literature

HIV mutation literature information.

A dynamic model of HIV integrase inhibition and drug resistance.

PMID: 20096702 2010 Journal of molecular biology

Result: During clinical studies of raltegravir, three pathways to resistance have been observed involving residues N155H, Q148H/K/R, and Y143C/R.

Discussion: In patients failing therapy with either raltegravir or elvitegravir, the mutations Y143R/C/H have been detected, but no mutations of H67 have been observed in patients.

Biochemical and pharmacological analyses of HIV-1 integrase flexible loop mutants resistant to raltegravir.

PMID: 20334344 2010 Biochemistry

Abstract: Resistance to raltegravir (RAL), the first HIV-1 integrase (IN) inhibitor approved by the FDA, involves three genetic pathways: IN mutations N155H, Q148H/R/K, and Y143H/R/C.

HIV-1 resistance patterns to integrase inhibitors in antiretroviral-experienced patients with virological failure on raltegravir-containing regimens.

PMID: 20388636 2010 The Journal of antimicrobial chemotherapy

Abstract: Four different patterns of IN mutations were observed: (i) emergence of Q148H/R with secondary mutations (n=5 patients); (ii) emergence of N155H, then replaced by a pattern including Y143C/H/R (n=3); (iii) selection of S230N (n=1); and (iv) no evidence of selection of IN mutations (n=2).

Abstract: The median plasma raltegravir Cmin was lower in patients with selection of the N155H mutation followed by Y143C/H/R compared with patients with Q148H/R and with patients without emerging mutations or without VF.

Abstract: The median raltegravir and elvitegravir fold changes (FCs) were 244 (154-647) and 793 (339-892), respectively,

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

Abstract: Characterization of the phenotypic evolution showed that the switch from N155H to Y143C/R was linked to an increase in resistance to RAL.

Abstract: The emergence of the N155H mutation was replaced by a pattern including the Y143R/C/H mutations in three patients with anti-HIV treatment failure.

Abstract: Wild-type (WT) IN and IN with mutations Y143C or Y143R were assayed in vitro in 3'end-processing, strand transfer and concerted integration assays.

Effect of raltegravir resistance mutations in HIV-1 integrase on viral fitness.

PMID: 20634701 2010 Journal of acquired immune deficiency syndromes (1999)

Introduction: Data from clinical trials show that RAL resistance involves IN mutations Y143C, Q148H or R or K or N155H, together with associated secondary mutations that result in higher levels of resistance.

Physical trapping of HIV-1 synaptic complex by different structural classes of integrase strand transfer inhibitors.

PMID: 20799722 2010 Biochemistry

Introduction: A third pathway having a Y143R/C mutation has been observed in a smaller patient population.

In-vitro phenotypic susceptibility of HIV-2 clinical isolates to the integrase inhibitor S/GSK1349572.

PMID: 20827161 2010 AIDS (London, England)

Abstract: We found a seven-, 13- and 18-fold increase in EC50 values to S/GSK1349572 for the HIV-2 double (T97A + Y143C; G140S + Q148R) and triple (G140T + Q148R + N155H) mutants, respectively, obtained from two raltegravir-experienced patients.

Polymorphisms of HIV-2 integrase and selection of resistance to raltegravir.

PMID: 21114823 2010 Retrovirology

Introduction: RAL resistance is not well documented for HIV-2, although cases of therapy failure have been associated with the emergence of variants carrying the Y143C, Q148K/R, or N155 H mutations, including Y143Y+T97A or Q148K, or Q148R+G140 S.

Extended use of raltegravir in the treatment of HIV-1 infection: optimizing therapy.

PMID: 21694899 2010 Infection and drug resistance

Abstract: The development of resistance to raltegravir mainly involved three resistance mutations in integrase gene: Q148H/K/R, N155H, and Y143C/H/R.

Discussion: A recent crystal structure study enabled to describe the interactions between HIV-1 integrase residue Tyr 143 and the methyloxadiazole group of raltegravir, which could explain the role of the Y143C/H/R mutations in the development of resistance to raltegravir.

Discussion: Moreover, the characterization of the phenotypic evolution showed that a switch from N155H to Y143C/R was linked to an increase in resistance to raltegravir.

HIV resistance to raltegravir.

PMID: 19959417 2009 European journal of medical research

Abstract: HIV resistance to raltegravir is the consequence of mutations located close to the integrase active site, which can be divided into three main evolutionary pathways: the N155H, the Q148R/H/K and the Y143R/C pathways.

Abstract: Resistance is frequently initiated by viruses carrying mutations of the N155H pathway, followed by emergence and further dominance of viral genomes carrying mutations of the Q148R/H/K or of the Y143R/C pathways, which express higher levels of resistance.

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