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.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
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.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
Introduction: However, a relatively high prevalence of Q151M has been observed in more recent studies of patients failing ART from LMICs (ranging 2-14% in these studies).
Introduction: Likewise the Q151M mutation causes intermediate/high-level resistance to zidovudine (ZDV), didanosine (DDI), stavudine (D4T), and abacavir (ABC) and low level resistance to tenofovir (TDF), lamivudine (3TC) and emtricitabine (FTC).
Introduction: The T69i mutation has been linked to DDI use whilst for Q151M an association with D4T has been observed, and most reports of the mutations occurring in Europe date to 10 or more years ago when the use of these drugs was still widespread.
Introduction: This paper reports changes in the prevalence of multi-drug resistance mutations Q151M and T69i in the UK-HDRD over time and evaluates outcomes in affected patients.|