literature

[Study on genotypic resistance mutations to antiretroviral drugs on HIV strains of treated and treatment-naive HIV-1 infectious patients in Hubei province].

PMID: 18396668 2007 Zhonghua liu xing bing xue za zhi

Abstract: Some protease (PR) drug-resistant mutations were found in these samples, such as D30N (2.27%), D30G (2.27%), M46I (4.55%), M46N (2.27%), I47V (4.55%), I84V (4.55%), I84L (2.27%), N88S (2.27%) and L90S (2.27%) that all belonged to major drug-resistant but A71T (29.55%) belonged to minor resistance mutations Five treated patients were detected having mutations associated RT drug resistance: M41L (5.26%), A62V (5.26%),D67N (5.26%),

PMID: 16430939 2006 Virology

Abstract: Using the chi2 test, we show a positive correlation between the nelfinavir-resistant D30N/N88D protease mutations and mutations at the p1-p6 cleavage site as compared to the other cleavage sites.

Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.

PMID: 16480273 2006 Journal of medicinal chemistry

Abstract: In PR(D30N), the inhibitor has a water-mediated interaction with the side chain of Asn30 rather than the direct interaction observed in PR, which is consistent with the relative inhibition.

Abstract: The inhibition constants (K(i)) of TMC-114 for mutants PR(D30N), PR(I50V), and PR(L90M) were 30-, 9-, and 0.14-fold, respectively, relative to wild-type PR.

Abstract: The potent new antiviral inhibitor TMC-114 (UIC-94017) of HIV-1 protease (PR) has been studied with three PR variants containing single mutations

PMID: 16527535 2006 Journal of clinical virology

Abstract: RESULTS: We cloned a set of GFP-PR reporters, some of which possess a simple, well-defined drug-resistant PR mutant (G48V L90M, V82A, A71V V82T I84V, D30N, K45I); another four complex PR mutants were obtained from patients undergoing HAART.

Trends in drug resistance mutations in antiretroviral-naive intravenous drug users of Rio de Janeiro.

PMID: 16628575 2006 Journal of medical virology

Abstract: Genotypic analysis revealed the presence of PR primary L90M, D30N, M46I, and V82A mutations in 7.9% of the post-HAART group, and a high frequency of secondary mutations (84.2%).

Impact of human immunodeficiency virus type 1 subtype C on drug resistance mutations in patients from Botswana failing a nelfinavir-containing regimen.

PMID: 16723586 2006 Antimicrobial agents and chemotherapy

Abstract: Among 16 human immunodeficiency virus-infected (subtype C) Batswana patients who failed nelfinavir (NFV)-containing regimens, the most prevalent mutation observed was D30N (54%), followed by L90M (31%).

Evidence of differential selection of HIV-1 variants carrying drug-resistant mutations in seroconverters.

PMID: 16759049 2006 Antiviral therapy

Abstract: Among the mutations not detected in viruses from SCs, the RT E44D, V1081, Q151M and Y188C/H/L, and the protease D30N, G48V and V82A/F/S/T substitutions appeared to be negatively selected.

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%).

Temporal characterization of drug resistance associated mutations in HIV-1 protease and reverse transcriptase in patients failing antiretroviral therapy.

PMID: 16841549 2006 The new microbiologica

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).

Rapid propagation of low-fitness drug-resistant mutants of human immunodeficiency virus type 1 by a streptococcal metabolite sparsomycin.

PMID: 17066895 2006 Antiviral chemistry & chemotherapy

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).