Abstract: In three other patients, viruses with N155H emerged at viral rebound either alone (2 months), followed by V151I (8 months) or alone (10 months), or together with V151I/G163RG (7 months).
Abstract: Loss of virus with the N155H mutation occurred in these patients when RAL therapy was terminated, despite maintenance of reverse transcriptase/polymerase resistance mutations.
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: These selective-advantage curves revealed that among single mutants, N155H had the highest and the widest (1 to 500 nM) selective-advantage profile.
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 tha
Dynamics of raltegravir resistance profile in an HIV type 2-infected patient.
PMID: 19618998
2009
AIDS research and human retroviruses
Abstract: The treatment failure of an RAL regimen in the HIV-2 patient studied was associated with the emergence of mutations via the N155H resistance pathway and subsequent switching to the Y143C mutational route.
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.
Pathway involving the N155H mutation in HIV-1 integrase leads to dolutegravir resistance.
Abstract: CONCLUSION: A continued low HIV-2 viral load seems to be enough to select the N155H mutation, which despite significantly impairing viral replication, shows a level of resistance sufficient to give a selective advantage to the virus that maintains this pathway of resistance to raltegravir overtime.
Abstract: Genotypic analysis at month 8 with raltegravir, revealed the development of N155H resistant mutation along with other changes in the HIV-2 integrase: V72I, I84V, A153G, N160K and S163S/G.
Loss of raltegravir susceptibility by human immunodeficiency virus type 1 is conferred via multiple nonoverlapping genetic pathways.
Abstract: Analysis of site-directed mutants indicated that E92Q in combination with N155H resulted in a higher level of resistance to raltegravir than N155H alone.
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
Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.
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, E92Q, G140S, Y143C/H/R Q148H/R/K and
The use of integrase inhibitors in treatment-experienced patients.
PMID: 19959414
2009
European journal of medical research
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, Q148H/K/R N155H) almost always in combination with at least one other mutation.
Introduction: The N155H or the Q148H/R/K alone are associated with high or intermediate levels of resistance that beca
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
AIDS (London, England)
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