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.
The dynamics of appearance and disappearance of HIV-1 integrase mutations during and after withdrawal of raltegravir therapy.
Abstract: Mutations Q148R (2 months) followed by G140A/Q148R and then G140A/Y143CHR/Q148R/G163R were detected in the virus from one patient, and these reverted to wild type when treatment was withdrawn, although clonal analysis identified maintenance of RAL resistance minority species at this time point.
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: 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 likely explains why N155H can be selected early in the course of RAL resistance evolution in vivo but is later replaced by genotypes that include Q148HKR.
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.
Loss of raltegravir susceptibility by human immunodeficiency virus type 1 is conferred via multiple nonoverlapping genetic pathways.
Abstract: Both N155H and Q148R(H)(K) mutations reduced the replication capacity, while the addition of secondary mutations either improved or reduced the replication capacity depending on the primary mutation.
Abstract: Clonal analysis demonstrated that N155H and Q148R(H)(K) occur independently, not in combination.
Abstract: The human immunodeficiency virus type 1 (HIV-1) integrase mutations N155H and Q148R(H)(K) that reduce susceptibility to the integrase inhibitor raltegravir have been identified in patients failing treatment regimens containing raltegravir.
Abstract: Viruses containing a Q148R(H) mutation together with a G140S
Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.
Introduction: Additionally, the major resistance mutations Q148H/RK and N155S have been shown to reduce replicative capacity.
Introduction: Major genetic pathways to integrase resistance, initially through N155H and shifting to Q148H/K/R-G140S or directly to Q148H/K/R-G140S, have been reported.
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
HIV mutation literature information.
PMID: 
2009
Journal of acquired immune deficiency syndromes (1999)
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