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: One of the conformations of Met90 in K45I/L90M has an unfavorably close contact with the carbonyl oxygen of Asp25, as observed previously in the L90M single mutant.
Longitudinal use of a line probe assay for human immunodeficiency virus type 1 protease predicts phenotypic resistance and clinical progression in patients failing highly active antiretroviral therapy.
PMID: 12019110
2002
Antimicrobial agents and chemotherapy
Abstract: Combinations of protease mutations (M46I, G48V, I54V, V82A or -F, I84V, and L90M) predicted phenotypic resistance to the protease inhibitor and to nelfinavir.
Genetic variation of the protease and reverse transcriptase genes in HIV-1 CRF04_cpx strains.
PMID: 12079565
2002
AIDS research and human retroviruses
Abstract: Substitutions classically associated with resistance to antiretroviral drugs were observed in six of seven samples, including G48V, V82A, L90M, M46I in the protease protein, and K70R, D69D/N, M184V, T215F, K103N in the reverse transcriptase protein.
Prevalence of mutations related to HIV-1 antiretroviral resistance in Brazilian patients failing HAART.
Abstract: The greatest increase in Ki was generally observed for the 184V mutant and least for the G48V/L90M mutant, and additional combinations of mutations did not result in improved inhibition profiles for the cyclic compounds.
Abstract: The overall structure-inhibitory profiles of the cyclic compounds were similar, and the inhibition of the V82A, 184V and G48V/L90M mutants were less efficient than of the wild-type enzyme.
Abstract: To allow a detailed structure-inhibition analysis, enzyme with single, double, triple and quadruple combinations of G48V, V82A, 184V and L90M substitutions was used.
Prevalence of HIV protease mutations on failure of nelfinavir-containing HAART: a retrospective analysis of four clinical studies and two observational cohorts.
Abstract: Although D30N confers little or no cross-resistance to other protease inhibitors (PIs) and has been shown to allow effective substitution of a second PI, L90M with secondary mutations is involved in broad cross-resistance to the class.
Abstract: Although L90M has been observed rarely to date under nelfinavir selection, data on the relative incidence of these two mutations on failure of first-line nelfinavir HAART are sparse.
Abstract: BACKGROUND: Both D30N and L90M in HIV-1 protease are primary resistance mutations that emerge under nelfinavir drug pressure.
Impact of human immunodeficiency virus type 1 subtypes on virologic response and emergence of drug resistance among children in the Paediatric European Network for Treatment of AIDS (PENTA) 5 trial.
PMID: 12195348
2002
The Journal of infectious diseases
Abstract: No differences were observed in the frequency of development of resistance mutations L90M (P=1.00) and D30N (P=.61) in B and non-B viruses.
Resistance mutations in HIV-infected patients experiencing early failure with nelfinavir-containing triple combinations.
Abstract: All six individuals harbored the D30N mutation, and none presented the L90M mutation.
Abstract: The D30N substitution, rather than L90M, is the most frequently recognized, which does not challenge the efficacy of further rescue interventions with other PIs.
Rapid phenotypic assay for human immunodeficiency virus type 1 protease using in vitro translation.
PMID: 12367727
2002
Journal of virological methods
Abstract: Three drug-resistant proteases carrying a single mutation, D30N, L90M, and V82F, were analyzed in the absence of the inhibitors.
HIV mutation literature information.
PMID: 
2002
Proteins
Browser Board
Co-occurred Entities
Filtrator
ViMRT