Result: 1a) the N155H variant replaced the Q148R variant and dominated the population together with the E138K + Q148K variant.
Result: 40 days after start of raltegravir, virus with Q148R had increased to 1.7% of the population and virus with E138K + Q148K had increased to 0.5%.
Result: NGS revealed very small populations at baseline containing Q148R and E138K (0.1% of the population.
Result: Population sequencing revealed presence of raltegravir resistance mutations (E138E/K + Q148Q/K/R + N155H/H) and raltegravir was discontinued from
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.
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.
Primary resistance to integrase strand transfer inhibitors in patients infected with diverse HIV-1 subtypes in sub-Saharan Africa.
PMID: 29462322
2018
The Journal of antimicrobial chemotherapy
Abstract: Major INSTI resistance mutations were detected only at <20% threshold, at a prevalence of 2.4% (2.5% in subtype A, 2.4% C, 0% D, 8.3% G and 2.4% in recombinants) and included T66A/I (0.7%), E92G (0.5%), Y143C/S (0.7%), S147G (0.2%) and Q148R (0.5%).
Prediction of the binding mode and resistance profile for a dual-target pyrrolyl diketo acid scaffold against HIV-1 integrase and reverse-transcriptase-associated ribonuclease H.
PMID: 29947629
2018
Physical chemistry chemical physics
Abstract: The results demonstrated that only three mutations in HIV-1 IN (Y143C, Q148R and N155H) and two mutations in HIV-1 RNase H (Y501R and Y501W) resulted in a reduction of JMC6F potency, thus indicating their potential role in providing resistance to JMC6F.
Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.
Abstract: However, three CAB selections resulted in Q148R/K followed by secondary mutations conferring high-level cross-resistance to all INSTIs.
Abstract: The development of Q148R/K with CAB can result in high-level cross-resistance to all INSTIs.
Abstract: Two EVG-resistant variants developed resistance to DTG, BIC and CAB through the additional acquisition of E138A/Q148R and S230N, respectively.
Introduction: One patient acquired virus with the Q148R mutation, conferring phenotypic resistance to RAL, EVG and CAB, in association with the K103N, E138G, and K238T, conferr
Temporal Patterns and Drug Resistance in CSF Viral Escape Among ART-Experienced HIV-1 Infected Adults.
PMID: 28328546
2017
Journal of acquired immune deficiency syndromes (1999)
Result: Two studies reported sequencing the integrase gene in CSF; N155H, L74I, and Q148R mutations were observed as single mutations in the integrase gene, and Y143C was observed in combination with T66I.
Discussion: Three CSF integrase mutations were identified in CSF (N155H, Y143C, and Q148R).
Lack of impact of pre-existing T97A HIV-1 integrase mutation on integrase strand transfer inhibitor resistance and treatment outcome.
Result: None of these pre-treatment integrase sequences contained primary integrase mutations most often associated with emergent EVG (T66I, E92Q, S147G, Q148R/H/K, and N155H) or RAL (Y143C/R/H, Q148H/K/R, and N155H) resistance.
Integrase strand-transfer inhibitor polymorphic and accessory resistance substitutions in patients with acute/recent HIV infection.
PMID: 27624569
2017
The Journal of antimicrobial chemotherapy
Abstract: CONCLUSIONS: Although signature InSTI substitutions (such as Y143R/C, N155H or Q148K/R/H) were not detected, polymorphisms and substitutions conferring low-level resistance to raltegravir and elvitegravir were frequently found in a baseline genotypic test.
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).