A Comparative Insight into Amprenavir Resistance of Mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 Protease Based on Thermodynamic Integration and MM-PBSA Methods.
PMID: 26317593
2015
Journal of chemical information and modeling
Abstract: Drug resistance of mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 protease (PR) was found in clinical treatment of HIV patients with the drug amprenavir (APV).
Exploring the drug resistance of V32I and M46L mutant HIV-1 protease to inhibitor TMC114: flap dynamics and binding mechanism.
PMID: 25562662
2015
Journal of molecular graphics & modelling
Introduction: It was found that, the mutations D30N and I50V results in the drug resistance to TMC114; however the changes due to mutations V82A, I84V and L90M are well adapted by TMC114.
Introduction: The resistance of inhibitor amprenavir, which is an analog of TMC114 to mutant V32I, I50V and I84V with an increase in the energetic contribution from the van der Waals interactions, was also explained in another study by Kar et al.
Introduction: utilized the crystallographic study to analyze the effectiveness of TMC114 to HIV-1-pr, with highly drug resistant mutants D30N, I50V, V82
Epidemiological Surveillance of HIV-1 Transmitted Drug Resistance in Spain in 2004-2012: Relevance of Transmission Clusters in the Propagation of Resistance Mutations.
Result: It is noteworthy that several major mutations associated to high level resistance to NRTIs (K65R, L74V, Y115F, M184V and T215Y), to NNRTIs (l100I, K101E, K103N/S, V106M, Y181C, Y188L and G190A) and to PIs (D30N, M46I/L, I54V/T, L76V, V82A,
Table: I84V
Effects of drug-resistant mutations on the dynamic properties of HIV-1 protease and inhibition by Amprenavir and Darunavir.
Abstract: Molecular dynamics simulations are performed to investigate the dynamic properties of wild-type HIV-1 protease and its two multi-drug-resistant variants (Flap + (L10I/G48V/I54V/V82A) and Act (V82T/I84V)) as well as their binding with APV and DRV inhibitors.
Introduction: indicated that the small structure difference of APV and DRV inhibitors lead to apparently different binding affinities towards WT HIV-1 PR and its two multi-drug-resistant (MDR) variants, namely Flap+ (L10I/G48V/I54V/V82A) and Act (V82T/I84V<
The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.
PMID: 29124158
2015
Biochemistry and biophysics reports
Introduction: L33F was initially identified as an accessory mutation to I54L/M, V32I+I47V, and I84V/I but is now recognized as a nonpolymorphic major drug resistance mutation.
Method: MDR769 L33F is based on the previously studied multi-drug resistant variant 769, MDR769, which contains the mutations Q7K, L10I, M36V, M46L, I54V, I62V, L63P, A71V, V82T, I84V, L90M.
Treatment-Emergent Mutations and Resistance in HIV-Infected Children Treated with Fosamprenavir-Containing Antiretroviral Regimens.
Result: At VF, the following major treatment-emergent PI mutations or mutation mixtures were detected: M46M/I, I50I/V, I54I/M/V, and I84I/V, and the virus developed FPV RS.
Assessing transmissibility of HIV-1 drug resistance mutations from treated and from drug-naive individuals.
Discussion: We show here that D30N, N88D/S and L90 M also have high transmissibility and that other SDRMs have higher (M41L, T215Rev and K219E/N/Q/R for NRTIs and K101E/P for the NNRTIs) or lower transmissibility (K70E/R, L74I/V, and T215Y/F for NRTIs; Y181C/I/V for NNRTIs and I84 V and I54A/L/M/S/T/V for protease inhibit
HIV-1 subtype characteristics of infected persons living in southwestern Greece.
Result: The 22 cases experiencing virologic failure presented with the following DRMs: M46I, F53LY, I54LTV, G73ST, L76V, V82AT, I84V, I185V, N88D, and L90M for PIs; L100I, K103NS, V179F Y181C, G190AS, V106A, K103N, and P225H for NNRTIs; and
Structural studies on molecular mechanisms of Nelfinavir resistance caused by non-active site mutation V77I in HIV-1 protease.
Introduction: L23I, D30N, E35G, M46I/L/V, G48V, I54L, G73S/T/C/A, T74S, V82A/F/S/T, I84V, N88D/S and L90M are other mutations correlated to NFV resistance.
Introduction: The other mutations which were co-occurring with DBM and TPM included major mutations like- M46IL, I54MV, I84V, L90M, N88S, V32I, PMID: 26397743
2015
Journal of molecular graphics & modelling
Method: Plasmid DNA encoding PR (subtype B of group M) with 20 mutations Q7K; L10F; I13V; I15V; D30N; V32I; L33F; E35D; M36I; S37N; I47V; I54L; Q58E; I62V; L63P; A71V; I84V; N88D; L89T and L90M (termed PR20) cloned between the Nde1 and BamH1 sites
HIV mutation literature information.
PMID: 
2015
Journal of chemical information and modeling
Browser Board
Co-occurred Entities
Filtrator
ViMRT