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.
Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.
PMID: 17209774
2006
AIDS research and human retroviruses
Abstract: In 16 patients having isolates with more than one combination of mutations at positions 30, 88, and 90, all exhibited one of the steps in the following progression: D30N-->D30N+N88D-->D30N+N88D+L90M-->D30N+N88D+L90M+(L33F+/-I84V or M46I/L+/-I54V).
Abstract: Second, D30N and L90M were negatively associated except in the presence of N88D, which facilitated the co-occurrence of D30N and L90M.
Abstract: Mutagenetic trees constructed form this cross-sectional data showed an ordered accumulation of the most prominent CS mutations along two pathways L90M-I84V-P453L and I54-V82-A431V followed by either M46L or L24I.
Performance of drug-resistance genotypic assays among HIV-1 infected patients with predominantly CRF02_AG strains of HIV-1 in Abidjan, Cote d'Ivoire.
Abstract: RESULTS: Major drug resistance mutations (protease: L90M; reverse transcriptase: M41L, K103N, V106M, M184V, Y181S, G190A, L210W, T215Y/F, and K219R) were detected in 1 subject with A subtype, 3 with subtype B, and 9 with subtype C.
[Study of resistance using the TRUGENE HIV-1 genotyping system and analysis of agreement between rule-based algorithms and virtual phenotyping].
PMID: 15757587
2005
Enfermedades infecciosas y microbiologia clinica
Abstract: For the IP: key mutations L90M (26.1%), M46I (18.1%) and V82AFTS (12.9%); and accessory mutations L63P (50.5%), A71V (27.2%), L10I (25.2%) and M36I (19.2%).
Novel human immunodeficiency virus type 1 protease mutations potentially involved in resistance to protease inhibitors.
PMID: 15855527
2005
Antimicrobial agents and chemotherapy
Abstract: K45R and K20T, which were associated with nelfinavir treatment, were specifically associated with D30N and N88D and with L90M, respectively.
Abstract: On the other hand, C95F, which was associated with treatment with saquinavir and indinavir, was highly expressed in clusters with either L90M and I93L or V82A and G48V.
Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.
PMID: 15871131
2005
The Journal of infectious diseases
Abstract: BACKGROUND: This work evaluates the role of subtype F human immunodeficiency virus type 1 (HIV-1) protease (PR) substitutions L89M and L90M in viral replication and resistance to PR inhibitors (PIs).
Abstract: CONCLUSION: The L89M mutation in subtype F viruses is a high genetic barrier to the accumulation of the L90M resistance mutation and can function as a resistance mutation, depending on the presence of other polymorphisms in the subtype F PR backbone.
[Genotypic resistence in patients infected with HIV and its correlation with therapy].
HIV mutation literature information.
PMID: 
2006
Antiviral chemistry & chemotherapy
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