Abstract: Any impact of the high prevalence of major accessory mutations, especially E157Q, requires long-term follow-up studies.
Abstract: One patient had a primary DRMs (0.3%, 1/270), but 17 (6.3%) had one major accessory DRM, of which 12 were E157Q.
Result: In addition, 17 of 270 (6.3%) patients had at least one major accessory DRM: T97A (n=3), E157Q (n=12), or A128T (n=2).
Result: Sequencing of samples collected 1216 and 1038 days earlier from these two patients showed that they had E157Q and the T97A mutations, respectively.
Result: Two RAL treated patients with E157Q and T97A mutations, respectively, failed to suppress viremia at month six.
Di
Phenotypic analysis of HIV-1 E157Q integrase polymorphism and impact on virological outcome in patients initiating an integrase inhibitor-based regimen.
PMID: 29342281
2018
The Journal of antimicrobial chemotherapy
Abstract: E157Q site-directed mutants in pNL4.3 and pCRF02_AG contexts were assessed in a recombinant phenotypic assay.
Abstract: Conclusions: Assessment of virological response in 39 patients initiating an INI-based regimen with E157Q-mutated virus, in combination with phenotypic analysis, suggests that particular attention should be paid to antiretroviral-naive patients and dolutegravir should be preferentially used in these patients.
Abstract: Objectives: To assess the phenotypic susceptibility of the E157Q polymorphism in HIV-1 integrase (IN) and the virological outcome of patients infected with E157Q-mutated virus initiating an IN inhibitor (INI)-based regimen.|mg
E157Q integrase strand-transfer inhibitor substitution in patients with acute/recent HIV infection.
Abstract: The E157Q mutation is polymorphic, found between 1.7% and 5.6% of viral sequences issued from ART-naive patients depending on the viral subtype; as well as acquired resistance emerging at failure of a raltegravir-based regimen in two case reports.
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.
Abstract: We reported data on phenotypic resistance level of E157Q mutants and virological response of patients harboring a E157Q virus initiating an INI-based regimen, showing that dolutegravir might be the most recommended INI in such patients.
Introduction: A case report in
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: Accessory mutations occurred at a prevalence of 15.1% at the >=20% threshold (23.1% in subtype A, 8.7% C, 11.6% D, 25% G and 23.8% in recombinants), and included L74I/M (10.4%), Q95K (0.5%), T97A (4%), E157Q (0.7%) and G163R/K (0.7%).
Prevalence of drug resistance in children recently diagnosed with HIV-1 infection in France (2006-17): impact on susceptibility to first-line strategies.
PMID: 29846602
2018
The Journal of antimicrobial chemotherapy
Abstract: Additionally, 3/60 (5%) strains had integrase inhibitor (INI)-related RAMs (an isolated E157Q mutation, which could mostly affect the susceptibility to raltegravir/elvitegravir rather than that to dolutegravir).
Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.
Abstract: EVG-resistant viruses (T66I/R263K, T66I/E157Q/R263K, and S153A/R263K) retained residual susceptibility when switched to DTG, BIC or CAB, losing T66I by week 27.
Abstract: Here, in vitro drug selections compared the development of resistance to DTG, BIC, CAB, EVG and RAL using clinical isolates from treatment-naive primary HIV infection (PHI) cohort participants (n = 12), and pNL4.3 recombinant strains encoding patient-derived Integrase with (n = 5) and without (n = 5) the E157Q substitution.
Abstract: The PMID: 30408827
2018
PloS one
Result: According to predictions from the Stanford HIVdb, phenotypic INSTI resistance (excluding potential low level) was identified in 0.7% (6/820) of cases (Fig 3B) due to the presence of the T66I (n = 1), the G163R or K (n = 4) or the combination of T97A and E157Q (n = 1) resulting in low level resistance to elvitegravir and raltegravir.
Characterization of minority HIV-1 drug resistant variants in the United Kingdom following the verification of a deep sequencing-based HIV-1 genotyping and tropism assay.
Result: Most of these minority drug resistance mutations were detected in the 67 cART-experienced individuals, e.g., the HIV-1 genotype of the following patients consisted of a mixture of majority and minority drug resistance mutations: patient SG79 (PR V11I 99.9%, K20I 99.9%; RT E44D 1.3%, D67N 1.1%, L100I 1.7%, M184V 84.9%, M184I 14.8%, K219Q 2.1%, INT E157Q 99.8%), patient SG86 (RT M184V 99.8%, INT L74M 97.9%, L74I 1.9%, E92Q 86
Resistance-Associated Mutations and Polymorphisms among Integrase Inhibitor-Naive HIV-1 Patients in Kuwait.
Abstract: However, the accessory mutation E157Q was found in 1 patient with CRF02_AG, and the polymorphic mutations L74M/I that may contribute to a reduced susceptibility to INSTIs in the presence of major mutations were observed in 6 (13.3%) patients with non-B subtypes and 1 (12.5%) patient with the B subtype.
Molecular evolution of HIV-1 integrase during the 20 years prior to the first approval of integrase inhibitors.
ViMRT
HIV mutation literature information.
PMID: 
2018
AIDS (London, England)
