Result: Q148R was present in 2.4% of the population and G163R in 2.7%.
Result: Mutations L74M, T97A and G163R appeared in nearly the entire viral population.
Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
Method: 26, September 2016), HIV-GRADE (http://www.hiv-grade.de, version January 16, 2017), and Rega (https://rega.kuleuven.be/cev/avd/software/rega-algorithm, v9.0.1, October 29, 2013) were considered: A49G, H51Y, V54I, L68IV, L74I, E92V, Q95K, H114Y, G118R, S119R, T124A, A128T, E138T, G140C, Y143AGS, P145S, Q146IKLPR, Q148EG, PMID: 28472323
2017
The Journal of antimicrobial chemotherapy
Result: Similarly, the acquisition of T66I followed by secondary mutations, including L74M, Q146K, and G163R, by small cluster viruses contributed to viral escape by week 24 (Figure7e and f).
Result: The infrequent appearance of S230R, E157Q, G163R or G59E minority species (<10%) occurred in some large cluster selections at selected weeks of pass
Discussion: The emergence of select mutations under dolutegravir pressure, including R263K (AGA AAA or AGG AAG), G163R (GGA AGA or GGG AGG) and E138K (GAA AAA, GAG AAG), may be related to APOBEC-mediated G A hypermutation.
Lack of impact of pre-existing T97A HIV-1 integrase mutation on integrase strand transfer inhibitor resistance and treatment outcome.
Introduction: Indeed, while T97A alone confers low-level to no effect on EVG and RAL susceptibility, respectively, additional integrase polymorphism(s) such as V72I, L74M, and/or G163R may serve a role to further reduce INSTI susceptibility before or during INSTI-based treatment.
Result: Among these 8 patients with emergent T97A alone, 4 patients co-developed a secondary INSTI RAM: V72N (1 TE patient on EVG/r+TDF+DRV), L74M (2 TE patients on RAL+ABC+LPV/r), and G163R (1 TN patient on EVG/COBI/FTC/TDF).
Result: Some secondary integr
Prevalence of Integrase Strand Transfer Inhibitors (INSTI) Resistance Mutations in Taiwan.
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,
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
Figure: Primary INSTI resistance mutations are T66I/A/K, E92Q/G, T97A, Y143C/H/R, S147G, Q148H/K/R, and N155H, and other INSTI resistance mutations are H51Y, L68I/V, V72A/N/T, L74M, Q95K/R, F121C/Y, A128T, E138A/K, G140A/C/S, P145S, PMID: 26546669
2016
The Journal of antimicrobial chemotherapy
Abstract: Three secondary INI-R changes appeared with variable frequency in INI-naive individuals carrying specific HIV-1 variants: L74M in CRF43_02G (33.3%); T97A in group P (50%), J (33.3%), CRF18_cpx (20%) and F2 (11.5%); and G163RK in CRF44_BF (100%), CRF46_BF (66.7%), CRF17_BF (28.6%), F1 (21.7%), CRF12_BF (16.7%) and CRF29_BF (12.5%).
Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.
PMID: 26626277
2015
Journal of translational medicine
Discussion: This includes T66IAK, E92Q, F121Y, G140SA, Y143HCR, Q146P, S147G, Q148KHR, and N155HS; (2) minor INI-resistance mutations were defined as non-polymorphic or minimally polymorphic mutations that reduce INI susceptibility H51Y, L74 M, T97A, E138AK, S153Y,
Integrase inhibitor (INI) genotypic resistance in treatment-naive and raltegravir-experienced patients infected with diverse HIV-1 clades.
PMID: 26311843
2015
The Journal of antimicrobial chemotherapy
Result: Of these, L74M, T97A, E138K, V151I and G163R were significantly associated (P < 0.01) with raltegravir exposure.
HIV mutation literature information.
PMID: 
2018
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