literature

N88D facilitates the co-occurrence of D30N and L90M and the development of multidrug resistance in HIV type 1 protease following nelfinavir treatment failure.

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: Third, D30N+

PMID: 17302250 2006 Antiviral therapy

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.

PMID: 15572008 2005 Journal of clinical virology

Abstract: For the protease gene, all three assays detected the I84V (n = 1), M46I (n = 1), and L90M (n = 1) mutations.

Drug-resistant HIV infection among drug-naive patients in Israel.

PMID: 15655750 2005 Clinical infectious diseases

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.

Low accumulation of L90M in protease from subtype F HIV-1 with resistance to protease inhibitors is caused by the L89M polymorphism.

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].

PMID: 15871775 2005 Medicina clinica

Abstract: Moreover, P mutations were detected in 59.38% of cases, being V82A, L90M and I84V the most frequent ones.

Diverse pattern of protease inhibitor resistance mutations in HIV-1 infected patients failing nelfinavir.

PMID: 15977242 2005 Journal of medical virology

Abstract: A surprisingly diverse pattern of primary PI mutations was seen: M46I (n=7), D30N (n=6), L90M (n=5), and V82A (n=4).

Treatment response and drug resistance in patients infected with HIV type 1 group O viruses.

PMID: 16060830 2005 AIDS research and human retroviruses

Abstract: One selected changes M41L, E44D, D67N, V75M, M184V, and T215Y at the RT, and G48M, F53L, I54V, V82A, and L90M at the protease.