Abstract: The most common UDS-detected DRM were NRTI in 18 subjects: M184V/I (11), TAMs(7) & K65R(4); PI DRMs were detected in 9 subjects: M46I/V(5), F53L(2), I50V(1), D30N(1), and N88S(1).
Result: Nineteen of 24 (79.2%) had any PI, N(t)RTI and/or NNRTI resistance mutations; 18/24 (75%) had N(t)RTI mutations: M184V/I (11), TAMs(7) and K65R (4), and 9/24 (37.5%) had PI mutations:
Interaction of I50V mutant and I50L/A71V double mutant HIV-protease with inhibitor TMC114 (darunavir): molecular dynamics simulation and binding free energy studies.
PMID: 22239286
2012
The journal of physical chemistry. B
Introduction: As for other approved PIs, several HIV-pr mutants were demonstrated to have drug resistance over the TMC114, like D30N and I50V, whereas L90M is well adapted by the TMC114.
Introduction: It was found that loss of H-bonds between Asp30 and TMC114 drives the drug resistance in D30N, whereas for I50V it is the increased polar solvation energies for the two residues Asp30' and Val50'.
Introduction: The drug resistance mechanism of such mutants was explored at the molecular level with all-atomistic MD simulation combined with molecular mechanics-Poisson/Boltzmann surface area (MM-PBSA) for the binding energies of TMC114 to D30N
RNA interference as a tool for exploring HIV-1 robustness.
Abstract: Importantly, the addition of a second-generation siRNA that matched the D30N mutation restored viral inhibition and delayed development of escape variants.
Abstract: Passages performed with both siRNAs prevented the emergence of the D30N escape mutant and forced the virus to develop new escape routes.
Abstract: The most common escape route was the D30N mutation.
The HIV type 1 protease L10I minor mutation decreases replication capacity and confers resistance to protease inhibitors.
PMID: 21142921
2011
AIDS research and human retroviruses
Abstract: Furthermore, viruses carrying the major mutation D30N or the minor mutation L10I showed a significant decrease in RC (p-value <0.05), whereas viruses carrying the minor mutation L63P had RC similar to wild-type virus.
Abstract: The prevalence of the minor mutation L10I had a pattern similar to that found for major mutations D30N, with a low prevalence (4.9%) in naive patients and significantly higher prevalence in treated patients.
Abstract: We characterized the HIV protease minor mutations, L10I, compared to the minor mutation, L63P, and the major mutation D30N and their impact on viral fitness and resistance to protease inhibitor
Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.
Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N, T69D/N, L210W, K219Q/E in RT and L10I/V, L63P, A71V/T, V77I in PR)
Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.
Abstract: Among these, we focused on associations between Gag-P453L, the P5' position of the p1/p6 cleavage-site mutation, and PR-D30N/N88D nelfinavir-resistant mutations, and attempted to clarify their virological significance in vitro by constructing recombinant clones.
Abstract: Furthermore, database analysis indicated that the P453L(Gag)/D30N(PR)/N88D(PR) association was not specific only to our clinical case, but was common among AIDS patients.
Abstract: Homology modeling analysis suggested that hydrogen bonds between the
Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.
PMID: 21537677
2011
Memorias do Instituto Oswaldo Cruz
Abstract: D30N also suppresses indinavir (IDV) resistance caused by the M46I mutation.
Abstract: Interestingly, in patients with viruses originally containing the D30N mutation who were treated with IDV or SQV, the virus either reversed this mutation or acquired N88D, suggesting an antagonistic effect of D30N upon exposure to these PIs.
Abstract: The human immunodeficiency virus type 1 (HIV-1) protease mutation D30N is exclusively selected by the protease inhibitor (PI) nelfinavir and confers resistance to this drug.
Abstract: We demonstrate that D30N increases the susceptibility to saquinavir (S
Selection of HIV resistance associated with antiretroviral therapy initiated due to pregnancy and suspended postpartum.
PMID: 21765365
2011
Journal of acquired immune deficiency syndromes (1999)
Method: An OLA was performed on all amplicons derived from plasma and PBMC using probes that detect mutations associated with high-level drug-resistance to NFV, codons D30N (AAT) and L90M (ATG), nucleoside reverse transcriptase inhibitors (NRTI) at codons K70R (AGA), M184V (GTG), and T215F/Y (TTC, TAC), and non-nucleoside reverse transcriptase inhibitors (NNRTI) at codons K103N (AAC), Y181C (TGT), and G190A (GCA) as described.
Structural and energetic analysis on the complexes of clinically isolated subtype C HIV-1 proteases and approved inhibitors by molecular dynamics simulation.
PMID: 20055526
2010
The journal of physical chemistry. B
Abstract: The effect of the V82I mutation on the association with chemicals and the reason for rare appearance of the D30N mutation in subtype C HIV-1 were discussed in terms of the change of geometry of the residues in HIV-1 protease.
HIV drug resistance surveillance using pooled pyrosequencing.
HIV mutation literature information.
PMID: 
2012
PloS one
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