Resistance to HIV integrase strand transfer inhibitors in Argentina: first interim survey.
PMID: 31037930
2019
Revista espanola de quimioterapia
Abstract: Predominant major mutations were N155H (35.1%), Q148H/R (15.8%) and G140A/S (14%).
Introduction: Different pathways against first-generation InSTIs were identified whose primary mutations include the substitutions N155H, Q148K/R/H, and Y143R/C.
Result: Predominant combinations of mutations were 140A/S + Q148H/R and N155H + G163K/R.
Result: Predominant major integrase resistance mutations were N155H (35.1%), Q148H/R (15.8%) and PMID: 31043606
2019
Nature communications
Introduction: An additional concern is the lack of information on the mutations selected with CAB in vivo and their potential impact on resistance to other INSTIs, as only two cases of CAB resistance have been reported in HIV-infected patients treated with CAB, both mediated by integrase mutation Q148R.
Discussion: In humans, treatment with CAB or CAB LA has been associated with rare instances of selection of Q148R.
Kinetics of Archived M184V Mutation in Treatment-Experienced Virally Suppressed HIV-Infected Patients.
PMID: 31430369
2019
The Journal of antimicrobial chemotherapy
Discussion: Additionally, any potential benefit of decreased viral fitness by M184V/I on the efficacy of dolutegravir/lamivudine may not outweigh the risk of virological failure with INSTI-R development, as it is possible for M184V and INSTI-R to co-develop while failing a dolutegravir/lamivudine regimen.In vitro studies further suggest that viral fitness defects can be overcome by drug resistance in the presence of antiretroviral drugs: HIV-1 with M184V and INSTI-R (E92Q, Q148R or N155H) grows more efficiently than WT HIV-1 in the presence of emtricitabine and the INSTI elvitegravir at physiological concentrations.
Delayed linkage to HIV care among asylum seekers in Quebec, Canada.
Result: One newly diagnosed patient, who was unknowingly prescribed functional monotherapy, developed full integrase inhibitor resistance (N155H, Q148R, S147G, E138K, and E92Q mutations).
Comparable In Vitro Activities of Second-Generation HIV-1 Integrase Strand Transfer Inhibitors (INSTIs) on HIV-1 Clinical Isolates with INSTI Resistance Mutations.
PMID: 31611362
2019
Antimicrobial agents and chemotherapy
Abstract: In this study, DTG, BIC, and CAB demonstrated a comparable activity on a panel of INSTI-resistant strains isolated from patients exposed to RAL, EVG, and/or DTG, with a significantly reduced susceptibility only with the pathway Q148H/K/R plus one to two additional INSTI mutations.
Raltegravir-Induced Adaptations of the HIV-1 Integrase: Analysis of Structure, Variability, and Mutation Co-occurrence.
Result: Curiously, four isolates showed mutations related to more than one of the three main resistance pathways: two from Italy, one with both N155H and Y143R and another with Q148H and Y143H; one from Canada with N155H and Y143C; and one from France with N155H and Q148R.
Result: The mutations that co-occur with Q148R, Q148H, N155H, Y143R, E138K, and T97A are shown in Table 3.
Result: The resistance-related mutations found in the network were L74M,
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: Primary INSTI resistance (-R) substitutions were T66I/A/K, E92Q/G, T97A, F121Y, Y143R/H/C, S147G, Q148H/K/R, N155H/S and R263K in IN.
Trend of HIV transmitted drug resistance before and after implementation of HAART regimen restriction in the treatment of HIV-1 infected patients in southern Taiwan.
Discussion: Major INSTI mutations have been previously detected in treatment-naive HIV-infected patients from Taiwan, however only one strain has been found to harbor Q148R.
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.
Impact of the HIV-1 genetic background and HIV-1 population size on the evolution of raltegravir resistance.
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
HIV mutation literature information.
PMID: 
2019
Revista espanola de quimioterapia
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