Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.
PMID: 16771502
2006
Journal of the American Chemical Society
Abstract: Exceptionally, some other mutations such as L90M cause drug resistance, although these appear at nonactive sites.
Abstract: In this study, we carried out computational simulations of L90M PR in complex with each of three kinds of inhibitors and one typical substrate, and we clarified the mechanism of resistance.
Abstract: The L90M mutation causes changes in interaction between the side chain atoms of the 90th residue and the main chain atoms of the 25th residue, and a slight dislocation of the 25th residue causes rotation of the side chain at the 84th residue.
Abstract: The difference in levels of resistance to the three inhibitors has been explained from energetic and structural viewpoints, which provides the suggestion for promising drugs keeping its efficacy even for the L90M mutant.
Linking HIV and antiretroviral drug resistance surveillance in Peru: a model for a third-generation HIV sentinel surveillance.
PMID: 16773026
2006
Journal of acquired immune deficiency syndromes (1999)
Abstract: The most frequently observed mutations in treatment-naive, chronically infected persons from Lima were M184V (1.7%), D30N (1.3%), L90M (1.3%), and L10I (1.3%).
High HIV type 1 subtype diversity and few drug resistance mutations among seropositive people detected during the 2005 second generation HIV surveillance in Madagascar.
PMID: 16796535
2006
AIDS research and human retroviruses
Abstract: According to the ANRS September 2005 DRM list and algorithm, no DRM was detected in the reverse transcriptase and only one strain bore three major DRM in the protease M46I, I84V, and L90M leading to resistance to indinavir, saquinavir, nelfinavir, atazanavir/ritonavir, and possibly lopinavir.
Temporal characterization of drug resistance associated mutations in HIV-1 protease and reverse transcriptase in patients failing antiretroviral therapy.
Abstract: From 1999 to 2003, resistance-mutations to drugs with high genetic-barrier significantly decreased (L90M/V82A/M46I/I54V/G73S/I84V/G48V for PIs; M41L/D67N/L210W/V1181 for NRTIs, p < 0.05), while mutations to drugs with low genetic-barrier increased (D30N in protease, M184V/K103N/V108I in reverse transcriptase, p < 0.05).
Virological responses to atazanavir-ritonavir-based regimens: resistance-substitutions score and pharmacokinetic parameters (Reyaphar study).
Abstract: The Reyaphar score included 12 baseline protease substitutions from the International AIDS Society USA list that were associated with poorer VR: L10I/F/R/V, K20I/M/R, L241, M461/L, 154L/M/T/V, L63P, A71I/L/V/T, G73A/C/F/T, V771, V82A/F/S/T, 184V, L90M and the polymorphism substitution Q58E.
Antiretroviral resistance in viral isolates from HIV-1-transmitting mothers and their infants.
Abstract: CONCLUSION: This functional assay allowed us to show for the first time that the L90M substitution, present in a primary HIV-2 isolate, modifies the HIV-2 Protease susceptibility to Saquinavir but not Lopinavir.
Method: The L90M mutant was constructed by PCR using the primers Fwd and 3-90LM.
Result: Among the 9 mutations observed in the MRT-8 Protease (4 conservative and 5 non-conservative), we focused on the 90th residue since the L90M substitution has already been classified as a major mutation in HIV-1 which confers resistance to SQV and LPV, and has been suggested to be associated with resistance to a yet undefined PI in HIV-2 Protease.
Result: The HIV-2ROD Protease was mutated and th
Quantitative SNP-detection method for estimating HIV-1 replicative fitness: application to protease inhibitor-resistant viruses.
Abstract: Almost identical results were obtained for L90M-mutated HIV-1 with or without saquinavir.
Abstract: HIV-1 can survive under indinavir pressure by acquiring M46I mutation, as with acquisition of the L90M mutation under saquinavir pressure.
Antiretroviral drug-resistant HIV-2 infection--a new therapeutic dilemma.
PMID: 17062187
2006
International journal of STD & AIDS
Abstract: Mutations at codons M184V and Q151M conferring resistance to nucleoside reverse transcriptase inhibitors (NRTIs) in HIV-1 infection were detected, as were mutations at codons V71I and L90M implying indinavir and nelfinavir resistance as well.
Rapid propagation of low-fitness drug-resistant mutants of human immunodeficiency virus type 1 by a streptococcal metabolite sparsomycin.
Abstract: In addition to wild-type HIV-1, sparsomycin also accelerated the replication of low-fitness, drug-resistant mutants carrying either D30N or L90M within HIV-1 protease, which are frequently found mutations in HIV-1-infected patients on highly active antiretroviral therapy (HAART).
Abstract: Of particular interest was that replication enhancement appeared profound when HIV-1 such as the L90M-carrying mutant displayed relatively slower replication kinetics.
HIV mutation literature information.
PMID: 
2006
Journal of the American Chemical Society
Browser Board
Co-occurred Entities
Filtrator
ViMRT