Abstract: The development of resistance to raltegravir mainly involved three resistance mutations in integrase gene: Q148H/K/R, N155H, and Y143C/H/R.
Discussion: However, 39 (29%) of the patients in the raltegravir arm of the EASIER study displayed at least one episode of low-level viremia on treatment and significant integrase resistance-associated mutations were detected in three subject (7.7%), including N155H in two subjects and P145S in one subject.
Discussion: Indeed, the level of phenotypic resistance to raltegravir associated with N155H is always much lower than that associated with Q148 or Y143 mutation (>100 times higher).
Discussion: Moreover, the characterizat
The G140S mutation in HIV integrases from raltegravir-resistant patients rescues catalytic defect due to the resistance Q148H mutation.
Introduction: Finally, we found that the G140S/Q148H mutant was much more resistant than the N155H mutant.
Introduction: We investigated the impact of the two main genetic resistance pathways (N155H and G140S/Q148H), on viral replication and the catalytic properties of recombinant INs.
Method: In parallel, the E92Q, G140S, Q148H, N155H and G140S/Q148H mutations were obtained by site-directed mutagenesis from pET-15b, containing the WT sequence.
Method: We studied the E92Q, PMID: 19165083
2009
AIDS (London, England)
Abstract: RESULTS: : Resistance to RAL appeared initially associated with selection of single variants (Y143R, Q148R N155H) in the majority of patients; however, in three patients, complex patterns of viral mutations were observed.
HIV-1 integrase polymorphisms are associated with prior antiretroviral drug exposure.
Introduction: These occur in one of two main pathways, either N155H or Q148H/K/R.
Introduction: We are aware of possibly two additional isolates, one from an Australian isolate bearing N155H in an INI-naive patient.
Introduction: in their review of the Stanford HIV Database in only 3 isolates (each with a single primary INI mutation N155H, Q148H and Q148K).
Quasispecies variant dynamics during emergence of resistance to raltegravir in HIV-1-infected patients.
PMID: 19221102
2009
The Journal of antimicrobial chemotherapy
Abstract: In most patients, raltegravir failure is associated with mutations in the IN gene, through two different genetic pathways: 155 (N155H) or 148 (Q148K/R/H).
Abstract: In the two patients switching from the 155 to the 148 pathway, clonal analysis showed that Q148R/H and N155H mutations were present on different strands, suggesting that these two pathways are independent.
Abstract: We observed a greater variability among quasispecies associated with the 155 pathway, and IC(50) determinations showed that the fold resistance to raltegravir, relative to wild-type, was 10 for the N155H mutant and 50 for the G140S+Q148H mutant.
Lack of primary mutations associated with integrase inhibitors among HIV-1 subtypes B, C, and F circulating in Brazil.
PMID: 19262402
2009
Journal of acquired immune deficiency syndromes (1999)
Abstract: Major mutations associated with elvitegravir or raltegravir in vivo resistance (Q148K/H/R, N155H) were not detected.
Characterization and structural analysis of HIV-1 integrase conservation.
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 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.
HIV mutation literature information.
PMID: 
2010
Infection and drug resistance
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