Transmitted drug resistance of HIV-1 strains among individuals attending voluntary counselling and testing in Taiwan.
PMID: 26404079
2016
The Journal of antimicrobial chemotherapy
Abstract: Among the seven major integrase mutations (T66I, E92Q, G140S, Y143C/H/R, S147G, Q148H/K/R and N155H), only one strain harbouring the Q148R mutation was detected.
Pathway involving the N155H mutation in HIV-1 integrase leads to dolutegravir resistance.
PMID: 26574015
2016
Antimicrobial agents and chemotherapy
Abstract: As a follow-up, the in vitro characteristics of mutant HIV-1 containing RT-K65R and/or RT-M184V with IN-Q148R or IN-N155H were also evaluated, alone and in combination, for potential interactions.
Abstract: In clinical trials of coformulated elvitegravir (EVG), cobicistat (COBI), emtricitabine (FTC), and tenofovir disoproxil fumarate (TDF), emergent drug resistance predominantly involved the FTC resistance substitution M184V/I in reverse transcriptase (RT), with or without the tenofovir (TFV) resistance substitution K65R, accompanied by a primary EVG resista
Efficacy and safety of antiretroviral regimens including raltegravir to treat HIV-infected patients with hemophilia.
Abstract: At Raltegravir failure, N155H was detected in four patients, and other secondary mutations were detected in five patients (71.4 %).
Abstract: CONCLUSION: This is a pilot study that demonstrates the possibility of properly identifying N155H and some secondary mutations 29-53 months after failure.
Abstract: In proviral DNA, N155H was detected by population sequencing in three patients (42.8 %), and UDS demonstrated a 9.77 % relative abundance of N155H in the remaining patient.
Conclusion: In summary, despite the limitations of our study, which is just a pilot study that should be confirmed in further studies, we have shown the proof of concept that for patients who failed a Raltegravir containing regimen in the past, who are currently virologically suppressed, and lack the resistance information at failure, studying
Introduction: However, the N155H and SH mutants, which emerge in patients treated with RAL, confer cross-resistance to EVG.|mgd
Result: Among the five compounds shown in Figure 6, those with the highest selectivity for ST over 3'-P were also the most susceptible to the SH and N155H mutants (Figures 6 and Supplementary Figure S3).
Result: They also suggest that 3'-P inhibition is an indicator of the ability of compounds to retain efficacy against the SH (and N155H) mutants.
Result: Together, these results reveal a significant correlation between the relative activity of a drug as a 3'-P inhibitor and its ability to overcome resistance to the SH mutant, and to a lesser extent, to the N155H mutant.
Result: We also tested the ST selectivity and resistance index relationships for the N155H mutant.
Maraviroc/raltegravir simplification strategy following 6 months of quadruple therapy with tenofovir/emtricitabine/maraviroc/raltegravir in treatment-naive HIV patients.
PMID: 27432606
2016
The Journal of antimicrobial chemotherapy
Abstract: N155H mutation was detected at failure in one patient.
Development and validation of a cell-based assay system to assess human immunodeficiency virus type 1 integrase multimerization.
PMID: 27474494
2016
Journal of virological methods
Introduction: It is of note, however, that RAL-resistant HIV-1 variants selected with RAL, that have acquired both Q148/H/K and/or N155H substitutions in IN, are cross-resistant to EVG.
Therapy-Emergent Drug Resistance to Integrase Strand Transfer Inhibitors in HIV-1 Patients: A Subgroup Meta-Analysis of Clinical Trials.
Abstract: The resistance of DTG is mainly shown in 13 integrase mutations (including T97T/A, E138E/D, V151V/I, N155H, Q148, Y143C/H/R, T66A and E92Q).
Abstract: The ten major integrase mutations (including N155H, Y143C/R, Q148H/R, Y143Y/H, L74L/M, E92Q, E138E/A, Y143C, Q148Q and
Development of a phenotypic susceptibility assay for HIV-1 integrase inhibitors.
PMID: 27737783
2016
Journal of virological methods
Abstract: While raltegravir resistance profiles presented a high cross-resistance to elvitegravir, dolutegravir maintained in-vitro activity in spite of the Y143R and N155H mutations, confirming the strong activity of dolutegravir against raltegravir-resistant viruses.
Drug resistant integrase mutants cause aberrant HIV integrations.
Abstract: More importantly, we show that at least two of the three clinically relevant drug resistant integrase mutants we tested, N155H and G140S/Q148H, which reduce the enzymatic activity of integrase, can cause the same sorts of aberrant integrations, even in the absence of drugs.
Conclusion: At least two of the three clinically relevant drug resistant integrase mutants we tested, N155H and G140S/Q148H, which reduce the enzymatic activity of integrase, caused aberrant integrations, even in the absence of any added drug.
HIV mutation literature information.
PMID: 
2016
The Journal of antimicrobial chemotherapy
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