literature

The HIV-1 integrase mutations Y143C/R are an alternative pathway for resistance to Raltegravir and impact the enzyme functions.

PMID: 20436677 2010 PloS one

Method: We followed-up the 50 mutations of resistance present at 32 positions: associated with in vitro or in vivo resistance to HIV-1 integrase inhibitors: H51Y, T66I/A/K, V72I, L74I/A/M, E92Q, T97A, T112I, F121Y, T125K, A128T, E138 K/A/D, G140R/C/H, Y143C/H/R, Q146K/P, S147G, Q148K/R/H, V151I,

PMID: 19290031 2009 AIDS reviews

Abstract: All primary signature mutations emerging in patients failing raltegravir (Y143R, Q148H/K/R, N155H) or elvitegravir (T66I, E92Q, S147G, Q148H/K/R, N155H), as well as secondary mutations (H51Y, T66A/K, E138K, G140S/A/C, Y143C/H, K160N, R166S, E170A, S230R, D232N, R263K) were complete

Resistance mutations in human immunodeficiency virus type 1 integrase selected with elvitegravir confer reduced susceptibility to a wide range of integrase inhibitors.

PMID: 18715920 2008 Journal of virology

Abstract: In addition, mutations that do not confer reduced susceptibility when present alone (H114Y, L74M, R20K, A128T, E138K, and S230R) are also discussed in relation to their position in the catalytic core domain and their proximity to known structural features of integrase.

Natural variation of HIV-1 group M integrase: implications for a new class of antiretroviral inhibitors.

PMID: 18687142 2008 Retrovirology

Result: Y226C/D/F/H, S230N/R, and D232N have been selected in vitro or in vivo by raltegravir and/or elvitegravir.

Discussion: Most accessory INI-resistance mutations including L74R, Q95K, E138A/K, H183P, Y226C/D/F/H, S230R, and D232N were also nonpolymorphic.

Development of resistance against diketo derivatives of human immunodeficiency virus type 1 by progressive accumulation of integrase mutations.

PMID: 14557631 2003 Journal of virology

Abstract: However, 3' processing and strand transfer activities of the recombinant integrases with two (T66I L74M) and three (T66I L74M S230R) mutations were notably lower than those of the wi

Abstract: The mutations T66I, L74M, and S230R emerged successively in the integrase gene.

Abstract: The virus with three mutations (T66I L74M S230R) was 10-fold less susceptible to L-708,906, while displaying the sensitivity of the wild-type virus to inhibitors of the RT or PRO or viral entry process.