Prevalence and virologic consequences of HIV-1 genotype mutations detected in a cohort of 161 Italian patients receiving a nelfinavir-based highly active antiretroviral therapy.
PMID: 12797395
2003
Journal of chemotherapy (Florence, Italy)
Abstract: In our HIV-infected population receiving a nelfinavir-based HAART, the D30N mutation has shown a low absolute frequency, while the detection of M184V substitution and the simultaneous occurrence of M184V, T215Y and K103N mutations were related to a more favorable virological response.
Abstract: On the whole, only 11 patients (7%) developed the D30N substitution, whose 6 was in association with the N88D mutation.
Patterns of point mutations associated with antiretroviral drug treatment failure in CRF01_AE (subtype E) infection differ from subtype B infection.
PMID: 12843744
2003
Journal of acquired immune deficiency syndromes (1999)
Abstract: The mutations, D30N, A71V, and N88D were found exclusively in patients with subtype B.
Parameters driving the selection of nelfinavir-resistant human immunodeficiency virus type 1 variants.
Abstract: Emergence of secondary mutations further increased the selective advantage of viruses harboring D30N.
Abstract: The advantage of the D30N mutant was mostly due to its resistance level, while the L90M mutation allowed preservation of infectivity coupled with minimal resistance.
Abstract: We investigated the parameters driving nelfinavir resistance, along the D30N and L90M evolutionary pathways.
Novel enzyme-linked minisequence assay for genotypic analysis of human immunodeficiency virus type 1 drug resistance.
PMID: 14605126
2003
Journal of clinical microbiology
Abstract: ELMA is a combination of hybridization and a 1-base extension reaction, and we designed the assay to detect five mutations conferring nucleoside analogue resistance (M41L, D67N, K70R, T215Y, and M184V) and six mutations conferring protease inhibitor resistance (D30N, M46I, G48V, V82A, I84V, and L90M).
Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.
Abstract: Our study shows that the M36I and A71V mutations provide a greater level of inhibitor cross-resistance combined with active site mutation D30N.
Abstract: The double mutants containing a combination of mutations D30N, M36I, and A71V displayed -0.5-fold to +6-fold changes in the K(i) of all inhibitors tested, with ritonavir and nelfinavir most affected.
Abstract: The variant containing mutation D30N displayed a 2-6-fold increase in K(i) for all inhibitors tested, with nelfinavir showing the greatest increase.
Abstract: We engineered protease mutants containing the active site mutation D30N alone and with the nonactive site polymorphisms PMID: 11748652
2002
Journal of medical virology
Abstract: However, some mutations detectable in some tissues were not seen in plasma (e.g., M46I and D30N in the protease).
Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.
PMID: 11850252
2002
Antimicrobial agents and chemotherapy
Abstract: L90M caused little impairment of the cleavage activities, but D30N was detrimental, although significant residual activity was observed.
Abstract: Among patients with nelfinavir treatment failure, we found that D30N acquisition was strongly suppressed when L90M preexisted.
Abstract: In contrast, D30N/L90M demonstrated severe impairment.
Abstract: In the disease course, the D30N and L90M clones readily evolved independently of each other, and later the D30N/L90M double mutants emerged.
Abstract: Supporting this notion, the D30N/L90M mutation was al
Evolution of primary protease inhibitor resistance mutations during protease inhibitor salvage therapy.
PMID: 11897594
2002
Antimicrobial agents and chemotherapy
Abstract: D30N persisted less frequently than L90M (50% versus 100%, respectively; P < 0.001) and V82A/F/T (50% versus 81%, respectively; P = 0.05).
Abstract: Among 78 patients meeting study selection criteria, baseline primary PI resistance mutations included L90M (42% of patients), V82A/F/T (27%), D30N (21%), G48V (6%), and I84V (4%).
Rapid and sensitive oligonucleotide ligation assay for detection of mutations in human immunodeficiency virus type 1 associated with high-level resistance to protease inhibitors.
PMID: 11923366
2002
Journal of clinical microbiology
Abstract: Oligonucleotides were designed to detect primary mutations associated with high-level resistance to amprenavir, nelfinavir, indinavir, ritonavir, saquinavir, and lopinavir, including amino acid substitutions D30N, I50V, V82A/S/T, I84V, N88D, and L90M.
Combining mutations in HIV-1 protease to understand mechanisms of resistance.
Abstract: D30N/V82S mutant showed lower stability than either of the two individual mutations, which is possibly due to concerted changes in the central P2-P2' and S2-S2' sites.
Abstract: Four double mutants, K45I/L90M, K45I/V82S, D30N/V82S, and N88D/L90M were selected for analysis on the basis of observations of increased or decreased stability or enzymatic activity for the respective single mutants.
Abstract: Mutations D30N, K45I, and V82S showed altered interactions with inhibitor residues at P2/P2', P3/P3'/P4/P4', and P1/P1', respective
HIV mutation literature information.
PMID: 
2003
Journal of chemotherapy (Florence, Italy)
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