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.
Drug Susceptibility and Viral Fitness of HIV-1 with Integrase Strand Transfer Inhibitor Resistance Substitution Q148R or N155H in Combination with Nucleoside/Nucleotide Reverse Transcriptase Inhibitor Resistance Substitutions.
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.
Discussion: Although for the remaining patient we could not demonstrate the failing mutation with Sanger sequencing, using a more sensitive test, resulted in the correct identification of the failing mutations [N155H (9.7 %) and T97A (12.42 %)] suggesting that, given the superiority of massive parallel sequencing, this should be the tool recommended for testing proviral DNA in virologically suppressed patients, although at present it is an expensive tool that may not be feasible in some laboratories.
Discussion: Secondly, only the N155H pathway was confirmed in some patients and it is possible that resistance pathways other than N155H, that could have emerged before N155H was established, may have been archived in the proviral DNA of the patients compromising DTG activity.
Selectivity for strand-transfer over 3'-processing and susceptibility to clinical resistance of HIV-1 integrase inhibitors are driven by key enzyme-DNA interactions in the active site.
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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