Abstract: Resistance selection experiments of JTP-0157602 led to the emergence of A128T and T174I mutations, which are located at the lens epithelium-derived growth factor/p75 binding pocket of IN.
Brief Report: Bictegravir/Emtricitabine/Tenofovir Alafenamide Efficacy in Participants With Preexisting Primary Integrase Inhibitor Resistance Through 48 Weeks of Phase 3 Clinical Trials.
PMID: 34897227
2022
Journal of acquired immune deficiency syndromes (1999)
Table: A128T
A highly potent and safe pyrrolopyridine-based allosteric HIV-1 integrase inhibitor targeting host LEDGF/p75-integrase interaction site.
Abstract: Y99H and A128T mutations at the LEDGF/p75 binding pocket render resistance to STP0404.
Method: Passages 4 and 14 viral supernatant collected were selected to illustrate the effect of single mutation (Y99H, passage 4) and double mutations (Y99H and A128T).
Method: p89.6 plasmid was applied for Quickchange kit (Invitrogen) to create Y99H single, A128T single, Y99H/A128T double mutants as well as two natural variants (A124N and T125A), and these 89.6 variant viruses were generated by transfecting 293T cells and culturing the produced viruses in CEMx174 cells.
Result: As shown in Fig 2, t
HIV-1 Subtype C Drug Resistance Mutations in Heavily Treated Patients Failing Integrase Strand Transfer Inhibitor-Based Regimens in Botswana.
Result: The four individuals failing DTG cART but with no documented prior exposure to RAL, their selected DRMs were E138K, G140A, Q148K, A128T; G118R, E138K; N155ND and T66A, G118R, E138EAKT Figure 3.
Absence of Integrase Inhibitor-Associated Resistance Among Antiretroviral Therapy-Naive HIV-1-Infected Adults in Guangdong Province, China, in 2018.
Abstract: Among them, no major resistance mutations to INSTIs were identified, and four accessory mutations, including T97A (0.12%, 1/827), A128T (0.24%, 2/827), E157Q (0.85%, 7/827), and G163R (0.24%, 2/827), were found in twelve individuals.
Conclusion
Result: The mutations were T97A (0.12%, 1/827), A128T (0.24%, 2/827), E157Q (0.85%, 7/827), and G163R (0.24%, 2/827).
Discussion: Two patient samples contained the A128T mutation, which is a relatively nonpolymorphic possibly INSTI-selected mutation that does not appear to reduce INSTI susceptibility.
Variability in HIV-1 Integrase Gene and 3'-Polypurine Tract Sequences in Cameroon Clinical Isolates, and Implications for Integrase Inhibitors Efficacy.
PMID: 32106437
2020
International journal of molecular sciences
Abstract: Integrase polymorphic and accessory RAMs found included T97A, E157Q, A128T, M50I, S119R, L74M, L74I, S230N, and E138D (0.3%-23.5% of samples).
Result: The proportion of AG and non-AG database samples harboring other INSTIs RAMs was not significantly different and T66A, N155K, A128T, S119R, and S230N were observed only in a very small number (1.4%) of database samples of non-AG genotypes (Table 4).
Result: Three
Switching to bictegravir/emtricitabine/tenofovir alafenamide maintained HIV-1 RNA suppression in participants with archived antiretroviral resistance including M184V/I.
PMID: 31430369
2019
The Journal of antimicrobial chemotherapy
Method: Secondary INSTI-R substitutions were M50I, H51Y, L68V/I, V72A/N/T, L74M, Q95K/R, G118R, S119P/R/T, F121C, A128T, E138K/A, G140A/C/S, P145S, Q146R/I/K/L/P, V151L/A, S153A/F/Y, E157K/Q, G163K/R and E
Resistance to HIV integrase strand transfer inhibitors in Argentina: first interim survey.
PMID: 31037930
2019
Revista espanola de quimioterapia
Table: A128T
Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.