Abstract: With EVG, T66I/A, E92G/V/Q, T97A or R263K (n = 16, 3, 2 and 1, respectively) arose by weeks 8-16, followed by 1-4 accessory mutations, conferring high-level resistance (> 100-fold) by week 36.
Table: T97A
Ex-vivo antiretroviral potency of newer integrase strand transfer inhibitors cabotegravir and bictegravir in HIV type 1 non-B subtypes.
Result: In addition, 17 of 270 (6.3%) patients had at least one major accessory DRM: T97A (n=3), E157Q (n=12), or A128T (n=2).
Result: One of the two patients who switched with suppressive viremia, maintained undetectable viral load, but one (with T97A) had a viral blip at month 6 (57 copies/mL) (Fig 3a).
Result: Sequencing of samples collected 1216 and 1038 days earlier from these two patients showed that they had E157Q and the T97A mutations, respectively.
Result: Two RAL treated patients with E157Q and Discussion: Instead, 17 (6.3%) patients had major INSTI accessory mutations (E157Q, T97A andA128T).
Impact of the HIV-1 genetic background and HIV-1 population size on the evolution of raltegravir resistance.
Result: In a later time-point, 169 days after start of raltegravir, this population was replaced by a variant with primary mutation Y143R and several secondary mutations including L74M, T97A and G163E.
Result: In a sample taken 28 days later, 77.5% of the population contained N155H, 15.4% had T97A and variants with Y143C were not detected anymore.
Result: Mutations L74M, T97A and G163R appeared in nearly the entire viral population.
Resistance to HIV Integrase Inhibitors: About R263K and E157Q Mutations.
Introduction: In the study of Anstett et al., L74M, E92Q, T97A, E157Q and G163R resistance mutations were introduced into NL4.3 subtype B HIV-1 vectors harboring N155H and R263K in tandem.
Introduction: They found that the addition of T97A, E157Q or G163R mutation somewhat improved the affinity of the double-mutant N155H-R263K for its target DNA substrate, while the presence of L74M or E92Q had a negative effect on this step.
Primary resistance to integrase strand transfer inhibitors in patients infected with diverse HIV-1 subtypes in sub-Saharan Africa.
PMID: 29462322
2018
The Journal of antimicrobial chemotherapy
Abstract: Accessory mutations occurred at a prevalence of 15.1% at the >=20% threshold (23.1% in subtype A, 8.7% C, 11.6% D, 25% G and 23.8% in recombinants), and included L74I/M (10.4%), Q95K (0.5%), T97A (4%), E157Q (0.7%) and G163R/K (0.7%).
Prevalence and clinical impact of minority resistant variants in patients failing an integrase inhibitor-based regimen by ultra-deep sequencing.
PMID: 29873733
2018
The Journal of antimicrobial chemotherapy
Abstract: Among 53 patients harbouring at least one resistance mutation detected by both techniques, the most dominant INSTI resistance mutations were N155H (45%), Q148H/K/R (23%), T97A (19%) and Y143C (11%).
Prevalence of resistance to integrase strand-transfer inhibitors (INSTIs) among untreated HIV-1 infected patients in Morocco.
Abstract: Primary INSTIs resistance mutation were absent, however secondary mutations L74IM, T97A were detected in four samples (5.2%).
Introduction: None of the primary amino acid mutations in IN positions 66, 92, 140, 143, 147, 148 and 155 listed in the Stanford resistance algorithm were found in this study, while secondary mutations L74IM and T97A associated with drug resistance to RAL and EVG were observed only in four patients (5.2%) (Additional file 1).
Introduction: The L74M was observed in one subtype B strain (KU609337) and T97A was observed in one CRF02_AG strain (KU609303).
Rapid Development of High-Level Resistance to Dolutegravir With Emergence of T97A Mutation in 2 Treatment-Experienced Individuals With Baseline Partial Sensitivity to Dolutegravir.
PMID: 30568974
2018
Open forum infectious diseases
Conclusion: T97A was not detected by Sanger sequencing or by next-generation sequencing (NGS; Illumina), which has a sensitivity of c.
Conclusion: A repeat INSTI genotype noted T97A (Supplementary Tables 2 and 3).
Conclusion: NGS detected T97A in addition to the previously detected integrase mutations (Supplementary Table 2).
Conclusion: Retrospective NGS analysis of a plasma sample from November 2015 (while the individual was on RAL) did not reveal the T97A mutation.
Conclusion: Thus T97A emerged within 8 weeks of consistent DTG therapy.
Figure: Impact of T97A mutation on phenotypic sensitivity to dolutegravir in HIV-1 isolates with baseline partial sensitivity to dolutegravir.|m
Raltegravir-intensified initial antiretroviral therapy in advanced HIV disease in Africa: A randomised controlled trial.
Result: One participant had predicted intermediate-level (mutations T97A+R263K) and two predicted high-level (N155H, T97A+Y143R/C) raltegravir resistance mutations (0.6% of those randomised, accounting for missing genotypes using probability weights).
Increasing proportions of HIV-1 non-B subtypes and of NNRTI resistance between 2013 and 2016 in Germany: Results from the national molecular surveillance of new HIV-diagnoses.
Result: According to predictions from the Stanford HIVdb, phenotypic INSTI resistance (excluding potential low level) was identified in 0.7% (6/820) of cases (Fig 3B) due to the presence of the T66I (n = 1), the G163R or K (n = 4) or the combination of T97A and E157Q (n = 1) resulting in low level resistance to elvitegravir and raltegravir.
HIV mutation literature information.
PMID: 
2018
Retrovirology
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