild-type virus.
High rate of early virological failure with the once-daily tenofovir/lamivudine/nevirapine combination in naive HIV-1-infected patients.
PMID: 19036752
2009
The Journal of antimicrobial chemotherapy
Abstract: Resistance genotypes for the nine Group 2 failing patients showed the mutations M184V/I (n = 3), K65R (n = 6), one or more NNRTI resistance mutations in all cases.
The rise and fall of K65R in a Portuguese HIV-1 Drug Resistance database, despite continuously increasing use of tenofovir.
PMID: 19038365
2009
Infection, genetics and evolution
Abstract: CONCLUSIONS: This study suggests that the use of certain TDF-based regimens caused the increase in K65R incidence over the last years.
Abstract: In this study, we evaluated the impact of these combinations on K65R selection over time.
Abstract: Incidence of K65R was calculated and compared with proportions of failing therapies in the respective year of sampling including TDF or didanosine plus stavudine and their respective frequency of K65R selection were analyzed using classical statistics and Bayesian Network Learning.
Abstract: OBJECTIVE: The overall prevalence of the K65R mutation in HIV-1 reverse transcriptase has increased in treatment-experienced patients, mostly attributed to the increasing use of tenofovir (TDF).
Abstract: RESULTS: The overal
Nucleoside and nucleotide analogs select in culture for different patterns of drug resistance in human immunodeficiency virus types 1 and 2.
PMID: 19064892
2009
Antimicrobial agents and chemotherapy
Abstract: In agreement with our previous findings, dual-drug combinations of TFV, ddI, ABC, d4T, ZDV, and 3TC preferentially selected for K65R in HIV-1 subtype C isolates.
Abstract: Recent findings suggest bidirectional antagonisms between the K65R mutation and thymidine analogue mutations in human immunodeficiency virus type 1 (HIV-1)-infected, treatment-experienced patients, yet little is known about HIV-2 in this regard.
Abstract: Since HIV-2 cultures did not develop K65R, an ultrasensitive allele-specific real-time PCR assay was developed to distinguish the presence of 65R from wild-type K65 after 16 cycles with a discriminatory ability of 0.1% against a population of wild-type virus.
Template usage is responsible for the preferential acquisition of the K65R reverse transcriptase mutation in subtype C variants of human immunodeficiency virus type 1.
Abstract: Template factors can therefore increase the probability of K65R development in subtype C HIV-1.
Abstract: We propose that a nucleotide template-based mechanism facilitates the acquisition of the K65R mutation in subtype C human immunodeficiency virus type 1 (HIV-1).
Abstract: When subtype C reverse transcriptase (RT) was employed to synthesize DNA from subtype C DNA templates, preferential pausing was seen at the nucleotide position responsible for the AAG-to-AGG K65R mutation.
Minority quasispecies of drug-resistant HIV-1 that lead to early therapy failure in treatment-naive and -adherent patients.
Abstract: The key mutations K65R, K103N, Y181C, M184V, and M184I in the reverse transcriptase were quantified by allele-specific real-time polymerase chain reaction performed on plasma samples before and during early virological treatment failure.
Emergence of multiclass drug-resistance in HIV-2 in antiretroviral-treated individuals in Senegal: implications for HIV-2 treatment in resouce-limited West Africa.
Abstract: HIV-1-associated thymidine analogue mutations (M41L, D67N, K70R, L210W, and T215Y/F) were not observed, with the exception of K70R, which was present together with K65R and Q151M in a strain from 1 patient.
Abstract: The reverse-transcriptase mutations M184V and K65R, which confer high-level resistance to lamivudine and emtricitabine in HIV-2, were found in strains from 43% and 9% of patients, respectively.
Abstract: ATP-mediated excision of TFV-or ZDV-terminated primer was decreased for K65R and for K65R+M184V RT compared to WT RT.
Abstract: At low dNTP concentration, K65R RT exhibited lower activity in single-cycle processivity assays while the K65R+M184V mutant showed diminished processivity independent of dNTP concentration.
Abstract: BACKGROUND: We investigated the effects of mutations K65R and K65R plus M184V on enzymatic function and mechanisms of drug resistance in subtype C reverse transcriptase (
Apricitabine does not select additional drug resistance mutations in tissue culture in human immunodeficiency virus type 1 variants containing K65R, M184V, or M184V plus thymidine analogue mutations.
PMID: 19223637
2009
Antimicrobial agents and chemotherapy
Abstract: Human immunodeficiency virus type 1 containing the reverse transcriptase mutation M184V or K65R or mutations M41L, M184V, and T215Y did not accumulate additional resistance mutations in the reverse transcriptase when increasing amounts of apricitabine drug pressure were applied.
HIV mutation literature information.
PMID: 
2009
International journal of infectious diseases
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