Introduction: Notably, HIV-1 RT Q151M is a critical mutation that confers multi-NRTI resistance, accompanied by A62V, V75I, F77L, and F116Y mutations (Q151M-complex).
Method: Antiviral assays (p24 assay) using wild-type HIV-1 (HIV-1WT) and replicable HIV-1 variants (HIV-1Q151M, HIV-1Q151M/Y115F/F116Y, and HIV-1Q151M/I63V/L74V) were also conducted as previously described.
Result: A recent structural study of HIV-1 RTQ151M-complex suggested that the F116Y mutation improves polymerization fitness, which might be caused by N-
The HIV-1 Reverse Transcriptase A62V Mutation Influences Replication Fidelity and Viral Fitness in the Context of Multi-Drug-Resistant Mutations.
Abstract: In particular, A62V was observed in various multi-dideoxynucleoside resistant (MDR) mutation complexes, including the Q151M complex (i.e., A62V, V75I, F77L, F116Y, and Q151M), and the T69SSS insertion complex, which has a serine-serine insertion between amino acid positions 69 and 70 (i.e., M41L, A62V, T69SSS, K70R, and T215Y).
Introduction: In particular, A62V is normally seen in different mutational arrangements, located mostly on the flexible beta3-beta4 loop region of the fingers sub-domain of
Risk factors and outcomes for the Q151M and T69 insertion HIV-1 resistance mutations in historic UK data.
Result: Data regarding accessory mutations to Q151M were available in 155 (86%) patients: A62V was present in 49 (32%), V75I in 62 (40%), F77L in 47 (30%) and F116Y in 99 (64%), and 75% of patients showed at least one accessory mutation.
Table: F116Y
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
PMID: 29084434
2018
AIDS research and human retroviruses
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.
Structural Insights into HIV Reverse Transcriptase Mutations Q151M and Q151M Complex That Confer Multinucleoside Drug Resistance.
PMID: 28396546
2017
Antimicrobial agents and chemotherapy
Abstract: Q151M and four associated mutations, A62V, V75I, F77L, and F116Y, were detected in patients failing therapies with dideoxynucleosides (didanosine [ddI], zalcitabine [ddC]) and/or zidovudine (AZT).
Abstract: The compensatory set of mutations in Q151Mc, particularly F116Y, restricts the side chain flexibility of M151 and helps restore the DNA polymerization efficiency of the enzyme.
Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
Method: Primary NRTI-R substitutions assessed were M41L, A62V, K65R, D67N, T69 insertions, K70E/R, L74I/V, V75I, F77L, Y115F, F116Y, Q151M, M184V/I, L210W, T215F/Y, and K219E/N/Q/R in RT.
Comparison of genotypic and virtual phenotypic drug resistance interpretations with laboratory-based phenotypes among CRF01_AE and subtype B HIV-infected individuals.
Result: Protease (PR) RAMs detected from this outlier sample were M46I, I47V and I84V, and reverse transcriptase (RT) RAMs were A62V, D67N, K70R, V75I, F116Y,
Discussion: The Q151M complex, consisting of Q151M, A62V, V75I, F77L and F116Y, is associated with resistance to all approved NRTIs except for tenofovir.
Biochemical characterization of a multi-drug resistant HIV-1 subtype AG reverse transcriptase: antagonism of AZT discrimination and excision pathways and sensitivity to RNase H inhibitors.
Abstract: We analyzed a multi-drug resistant (MR) HIV-1 reverse transcriptase (RT), subcloned from a patient-derived subtype CRF02_AG, harboring 45 amino acid exchanges, amongst them four thymidine analog mutations (TAMs) relevant for high-level AZT (azidothymidine) resistance by AZTMP excision (M41L, D67N, T215Y, K219E) as well as four substitutions of the AZTTP discrimination pathway (A62V, V75I, F116Y and Q151M).
Introduction: In HIV-2, AZT discrimination is characterized by the mutations A62V, V75I, F77I, F116Y
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
HIV mutation literature information.
PMID: 
2019
PloS one
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