Switching to bictegravir/emtricitabine/tenofovir alafenamide maintained HIV-1 RNA suppression in participants with archived antiretroviral resistance including M184V/I.
PMID: 31430369
2019
The Journal of antimicrobial chemotherapy
Method: Primary NRTI-R substitutions were M41L, K65R/E/N, D67N, T69 insertions, K70E/R, L74V/I, Y115F, Q151M, M184V/I, L210W, T215Y/F and K219E/Q/N/R in RT.
Table: Q151M
HIV-1 Reverse Transcriptase Promotes Tumor Growth and Metastasis Formation via ROS-Dependent Upregulation of Twist.
PMID: 31885806
2019
Oxidative medicine and cellular longevity
Result: The most frequent mutation of resistance to NRTI worldwide is M184V/I, followed by K65R/N, L74V/I, Y115F, and Q151M, and the most prevalent for FSU_A is M184V, followed by K65R/N.
Genetic diversity and antiretroviral resistance-associated mutation profile of treated and naive HIV-1 infected patients from the Northwest and Southwest regions of Cameroon.
HIV Drug Resistance Mutations in Patients with HIV and HIV-TB Coinfection After Failure of First-Line Therapy: A Prevalence Study in a Resource-Limited Setting.
PMID: 31117863
2019
Journal of the International Association of Providers of AIDS Care
Table: Q151M
Discussion: Q151M mutations cause intermediate-/high-level resistance to AZT, ddI, d4T, and ABC with low-level resistance to TDF, 3TC, and FTC.
Discussion: Also, in combination with accessory mutations at positions 62, 75, 77, and 116, Q151M confers high-level resistance to AZT, ddI, d4T, and ABC and intermediate-level resistance to TDF, 3TC, and FTC.
Discussion: The Q151M mutation was observed in 2 patients with HIV alone.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
PMID: 29753024
2018
Infection, genetics and evolution
Abstract: This study reveals the antiretroviral efficacy of obtained two best ligands and delivers the hits against HIV-1 reverse transcriptase Q151M mutant.
Abstract: To discover potential hits, we docked 49 antiretroviral analogs (n = 6294) against HIV-1 reverse transcriptase Q151M mutant & its wild-type form and narrow downed their number in three sequential modes of docking using Schrodinger suite.
Distinct Pattern of Thymidine Analogue Mutations with K65R in Patients Failing Tenofovir-Based Antiretroviral Therapy.
PMID: 29084434
2018
AIDS research and human retroviruses
Introduction: As expected, patients failing AZT-based therapy did not develop mutations K65R, K70E, L74V, or Y115F, and only rarely were DRMs from the Q151M complex seen.
Introduction: However, in the 31 patients with no K65R present at S2, 6 had intermediate or high-level resistance to AZT: 4 were caused by TAM-2 DRMs, 1 by T215Y, and 1 by Q151M-complex mutations Q151M, A62V, V75I, F77L, F116Y.
HIV-1 with HBV-associated Q151M substitution in RT becomes highly susceptible to entecavir: structural insights into HBV-RT inhibition by entecavir.
Abstract: Here, we demonstrate that a Q151M substitution alone at the nucleotide-binding site (N-site) of human immunodeficiency virus type-1 (HIV-1) RT renders HIV-1 highly sensitive to entecavir (ETV), a potent nucleoside analogue RT inhibitor (NRTI) against HBV.
Abstract: We thus solved the crystal structures of HIV-1 RTQ151M:DNA complex with bound dGTP or ETV-triphosphate (ETV-TP).
Introduction: Based on the structures of RTQ151M together with the results of the antiviral assay, possible mechanisms of ETV-TP action on HIV-1/HBV RT and of the reported ETV resistance are discussed.
Introduction: In this study, we showed that the PMID: 29892199
2018
Infection and drug resistance
Discussion: Since the majority of these patients (40.4%) received the first-line regimens containing zidovudine, its influence on the detection of RAMs or Q151M complex can be neglected.
Risk factors and outcomes for the Q151M and T69 insertion HIV-1 resistance mutations in historic UK data.
Conclusion: Our data confirm that modern ART and laboratory monitoring have greatly reduced the occurrence of
Method: Few data are available before this period, as resistance testing was not widely available, with no recorded observations of either Q151M or T69i mutations.
Method: Multivariable Cox regression was used to investigate the factors associated with successful viral suppression following detection of either the Q151M or T69i mutation.
Method: Presence or absence of the K65R mutation was also included as a predictor, and analyses were also conducted including the respective accessory mutations for Q151M and T69i.
Method: To investigate the association between Q151M and 69i and mortality, we carried out a matched cohort analysis of comparable patients in whom ART data were available.
HIV mutation literature information.
PMID: 
2019
Infection and drug resistance
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