HIV-1 acquired drug resistance to integrase inhibitors in a cohort of antiretroviral therapy multi-experienced Mexican patients failing to raltegravir: a cross-sectional study.
High resistance to reverse transcriptase inhibitors among persons infected with human immunodeficiency virus type 1 subtype circulating recombinant form 02_AG in Ghana and on antiretroviral therapy.
Abstract: Additionally, and at a lower level, protease inhibitor (PI)-resistance mutations, M46I, I54 V, V82A, L90 M, and I471 V, were also present in the sequences from antiretroviral therapy (ART)-experienced individuals.
High prevalence of integrase mutation L74I in West African HIV-1 subtypes prior to integrase inhibitor treatment.
PMID: 32105319
2020
The Journal of antimicrobial chemotherapy
Table: V82A
Drug Resistance Mutations Against Protease, Reverse Transcriptase and Integrase Inhibitors in People Living With HIV-1 Receiving Boosted Protease Inhibitors in South Africa.
Result: The most common major PI RAMs observed were M46I and V82A (n = 12; 12%); I54V (n = 10; 10%); I84V and L76V (n = 7; 7%); I47A/V (n = 3; 3%); I50L/V (n = 2; 2%); and V32I (n = 2; 2%) (Table 1).
Table: V82A
Discussion: The M46I and V82A RAMs were the most common mutations observed in patients receiving LPV/r compared with ATV/r.
Discussion: The most common
Discussion: We identified a low frequency of M46I and V82A in patients receiving ATV/r as their bPIs.
HIV-1 Gag mutations alone are sufficient to reduce darunavir susceptibility during virological failure to boosted PI therapy.
PMID: 32556165
2020
The Journal of antimicrobial chemotherapy
Result: As shown in Figure 4(a), recombinant viruses from PT1, PT3 and PT6 were fully susceptible to darunavir in accordance with the high genetic barrier of the drug, even in the presence of I54V and V82A protease mutations, as predicted by Stanford for the T2 clonal viruses 5 and 8 from PT3.
Result: Clonal sequences were also analysed using the Stanford HIVdb database, and clones were predicted to be PI susceptible, except the clones containing I52V and V82A, which were predicted to have intermediate resistance to lopinavir and be fully susceptibility to darunavir.
Result: In the case of PT3, we were able to detect a cluster of clonal sequences [C5, C6, C8 and C10 (Figure S1B)] containing drug resistance mutations I52V and PMID: 33014372
2020
SAGE open medicine
Table: V82A/S
Patterns of acquired HIV-1 drug resistance mutations and predictors of virological failure in Moshi, Northern Tanzania.
Result: One participant (K38) who had previously used ritonavir-boosted lopinavir had L24I, L33F, I54V, and V82A mutations which together reduce the susceptibility of ritonavir-boosted lopinavir.
Table: V82A
Genotyping and antiretroviral drug resistance of human immunodeficiency Virus-1 in Jazan, Saudi Arabia.
Abstract: Mutations associated with antiretroviral drugs include (V82A+I84IV), (L10F+Q58E), (L10F+V82Y), L10FV, L33LF, L89LMV, M184V, E138A, V106I, and V179VD.
Result: One patient had multi-drug mutation; the mutations (V82A + I84IV) and (L10F + Q58E) were found in the protease region while mutation M184 V
Multiple Molecular Dynamics Simulations of the Inhibitor GRL-02031 Complex with Wild Type and Mutant HIV-1 Protease Reveal the Binding and Drug-Resistance Mechanism.
Abstract: To elucidate the binding mechanism of HIV-1 protease with promising inhibitor GRL-02031 and further to probe the resistance mechanism associated with mutations (I47V, L76V, V82A, and N88D) to the inhibitor, we applied multiple molecular dynamics (MMD) simulations along with energy analysis by the molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) and solvated interaction energy (SIE) methodology on specific HIV-1 protease with GRL-0231 complexes.
HIV mutation literature information.
PMID: 
2020
EClinicalMedicine
Browser Board
Co-occurred Entities
Filtrator
ViMRT