Result: The major cluster (A), contains two mutations in the main resistance-related positions (Q148H and N155H), as well as the major resistance mutation G140S.
Result: The resistance-related mutations found in the network were L74M, L74I, T97A, E138K, G140S, Y143R, Q148H, Q148R, N155H, E157Q, G163R, M50I, and S119R.
Result: This observation highlights the fact that T97A does not play a rol
A Trial of a Single-tablet Regimen of Elvitegravir, Cobicistat, Emtricitabine, and Tenofovir Disoproxil Fumarate for the Initial Treatment of Human Immunodeficiency Virus Type 2 Infection in a Resource-limited Setting: 48-Week Results From Senegal, West Africa.
Abstract: The 1 subject with virologic failure had multidrug-resistant HIV-2 (reverse transcriptase mutation: K65R; integrase mutations: G140S and Q148R) detected at week 48.
Long-term efficacy of dolutegravir in treatment-experienced subjects failing therapy with HIV-1 integrase strand inhibitor-resistant virus.
PMID: 29077927
2018
The Journal of antimicrobial chemotherapy
Abstract: A higher risk of VF was independently associated with baseline viral load >100000 copies/mL (adjusted HR = 4.73, 95% CI = 1.33-16.78, P = 0.016) and with >=1 INSTI mutations plus Q148H/K/R/N and the G140S/A/C as compared with other subjects (adjusted HR = 4.18, 95% CI = 1.32-13.23, P = 0.015).
Ex-vivo antiretroviral potency of newer integrase strand transfer inhibitors cabotegravir and bictegravir in HIV type 1 non-B subtypes.
Method: For BIC, the presence of E138K/Q148R, G140S/Q148R or N155H/Q148R was interpreted as high level resistance.
Method: For CAB, the presence of E138A/Q148R, E138K/Q148K, E138K/Q148R, G140C/Q148R, G140S/Q148R, or Q148R/N155H was interpreted as high-level resistance.
Result: Five patients (21%) with multiple mutations ( PMID: 29304821
2018
Retrovirology
Result: 1e) by double mutant G140S + Q148H.
Result: 1e) mutations from all three major resistance pathways including double mutants with secondary mutations were observed with G140S + Q148H being the most frequently occurring double mutant.
Result: N155H was found in 14.4%, of the population, Q148H in 7.5% of which approximately half (4.1%) in combination with G140S and the remainder in combination with E157D.
Result: G140S was probably not selected because it required two nucleotide changes in this HXB2 background; G140A and E138K required just one.
Result: Population sequencing
Resistance to HIV Integrase Inhibitors: About R263K and E157Q Mutations.
Introduction: They showed that the presence of the E92Q or N155H resistance mutations was compatible with the emergence of R263K, whereas no R263K selection was observed in presence of G140S-Q148R, E92Q-N155H, G140S, Y143R and Q148R resistance mutations.
Novel secondary mutations C56S and G149A confer resistance to HIV-1 integrase strand transfer inhibitors.
Abstract: During passage with Q148H virus, G140S arose by day 14, followed by G149A and C56S.
Abstract: Signature mutant viruses G140S/Q148H in which C56S and G149A were added acquired further INSTI resistance in conjunction with diminished integration activity, which yielded slower growth under drug-free conditions.
Durable suppression of HIV-1 with resistance mutations to integrase inhibitors by dolutegravir following drug washout.
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: With the G140S/Q148H virus, levels of integration were not significantly affected by the presence o
Rapid Development of High-Level Resistance to Dolutegravir With Emergence of T97A Mutation in 2 Treatment-Experienced Individuals With Baseline Partial Sensitivity to Dolutegravir.
PMID: 30568974
2018
Open forum infectious diseases
Conclusion: In November 2014, a PhenoSense Integrase GT assay detected DRMs to NRTI, NNRTI, PI, and the
Introduction: T97A is an accessory mutation frequently co-selected with additional drug resistance mutations (DRMs) including Q148H and G140S in individuals failing raltegravir (RAL) or elvitegravir (EVG) therapy and contributes substantially to resistance to these first-generation INSTIs.
Discussion: In an analysis of individual derived isolates with E138K, G140S, and Q148H, the FC to bictegravir is reported to be as high as 19-fold (2-19), whereas baseline DTG FC was 63 (3-63).
Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.
Abstract: One EVG-resistant variant (T66I) acquired L74M/G140S/S147G, L74M/E138K/S147G and H51Y with DTG CAB and BIC, respectively.
Result: For isolate 5326, the progressive accumulation of Q148K/G140S/G147GS resulted in increasingly high cross-resistance to CAB, RAL and EVG while retaining susceptibility to DTG and BIC (Table 3).
Result: In contrast, the loss of T66I in 14624 was accompanied by the acquisition of L74M/E138K/S147G/
HIV mutation literature information.
PMID: 
2019
Frontiers in microbiology
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