Abstract: CONCLUSIONS: The major IN mutations E92Q, Q148K/R/H, N155H and E157Q (implicated in the resistance of IN inhibitors RAL and EVG) are highly conserved between subtypes B and CRF02_AG and display a similar genetic barrier.
Virological and immunological response in HIV-1-infected patients with multiple treatment failures receiving raltegravir and optimized background therapy, ANRS CO3 Aquitaine Cohort.
PMID: 19336453
2009
The Journal of antimicrobial chemotherapy
Abstract: Raltegravir-related mutations emerged in 9 of 11 failing patients (82%): Q148H/R (n = 5), N155S/H (n = 3) and S230N (n = 1).
Evolution of raltegravir resistance during therapy.
PMID: 19447792
2009
The Journal of antimicrobial chemotherapy
Abstract: The Q148R/H was detected only in subtype B.
Abstract: The Q148R/H was mostly detected after short exposure to raltegravir, while the Y143R was observed only after prolonged raltegravir exposure.
Abstract: The primary mutations N155H, Q148R/H or Q143R were observed during raltegravir therapy.
Abstract: We detected an association between the presence of the T206S in the baseline genotype and the absence of the primary Q148R/H mutation or any secondary mutation accompanying the N155H following raltegravir failure.
Selective-advantage profile of human immunodeficiency virus type 1 integrase mutants explains in vivo evolution of raltegravir resistance genotypes.
Abstract: After prolonged viral escape, mutants of the N155H pathway are replaced by mutants of the Q148HKR pathway.
Abstract: Among double mutants, the highest and widest selective-advantage profile was seen with G140S+Q148H.
Abstract: Despite the higher 50% inhibitory concentration, Q148H displayed a lower and narrower (10 to 100 nM) selective-advantage profile.
Abstract: The emergence of human immunodeficiency virus type 1 resistance to raltegravir, an integrase strand transfer inhibitor, follows distinct and independent genetic pathways, among which the N155H and Q148HKR pathways are the most frequently encountered in treated patients.
Abstract: This finding
HIV-1 IN alternative molecular recognition of DNA induced by raltegravir resistance mutations.
PMID: 19623602
2009
Journal of molecular recognition
Abstract: Virologic failure during treatment with raltegravir, the first effective drug targeting HIV integrase, is associated with two exclusive pathways involving either Q148H/R/K, G140S/A or N155H mutations.
Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.
Result: Of the 38 major and minor integrase inhibitor resistance associated codons, 44, 61, 66, 92, 121, 140, 143, 147, 148, 155, 226 and 263 were the only positions absolutely conserved across all 342 sequences and these included six primary resistance-associated mutations for raltegravir and elvitegravir (T66I
Discussion: In this population-based review of all sites associated with integrase inhibitor resistance in 342 natural isolates of HIV-1 obtained from two geographically distinct cohorts in Switzerland and Australia, we observed that the primary raltegravir and elvitegravir resistance mutations T66I, E92Q, G140S, Y143C/H/R, Q148H/R/K and N155H were absent.
The use of integrase inhibitors in treatment-experienced patients.
PMID: 19959414
2009
European journal of medical research
Abstract: Tolerance was remarkably good and virological failure was often associated with selection of integrase gene resistance mutations following the Y143C/H/R, Q148H/K/R o less frequently the NI55H paths.
Introduction: A genotypic resistance test could be performed in 38 of these patients of whom 35 selected resistance mutations in the integrase gene following the N155H or the Q148H/R/K path almost always associated with one additional mutation.
Introduction: Overall, by week 96 resistance tests were available for 112 raltegravir treated patients of whom 73% had integrase mutations at one of the three positions (Y143C/H/R,
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.
Mutations associated with failure of raltegravir treatment affect integrase sensitivity to the inhibitor in vitro.
PMID: 18227187
2008
Antimicrobial agents and chemotherapy
Abstract: All the mutations identified altered the activities of integrase protein: both 3' processing and strand transfer activities were moderately affected in the E92Q mutant; strand transfer was markedly impaired in the N155H mutant; both activities were strongly impaired in the G140S Q148H mutant; and the E157Q mutant was almost completely inactive.
Abstract: At least four genetic profiles (E92Q, G140S Q148H, N155H, and E157Q) can be associated with in vivo treatment failure and resistance to raltegravir.
Abstract: Four different mutation profiles were identified in these nine patients
HIV mutation literature information.
PMID: 
2009
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