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: A62V
Trends in the Molecular Epidemiology and Genetic Mechanisms of Transmitted Human Immunodeficiency Virus Type 1 Drug Resistance in a Large US Clinic Population.
Method: Several additional DRMs not on the SDRM list were analyzed including (1) the primarily tenofovir disoproxil fumarate (TDF)-selected DRMs A62V, K65N, and K70G/N/Q/S/T and (2) the primarily rilpivirine (RPV)-selected DRMs E138A/G/K/Q, of which E138A is polymorphic, occurring in 1%-4% of viruses from ART-naive individuals.
Result: A62V, a non-SDRM TDF-associated accessory DRM, occurred in 10 individuals.
Genetic diversity and antiretroviral resistance-associated mutation profile of treated and naive HIV-1 infected patients from the Northwest and Southwest regions of Cameroon.
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: A62V
Distinct Pattern of Thymidine Analogue Mutations with K65R in Patients Failing Tenofovir-Based Antiretroviral Therapy.
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.
HIV-1C proviral DNA for detection of drug resistance mutations.
Result: G190A, E138A/G) were found concurrently both in viral RNA and proviral DNA, in two patients resistance mutations (M46I and G190E) were detected only in viral RNA, and in five patients archived transmitted drug resistance mutations (M230I, G73S, M184I, M46I, and A62V) in proviral DNA were identified.
Result: NRTIs related mutations M184I and A62V were only found in proviral DNA (Table 2).
Table: A62V
The HIV-1 Reverse Transcriptase A62V Mutation Influences Replication Fidelity and Viral Fitness in the Context of Multi-Drug-Resistant Mutations.
Result: In contrast, the two MDR complexes with A62V, as well as the A62V mutant, had a reduced replication capacity compared to that of wt virus (Figure 3).
Result: In the absence of AZT, the A62V mutant alone had significantly reduced viral replication fitness, while the T69SSS insertion complex with A62V had a non-statistically significant decrease in fitness (Figure 5A).
Result: In the presence of AZT, all MDR mutant complexes, except for the T69SSS insertion complex without A62V, had a statistically significant increase in virus fitness (Figure 5B).
Result: In this assay, all four MDR mutants (i.e., Q151M complex with or without A62V, and the PMID: 30409215
2018
AIDS research and therapy
Result: Most of the minority mutations in viruses from both groups of naive patients were observed in the RT, e.g., M41L, E44D, A62V, K65R, D67N, D67G, V75I, L100I, K103N, K103R, V188I, M184I, L210W, K219Q, Y318F, etc., although a number of minority mutations associated with resistance to PI (L10F, V11I, M46I/
Virological response, HIV-1 drug resistance mutations and genetic diversity among patients on first-line antiretroviral therapy in N'Djamena, Chad: findings from a cross-sectional study.