Abstract: DESIGN AND METHODS: MT-2 cells infected with wild-type, R263K or G140S/Q148H HIV-1 clones were treated with DTG, RAL or EVG for 3 days.
Abstract: Now, we performed DTG, EVG and RAL washout experiments to compare the recovery of viral integration and production of 2-long terminal repeat (LTR) circles using wild-type HIV-1 clones, R263K viruses with low-level resistance to DTG and viruses with G140S/Q148H mutations showing cross-resistance against all currently approved INSTIs.
Abstract: RESULTS: Viral integration did not resume for up to 8 days after DTG washout from the wild-type or R263K infections but increased soon
Prevalence of resistance to integrase strand-transfer inhibitors (INSTIs) among untreated HIV-1 infected patients in Morocco.
Introduction: Regarding DTG R263K resistance mutation, no strain from our study exhibited this mutation, whereas the L101I and T124A mutations were found in 26 and 12 strains, respectively.
The S230R Integrase Substitution Associated With Virus Load Rebound During Dolutegravir Monotherapy Confers Low-Level Resistance to Integrase Strand-Transfer Inhibitors.
PMID: 29617824
2018
The Journal of infectious diseases
Abstract: Conclusions: Our data indicate that the S230R substitution is comparable to the previously reported R263K substitution in some respects.
Abstract: Virologic failure during DTG monotherapy can occur through the development of the S230R or R263K mutation, without the need for high-level DTG resistance.
HIV-1 Resistance Dynamics in Patients With Virologic Failure to Dolutegravir Maintenance Monotherapy.
PMID: 29617822
2018
The Journal of infectious diseases
Abstract: INSTI-RAMs (S230R, R263K, N155H, and E92Q+N155H) were detected in 4 patients, no INSTI-RAMs were detected in 4 patients, and sequencing of the integrase gene was unsuccessful in 2 patients.
Progressive emergence of an S153F plus R263K combination of integrase mutations in the proviral DNA of one individual successfully treated with dolutegravir.
Abstract: Further in vitro studies on R263K mutants showed a moderate increase in phenotypic resistance level and a drastic reduction in viral replicative capacity.
Abstract: The R263K mutation was the first mutation rarely found selected at time of virological failure in patients failing a first-line dolutegravir-based treatment.
Abstract: The aim of this manuscript was to review main in vivo and in vitro knowledge about two particular integrase resistance-associated mutations: R263K and E157Q.
Introduction: A few additional VF occurred in the SAILING trial after W48 and R263K mutation was detected in one of them.
Introduction: assessed the impact of adding the M184I/V mutation to a R26
ACTG A5353: A Pilot Study of Dolutegravir Plus Lamivudine for Initial Treatment of Human Immunodeficiency Virus-1 (HIV-1)-infected Participants With HIV-1 RNA <500000 Copies/mL.
Abstract: Three participants with VF, had undetected plasma dolutegravir at >=1 time points; the M184V and R263R/K mutations developed in 1 participant.
Ex-vivo antiretroviral potency of newer integrase strand transfer inhibitors cabotegravir and bictegravir in HIV type 1 non-B subtypes.
Method: Additionally, if the M50I/R263K mutation was present, we termed it as intermediate resistance to BIC.
Discussion: A selection of R263K/M50I has been described in virus outgrowth assay for BIC that resulted 2.8-fold reduction of BIC-susceptibility, but M50I alone did not have any effect.
Discussion: In breakthrough selections, M50I emerges after R263K and provides replication advantage to R263K containing virus.
Discussion: Mutation R263K mutation has been shown to confer 2- to 5-fold resistance to DTG, with decreased viral replication and strand transfer activity.
Molecular evolution of HIV-1 integrase during the 20 years prior to the first approval of integrase inhibitors.
Method: Major INSTI resistance mutations (T66I, E92Q, F121Y, Y143CHR, S147G, Q148HKR, N155H) that confer substantial phenotypic resistance to at least one of the currently approved INSTI as well as minor INSTI resistance mutations (T66AK, L74 M, E92G, T97A, E138AK, G140AS, R263K) that increase INSTI resistance and/or viral
Antiviral Activity of Bictegravir and Cabotegravir against Integrase Inhibitor-Resistant SIVmac239 and HIV-1.
PMID: 28923862
2017
Antimicrobial agents and chemotherapy
Abstract: In both single and multiple rounds of HIV-1 infections, BIC remained active against the Y143R, N155H, R263K, R263K/M50I, and R263K/E138K mutants (<=4-fold increase in EC50).
Abstract: In single cycle SIV infections, none of the E92Q, T97A, Y143R, or N155H substitutions had a significant effect on susceptibility to BIC (<=4-fold increase in EC50), whereas G118R and R263K conferred ~14-fold and ~6-fold increases in EC50, respectively.
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).
HIV mutation literature information.
PMID: 
2018
AIDS (London, England)
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