Result: One individual that was infected through homosexual contact, exhibited a high level of resistance to nelfinavir with ritonavir (NFV/r) with a D30N mutation and conferred intermediate resistance to all nucleoside reverse transcriptase inhibitors (NRTIs) with T69ins.
Table: D30N
Increasing trends in primary NNRTI resistance among newly HIV-1-diagnosed individuals in Buenos Aires, Argentina.
PMID: 24093951
2013
Journal of the International AIDS Society
Method: Sequences were analyzed to identify mutations associated with reduced susceptibility to protease and RT inhibitors, as reported by the International AIDS Society-USA in 2010: RT-M41L, A62V, K65R, D67N, 69 insert, K70R, L74V,V75I, F77L, L100I, K101P, K103N, V106A, V106M, V108I, Y115F, F116Y,
Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
Discussion: In addition, mutation frequencies in A/AE-infected patients genotyped prior to 2001, who were initially given mono- or 2-drug therapy, were similar to those found in the general B-population, except that D30N was not found in any of the 9 A/AE patients failing NFV while it was found in 23% of B-patients failing this drug.
Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.
Method: The following resistance mutations were scored: to nucleoside reverse transcriptase inhibitors (NRTIs): M41L, K65R, D67N/G/E, T69D/insertion, K70R/E, L74V/I, V75M/T/A/S, F77L, Y115F, F116Y, Q151M, M184V/I, L210W, T215Y/F/I/S/C/D/V/E, K219Q/EN/R; to non-nucleoside revers
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
Virologic failures on initial boosted-PI regimen infrequently possess low-level variants with major PI resistance mutations by ultra-deep sequencing.
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:
Potent antiviral HIV-1 protease inhibitor GRL-02031 adapts to the structures of drug resistant mutants with its P1'-pyrrolidinone ring.
PMID: 22401672
2012
Journal of medicinal chemistry
Introduction: However, N88D is common in association with D30N, which exerts a synergistic effect on resistance to NFV, and the double mutant shows 260-fold increased Ki value for NFV compared to wild-type.
Discussion: Moreover, D30N is one of the major mutations associated with NFV resistance.
Discussion: The dynamic side chain position of Asp30 has been observed in various D30N single mutants and double mutants such as D30N/N88D and D30N/N88S.
Prevalence of HIV Drug Resistance Mutations in HIV Type 1 Isolates in Antiretroviral Therapy Naive Population from Northern India.
Abstract: One patient had a major RT mutation M184V, known to confer resistance to lamivudine, and another had a major protease inhibitor (PI) mutation D30N that imparts resistance to nelfinavir.
Result: One patient (1.47%) had RT mutation, M184V that imparts resistance to NRTIs, lamivudine, and emtricitabine, and another (1.47%) had a major PI mutation, D30N, conferring resistance to nelfinavir.
Discussion: One participant (1.5%) in our study had a major PI mutation, D30N, in the protease gene.
HIV-1 protease with 20 mutations exhibits extreme resistance to clinical inhibitors through coordinated structural rearrangements.
Result: D30N is the only mutation of a charged first shell residue in PR20 and second shell mutation N88D may compensate for the altered charge.
Result: Also, in vitro studies show that combining the two mutations D30N and L90M results in PR that exhibits high levels of resistance to nelfinavir.
Result: Analysis of mutation patterns in eight thousand and sixty virus isolates reveals that N88D is positively associated with D30N, and facilitates the occurrence of major resistance mutations D30N and L90M resulting in multidrug resistance.
ViMRT
HIV mutation literature information.
PMID: 
2013
The Journal of infectious diseases
