High prevalence of integrase mutation L74I in West African HIV-1 subtypes prior to integrase inhibitor treatment.
PMID: 32105319
2020
The Journal of antimicrobial chemotherapy
Introduction: A good example is G118R in integrase, a polymorphism that confers significant integrase strand transfer inhibitor (INSTI) resistance.
Integrase strand transfer inhibitor (INSTI)-resistance mutations for the surveillance of transmitted HIV-1 drug resistance.
PMID: 31617907
2020
The Journal of antimicrobial chemotherapy
Abstract: Among the 29 relatively common INSTI-selected mutations, 24 emerged as candidates for inclusion on a list of INSTI surveillance drug-resistance mutations: T66A/I/K, E92G/Q, G118R, F121Y, E138A/K/T, G140A/C/S, Y143C/H/R/S, S147G, Q148H/R/K, N155H, S230R and R263K.
Virologic failure after 48 weeks of raltegravir-based regimen in low HIV-1 incidence setting.
Abstract: Primary mutations (Y143C, N155H, T66I, G118R, E138K) conferring high level resistance to raltegravir were detected in only three patients.
Result: Among patients with M184V mutation, two had mutations at position 138 of reverse transcriptase that is associated with low-level resistance to the NNRTI, rilpivirine, and three had major mutations (Y143C, N155H, T66I, G118R, E138K) conferring high level resistance to RAL (Table 2).
Table: G118R
Discussion:
Occurrence of the S230R integrase strand inhibitor mutation in a treatment-naive individual case report.
Abstract: It was also found that the drug resistance mutations Q148K/G140S and G118R/E138K significantly reduce the catalytic activity of IN_CRF and its sensitivity to the strand transfer inhibitor raltegravir.
Method: Consensus IN_CRF and IN_A proteins and those with the mutations Q148K/G140S and G118R/E138K were expressed in Escherichia coli strain Rosetta (DE3) (Novagen) and purified according to .
Method: The vectors encoding IN_CRF with substitutions Q148K/G140S and PMID: 30381490
2019
Journal of virology
Abstract: Some mutations, such as G118R, previously shown to severely impair the replication capacity in vitro, were associated with more sustained virological and immunological benefits of continued DTG therapy, while other mutations, such as E92Q and G140A/Q148K, were associated with more variable outcomes.
Development of the R263K Mutation to Dolutegravir in an HIV-1 Subtype D Virus Harboring 3 Class-Drug Resistance.
PMID: 30648124
2019
Open forum infectious diseases
Introduction: Dolutegravir monotherapy in naive patients, on the other hand, is associated with more frequent selection of drug resistance mutations such as R263K, G118R, S230, and possibly resistance mutations outside the integrase gene.
Drug resistance emergence in macaques administered cabotegravir long-acting for pre-exposure prophylaxis during acute SHIV infection.
Result: Likewise, the G118R and A122T substitutions identified in plasma sequences from macaque CH54 were also detected in rectal fluids between days 71 and 120.
Result: Macaque CH54 acquired both G118R and A122T at day 57.
Result: Of all the mutations identified in vivo, E92Q, E92G, G118R, and G140R were associated with resistance to INSTI.
Result: Overall, these findings demonstrate that G118R, G140R, and E92Q/G selected during CAB LA treatment are associated with resistance to CAB and cross-resistance to other integra
Raltegravir-Induced Adaptations of the HIV-1 Integrase: Analysis of Structure, Variability, and Mutation Co-occurrence.
Conclusion: S119R could have a substantial impact on how the IN binds to the tDNA, as well as G118R.
Result: G118R is considered an accessory mutation and shows a significant reduction in RAL susceptibility.
Result: However, it is not clear how the presence of G118R affects the variability in the neighbor S119.
Result: It is also important to note that its neighbor G118 may show the mutation G118R.
Result: It is known that arginine residues are commonly found in interfaces between proteins and DNA minor grooves, it could be possible that mutation S119R, as well as G118R, enhances the DNA binding, and therefore acts as a compensatory mechanism for primary resistance mutations.
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
HIV mutation literature information.
PMID: 
2020
The Journal of antimicrobial chemotherapy
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