Method: Participants with a history of genotypic/phenotypic drug resistance to protease inhibitors (PIs) or with HIV-1 genotypic drug resistance to PIs at baseline (including D30N, M46I/L, I47V/A, G48V, I50L, I54M/L, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, or L90M) were excluded, despite any reported effects of PI resistance or resistance
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 PI-R substitutions were D30N, V32I, M46I/L, I47V/A, G48V, I50V/L, I54M/L, Q58E, T74P, L76V, V82A/F/L/S/T, N83D, I84V, N88S and L90M in PR.
Table: N88S
Drug Resistance Mutation L76V Alters Nonpolar Interactions at the Flap-Core Interface of HIV-1 Protease.
Discussion: Mutation L76V is not unusual in this respect; mutations L90M and N88D/S also have no direct interactions with inhibitors, yet are strongly associated with resistance to one or more clinical inhibitors.
Drug Resistance Mechanism of L10F, L10F/N88S and L90M mutations in CRF01_AE HIV-1 protease: Molecular dynamics simulations and binding free energy calculations.
PMID: 28645089
2017
Journal of molecular graphics & modelling
Abstract: In this work, we examined the effect of non active site mutations L10F, L10F/N88S and L90M with nelfinavir using molecular dynamics simulation and binding free energy calculations.
Abstract: Our present study shed light on the resistance mechanism of the strongly linked mutation L10F/N88S observed experimentally in AE subtype.
Abstract: The benzamide moiety of nelfinavir shows large positional deviation in L10F and L10F/N88S complexes and the L10F/N88S mutation changes the hydrogen bond between the side chain atoms of 30th residue and the 88th residue.
Abstract: The simulations suggested th
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 PI-R substitutions assessed were D30N, V32I, L33F, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/S/T, I84V, N88S, and L90M in PR.
Treatment Outcomes and Resistance Patterns of Children and Adolescents on Second-Line Antiretroviral Therapy in Asia.
PMID: 27355415
2016
Journal of acquired immune deficiency syndromes (1999)
Result: Data on PI resistance mutations were available among 50 (68%) children, and included any major LPV mutation (L76V, V82A, V82S; 8%), >=6 LPV mutations (2%), any major darunavir (DRV) mutation (I84V, L76V; 2%), and any major ATV mutation (I84V, N88S; 4%) (Table 2).
HIV Drug Resistance in Antiretroviral Treatment-Naive Individuals in the Largest Public Hospital in Nicaragua, 2011-2015.
Result: Most PI SDRMs were present only as low-abundance variants under the 5% threshold, including L23I, D30N, I47V, I50V, F53L, I54T, G73S, V82A, N83D, I84V, I85V, N88DS, and L90M (Fig 2).
The Antiviral Activity of Approved and Novel Drugs against HIV-1 Mutations Evaluated under the Consideration of Dose-Response Curve Slope.
Method: M46I, I54V, V82A, M46IN88S, G48VI54V, M46IV82TI84V, and G48VI54VV82A mutations were introduced into the PR coding region, and K103N, Y181C, K103NY181C, K101Q, K101QY181C, K101QH221Y, PMID: 26558396
2015
PloS one
HIV mutation literature information.
PMID: 
2020
SAGE open medicine
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