Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.
Result: Our analysis showed that mutations A62V, Y181C, G190A, H208Y and T215F could cluster with the first group, although the association was weaker than for A98G, Q174R, I178L and L228H.
Table: A62V
HIV-1 drug resistance genotyping from antiretroviral therapy (ART) naive and first-line treatment failures in Djiboutian patients.
Discussion: Q151M is a primary mutation that in vivo can be co-selected together with a group of secondary mutations (A62V, V75I, F77L and F116Y) that confers a cross-resistance with all NRTIs.
Effect of translocation defective reverse transcriptase inhibitors on the activity of N348I, a connection subdomain drug resistant HIV-1 reverse transcriptase mutant.
PMID: 23273211
2012
Cellular and molecular biology (Noisy-le-Grand, France)
Abstract: In this study we tested EFdA-triphosphate (TP) together with a related compound, ENdA-TP (4'-ethynyl-2-amino-2'-deoxdyadenosine triphosphate) against HIV-1 RTs that carry clinically relevant drug resistance mutations: N348I, D67N/K70R/L210Q/T215F, D67N/K70R/L210Q/T215F/N348I, and A62V/V5I/F77L/F116Y/Q151M.
Introduction: In this study we determine the ability of TDRTIs to block reverse transcription
Low prevalence of transmitted K65R and other tenofovir resistance mutations across different HIV-1 subtypes: implications for pre-exposure prophylaxis.
PMID: 23305651
2012
Journal of the International AIDS Society
Table: A62V
The HIV-1 Reverse Transcriptase A62V Mutation Influences Replication Fidelity and Viral Fitness in the Context of Multi-Drug-Resistant Mutations.
Abstract: We demonstrate that F61A causes a strong bias to the posttranslocational state, while A62V shows a subtle bias toward pretranslocation regardless of the mutational background.
Abstract: We employed site-specific footprinting, binding assays, and DNA-synthesis inhibition experiments to study F61A and A62V, alone and against a background of known drug-resistance mutations.
Abstract: We focused on substitution F61A and the neighboring A62V that is frequently associated with drug-resistance-conferring mutations.
Abstract: We propose that a binary, pretranslocated complex in a closed conformation is stabilized with A62V and destabilized with F61A.
"K70Q adds high-level tenofovir resistance to ""Q151M complex"" HIV reverse transcriptase through the enhanced discrimination mechanism."
1Abstract: HIV-1 carrying the ""Q151M complex"" reverse transcriptase (RT) mutations (A62V/V75I/F77L/F116Y/Q151M, or Q151Mc) is resistant to many FDA-approved nucleoside RT inhibitors (NRTIs), but has been considered susceptible to tenofovir disoproxil fumarate (TFV-DF or TDF)."
Introduction: This RT contains the Q151M mutation together with a cluster of four additional mutations (A62V/V75I/F77L/F116Y).
Discussion: Also,
A Leu to Ile but not Leu to Val change at HIV-1 reverse transcriptase codon 74 in the background of K65R mutation leads to an increased processivity of K65R+L74I enzyme and a replication competent virus.
Discussion: For example, in contrast to the severe replication defect conferred by L74V mutation in the background of K65R, RT mutation A62V and S68G have been shown to improve replication capacity of virus when selected in the same genome that contain K65R mutation.
The evolution of HIV-1 reverse transcriptase in route to acquisition of Q151M multi-drug resistance is complex and involves mutations in multiple domains.
Abstract: The emergence of Q151M MDR occurred in the order A62V, V75I, and finally Q151M on the same genome at 4, 17 and 37 months after initiation of therapy, respectively.
Introduction: The Q151M MDR complex is composed of the Q151M mutation, which is normally the first to appear, followed by at least two of the following four mutations: A62V, V75I, F77L and F116Y.
Result: Genetic linkage analysis of the single genomes at 4, 17 and 37 months showed that the patient acquired the Q151M MDR mutations in the order: A62V, V75I and finall
Genotypic resistance at viral rebound among patients who received lopinavir/ritonavir-based or efavirenz-based first antiretroviral therapy in South Africa.
PMID: 21694608
2011
Journal of acquired immune deficiency syndromes (1999)
Result: One participant who received EFV+d4T+3TC had four RT mutations (A62V, K65R, M184V, and K219E) in addition to two NNRTI-associated mutations.
HIV mutation literature information.
PMID: 
2012
Retrovirology
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