Abstract: This variant possessed the ritonavir-resistance-associated mutations in the active-site (V32I and V82A) and nonactive-site mutations (K20R, L33F, M36I, L63P, A71V, and L90M).
Alternative, age- and viral load-related routes of nelfinavir resistance in human immunodeficiency virus type 1-infected children receiving highly active antiretroviral therapy.
PMID: 15545865
2004
The Pediatric infectious disease journal
Abstract: The prevalence of L90M was similar to that of D30N.
Abstract: There was a significant correlation with a higher viral load and lower age and the occurrence of L90M.
Clinically relevant interpretation of genotype and relationship to plasma drug concentrations for resistance to saquinavir-ritonavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients.
PMID: 15561845
2004
Antimicrobial agents and chemotherapy
Abstract: Adjusted in a multivariate analysis, taking into account all the confounding factors, such as the nucleoside used, five mutations were combined in a resistance score associated with a reduced virological response to an SQV-plus-RTV regimen: L24I, I62V, V82A/F/T/S, I84V, and L90IM.
A major role for a set of non-active site mutations in the development of HIV-1 protease drug resistance.
Abstract: This mutant protease contains 11 mutations, 10 of which are located outside the active site (L10I/M36I/S37D/M46I/R57K/L63P/A71V/G73S/L90M/I93L) and 1 within the active site (I84V).
Drug resistance mutations and outcome of second-line treatment in patients with first-line protease inhibitor failure on nelfinavir-containing HAART.
Abstract: CONCLUSION: In patients failing nelfinavir-containing HAART, D30N was detected frequently and L90M occasionally.
Abstract: Ten patients had D30N (38%), five patients had L90M (19%), two patients had V82A/F (8%) and two patients had M46I/L (8%).
Abstract: Two patients had both D30N and L90M.
HIV-1 reverse transcriptase and protease resistance mutations selected during 16-72 weeks of therapy in isolates from antiretroviral therapy-experienced patients receiving abacavir/efavirenz/amprenavir in the CNA2007 study.
Abstract: Mutations D30N, G48V, N88D/S, L90M and 154V were de-selected, and mutations I50V, I or V to 54M/L, I84V, M46I/L, L33F, I47V as well mutations at position 10 were observed in 20/49 (41%) isolates.
Elucidation of HIV-1 protease resistance by characterization of interaction kinetics between inhibitors and enzyme variants.
Abstract: The kinetics of the interaction between drug-resistant variants of HIV-1 protease (G48V, V82A, L90M, I84V/L90M, and G48V/V82A/I84V/L90M) and clinically used inhibitors (amprenavir, indinavir, nelfinavir, ritonavir, and saquinavir) were determined using biosensor technology.
Natural polymorphisms of protease in protease inhibitor-naive HIV-1 infected patients in Korea: a novel L63M in subtype B.
PMID: 12892062
2003
AIDS research and human retroviruses
Abstract: One patient (2.3%) harbored a primary resistance-conferring mutation, L90M along with L63P and A71V, and all 43 strains showed some secondary associated with drug resistance.
Quality control trial for human immunodeficiency virus type 1 drug resistance testing using clinical samples reveals problems with detecting minority species and interpretation of test results.
PMID: 12904355
2003
Journal of clinical microbiology
Abstract: resistant minorities of L90M in the protease, which were determined to about 12% by real-time amplification, were only detected by one-fourth of the participants; (ii).
Parameters driving the selection of nelfinavir-resistant human immunodeficiency virus type 1 variants.
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.
HIV mutation literature information.
PMID: 
2004
Biochemistry
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