Abstract: RESULTS: We detected integrase inhibitor resistance (T66I/T) at baseline in one patient sample.
HIV-1 strains belonging to large phylogenetic clusters show accelerated escape from integrase inhibitors in cell culture compared with viral isolates from singleton/small clusters.
PMID: 28472323
2017
The Journal of antimicrobial chemotherapy
Abstract: With elvitegravir, large cluster variants more rapidly acquired first mutations (T66I, A92G, N155H or S147G) by week 8 followed by sequential accumulation of multiple mutations leading to viral escape (>10 muM) by week 24.
Introduction: Resistance to elvitegravir and raltegravir occurs via several mutational pathways, including: (i) N155H or G140A/G148RHQ pathways conferring raltegravir and elvitegravir cross-resistance; (ii) T66I or E92Q/G elvitegravir-specific pathways; or (iii) the Y143R/H/C raltegravir-specific resistance pathway.
Result: By week 24, the dominant virus coexpressed PMID: 28328546
2017
Journal of acquired immune deficiency syndromes (1999)
Result: Two studies reported sequencing the integrase gene in CSF; N155H, L74I, and Q148R mutations were observed as single mutations in the integrase gene, and Y143C was observed in combination with T66I.
Lack of impact of pre-existing T97A HIV-1 integrase mutation on integrase strand transfer inhibitor resistance and treatment outcome.
Result: None of these pre-treatment integrase sequences contained primary integrase mutations most often associated with emergent EVG (T66I, E92Q, S147G, Q148R/H/K, and N155H) or RAL (Y143C/R/H, Q148H/K/R, and N155H) resistance.
Antiviral Activity of Bictegravir (GS-9883), a Novel Potent HIV-1 Integrase Strand Transfer Inhibitor with an Improved Resistance Profile.
PMID: 27645238
2016
Antimicrobial agents and chemotherapy
Result: Of the five mutations that emerged in EVG breakthrough selections, only T66I is a known mutation associated with INSTI resistance.
Result: The EVG selection experiment resulted in the successive emergence of R263K and T66I in P2 day 20 and P6 day 56, respectively.
Result: Virus variants that emerged in the presence of EVG or RAL frequently encoded mutations commonly observed in patients treated with these earlier approved INSTIs (e.g., T66I, E92G/V, Q148R, and N155H).
HIV-1 Epidemiology, Genetic Diversity, and Primary Drug Resistance in the Tyumen Oblast, Russia.
Method: Besides these three major mutations, the integrase substitutions with a Stanford HIVdb score 10 to at least one INSTI were included, such as H51Y, T66A/I/K, L74M, E92G/Q/V, Q95K, T97A, F121Y, E138A/K, G140S/C/A, Y143G/K/S/A, P145S, Q146P, S147G, V151A/L, S153F/Y, N155S/T,
Effect on HIV-1 viral replication capacity of DTG-resistance mutations in NRTI/NNRTI resistant viruses.
Introduction: More recently, we have shown that the T66I/R263K combination severely impaired both integrase strand-transfer activity and viral replicative capacity.
Introduction: The T66I/R263K virus was slightly more susceptible to DTG when viruses containing R263K alone were studied but highly resistant to EVG, which explains the emergence of this combination with EVG but not DTG.
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.
Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.
PMID: 26626277
2015
Journal of translational medicine
Abstract: Neither major resistance-associated IN mutations (T66I/A/K, E92Q/G, T97A, Y143HCR, S147G, Q148H/R/K, and N155H) nor silent mutations known to change the genetic barrier were observed.
Conclusion: None of the previously reported major mutations (T66AIK, E92Q, Y143RCH, S147G, Q148HRK and N155H) associated with resistance to INIs were observed in HIV-1C Ethiopian isolates, indicating that
HIV mutation literature information.
PMID: 
2017
Journal of clinical virology
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