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


  Prevalence of drug resistance mutations among ART-naive and -experienced HIV-infected patients in Sierra Leone.
 PMID: 30989237       2019       The Journal of antimicrobial chemotherapy
Result: No RAMs were observed to INSTIs; only the polymorphisms E157Q (n = 2), G163KR (n = 2) and T97A (n = 1) were observed, which have minimal effect on INSTI susceptibility.


  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


  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


  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


  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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