literature

HIV mutation literature information.

Predicted antiviral activity of tenofovir versus abacavir in combination with a cytosine analogue and the integrase inhibitor dolutegravir in HIV-1-infected South African patients initiating or failing first-line ART.

PMID: 30380053 2019 The Journal of antimicrobial chemotherapy

Result: Fifteen participants had integrase DRM20% (15/83, 18.1%), including Q148R conferring low-level resistance to dolutegravir, and some accessory integrase mutations were also found: L74I/M (n = 12/15, 80.0%), E157Q (n = 1) and G163R (n = 1).

Result: While no major mutation was described for dolutegravir resistance, we found some accessory integrase mutations in 98/524 (18.7%), such as L74I/M (n = 81/98, 82.7%), T97A (n = 8/98, 8.2%) and E157Q (n = 5/98, 5.1%), and more sporadically E138D/K (n = 2), V151I (n = 1) and G163R

High predictive efficacy of integrase strand transfer inhibitors in perinatally HIV-1-infected African children in therapeutic failure of first- and second-line antiretroviral drug regimens recommended by the WHO.

PMID: 30891603 2019 The Journal of antimicrobial chemotherapy

Abstract: Two (2/18; 11.1%) viruses from children treated with a first-line regimen had INSTI DRMs at codon 138 (E138K and E138T), which is known to harbour major resistance mutations, and also had the accessory mutations L74I, G140K, G140R and G163R.

Result: In addition, the HIV-1 strain harbouring the E138K DRM also displayed accessory mutations G140K, G163R (Table 2) and APOBEC-related mutations not associated with resistance, including G82E, E85K, G106K, D116N, D167N

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

Resistance to HIV integrase strand transfer inhibitors in Argentina: first interim survey.

PMID: 31037930 2019 Revista espanola de quimioterapia

Result: Predominant combinations of mutations were 140A/S + Q148H/R and N155H + G163K/R.

Table: G163K/R

Table: G163R

Raltegravir-Induced Adaptations of the HIV-1 Integrase: Analysis of Structure, Variability, and Mutation Co-occurrence.

PMID: 31551948 2019 Frontiers in microbiology

Result: The latter co-occurs with G163R, which is an accessory mutation to the N155H pathway selected in patients receiving RAL.

Result: The resistance-related mutations found in the network were L74M, L74I, T97A, E138K, G140S, Y143R, Q148H, Q148R, N155H, E157Q, G163R, M50I, and S119R.

Table: G163R

Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.

PMID: 30119633 2018 Retrovirology

Result: Two other variants, 14947 and 6343, acquired R263K/S153A and S153Y/G163R variants.

Table: G163R

Impact of the HIV-1 genetic background and HIV-1 population size on the evolution of raltegravir resistance.

PMID: 29304821 2018 Retrovirology

Result: Q148R was present in 2.4% of the population and G163R in 2.7%.

Result: Mutations L74M, T97A and G163R appeared in nearly the entire viral population.

Resistance to HIV Integrase Inhibitors: About R263K and E157Q Mutations.

PMID: 29346270 2018 Viruses

Introduction: In the study of Anstett et al., L74M, E92Q, T97A, E157Q and G163R resistance mutations were introduced into NL4.3 subtype B HIV-1 vectors harboring N155H and R263K in tandem.

Introduction: They found that the addition of T97A, E157Q or G163R mutation somewhat improved the affinity of the double-mutant N155H-R263K for its target DNA substrate, while the presence of L74M or E92Q had a negative effect on this step.

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%).

Increasing proportions of HIV-1 non-B subtypes and of NNRTI resistance between 2013 and 2016 in Germany: Results from the national molecular surveillance of new HIV-diagnoses.

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.

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