Abstract: We identified a patient who possessed a protease (PR) inhibitor-resistant HIV-1 with a major mutation consisting of L90M before the initiation of therapy.
Lack of persistent drug-resistant mutations evaluated within and between treatment interruptions in chronically HIV-1-infected patients.
Abstract: In the remaining six patients, the following patterns of mutations associated with viral resistance were found: one mutation (K70R), which was observed in one patient during the 1st TI and persisted during follow-up; two mutations (L90M, M184V), which were observed in four patients during the 1st TI and were intermittently present or lost following extended TI, treatment reinitiation and/or during subsequent TI; and evolution of two mutations (M184V, K219E) observed in two patients.
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).
Multidrug resistance to HIV-1 protease inhibition requires cooperative coupling between distal mutations.
Abstract: A mutant containing only the four active site mutations (V82A/I84V/M46I/I54V) only showed a small cooperative effect, suggesting that the mutations at the dimer interface (L10I/L90M) play a major role in eliciting a cooperative response.
Abstract: This mutant (MDR-HM) contains six amino acid mutations (L10I/M46I/I54V/V82A/I84V/L90M) located within and outside the active site of the enzyme.
Abstract: To understand the origin of resistance, three submutants containing mutations in specific regions were also studied, i.e., the active site (
Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.
PMID: 14624368
2003
The Journal of infectious diseases
Abstract: In 14 of 25 and in 3 of 25 subjects, the M184V and the L90M mutations, respectively, were detected as minor populations, at different times during STI.
Abstract: Minor populations of drug-resistant variants were detected by quantitative real-time polymerase chain reaction, by use of allele-discriminating oligonucleotides for 2 key resistance mutations: L90M (protease) and M184V (reverse transcriptase).
Plasma drug levels, genotypic resistance, and virological response to a nelfinavir plus saquinavir-containing regimen.
Abstract: A higher number of mutations in the protease gene (12 versus 8;P = 0.001), and the L90M mutation (36% versus 67%; P = 0.001) were associated with treatment failure.
Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.
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%).
Abstract: HIV-1 isolates from 38 (49%) patients failing PI salvage therapy developed new primary PI resistance mutations including L90M, I84V, V82A,
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.
Evolution of human immunodeficiency virus type 1 populations after resumption of therapy following treatment interruption and shift in resistance genotype.
PMID: 11992288
2002
The Journal of infectious diseases
Abstract: Sixty-two percent of patients in whom the V82A and L90M protease mutations were no longer detectable by conventional genotyping still harbored minority resistant variants, in proportions ranging from 0.1% to 21%.
HIV mutation literature information.
PMID: 
2003
Microbiology and immunology
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