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: 16472877 2006 Antiviral research

Abstract: Results demonstrate that HIV-1 variants selected at increasing CPV concentrations contained multiple substitutions in diverse patterns including L100I, Y181C, G190E and/or L234I in various combinations with K101R/E, K103T, V106A/I, V108I, E138K, T139K, A158T, V179D/I/G, Y188D, V189I, G190A, F227C, W229R, L234F,

The development of drug resistance mutations K103N Y181C and G190A in long term Nevirapine-containing antiviral therapy.

PMID: 16504235 2006 Virology

Abstract: In the absence of efavirenz, the fitness hierarchy was G190S < G190A < K103N < wild-type.

Abstract: We evaluated the replication efficiency of the HIV reverse transcriptase (RT) mutants K103N, G190A, and G190S, which confer resistance to the non-nucleoside RT inhibitor efavirenz, using growth competition assays in cell culture.

Phenotypic drug resistance patterns in subtype A HIV-1 clones with nonnucleoside reverse transcriptase resistance mutations.

PMID: 16545016 2006 AIDS research and human retroviruses

1Abstract: Six clones had no NNRTI resistance-associated mutations (""wild type""), eight had K103N, nine had Y181C, five had G190A, and one had Y181S."

Abstract: One wild-type clone had reduced susceptibility to NVP, delavirdine (DLV), and efavirenz (EFV), one clone with K103N was susceptible to all three NNRTIs, and one clone with G190A had extreme hypersusceptibility to DLV.

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: All ten samples with the M184V mutation, three with the K65R, two with the G190A mutation, one with the K103N mutation, and one with the V75T mutation were detected similarly by all three assays.

Characterization of mutations in CRF01_AE virus isolates from antiretroviral treatment-naive and -experienced patients in Singapore.

PMID: 15608517 2005 Journal of acquired immune deficiency syndromes (1999)

Abstract: There were differences between CRF01_AE and subtype B viruses in several drug resistance mutations including the following: D67N, L210F, K101E, V106M, V179I/D, G190A/S/E, and G48V (which were more common in CRF01_AE virus) and M41L, T215Y, and V82A (which were less common in CRF01_AE virus).

Emergence of antiretroviral resistance in HIV-positive women receiving combination antiretroviral therapy in pregnancy.

PMID: 15627034 2005 AIDS (London, England)

Abstract: Seven primary mutations, V106A (one), Y181C (two), G190A (one), K101E (one), M184V (one), T215S (one) were detected in five (13%) women.

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 ITINN K103N (25.8%), Y181C (11.2%) and G190A (10.9%).

4-Benzyl and 4-benzoyl-3-dimethylaminopyridin-2(1H)-ones: in vitro evaluation of new C-3-amino-substituted and C-5,6-alkyl-substituted analogues against clinically important HIV mutant strains.

PMID: 15771439 2005 Journal of medicinal chemistry

Abstract: When tested further, it was shown that these molecules, and in particular compound 35, are globally more active than 9, 10, and efavirenz against an additional eight single [L100I, K101E, V106A, E138K, V179E, G190A/S, and F227C] and four double HIV mutant strains [L100I + K103N, K101E + K103N, K103N + Y181C, and F227L + V106A], which are clinically relevant.