Management of a human immunodeficiency virus case with discordant antiviral drug resistance profiles in cerebrospinal fluid compared with plasma: a case report.
PMID: 35164871
2022
Journal of medical case reports
Abstract: A discordant protease inhibitor mutation/wild-type T74PT in plasma but not in cerebrospinal fluid indicated poor central nervous system penetration due to the selective pressure of drug therapy.
Conclusion: However, discordantly, the accessory nonpolymorphic PI T74TP mutation mixed with wild type appeared only in the plasma but not CSF.
Discussion: Although the T74P mutation is described as nonpolymorphic, the T74TP mutation was mixed with wild type, which has sporadically been reported.
Discussion: The discordant finding of the PI T74TP mutation/wild type in the plasma but not CSF indicates a selective drug pressure in plasma and not in the CSF caused by insuf
Emergence of Resistance in HIV-1 Integrase with Dolutegravir Treatment in a Pediatric Population from the IMPAACT P1093 Study.
PMID: 34694878
2022
Antimicrobial agents and chemotherapy
Table: T74P
Brief Report: Bictegravir/Emtricitabine/Tenofovir Alafenamide Efficacy in Participants With Preexisting Primary Integrase Inhibitor Resistance Through 48 Weeks of Phase 3 Clinical Trials.
PMID: 34897227
2022
Journal of acquired immune deficiency syndromes (1999)
Table: T74P
Detection of Gag C-terminal mutations among HIV-1 non-B subtypes in a subset of Cameroonian patients.
Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F, K43T, F53L, Q58E, A71IL, G73STCA, T74P, N83D, and L89V) are assumed to have ancillary roles such as compensation for lower efficiency of proteolysis caused by major mutations; major resistance mutations (V32I, M46IL, I47VA, G48VM, PMID: 35061671
2022
PloS one
Table: T74P
Temporal Trends in HIV-1 Mutations Used for the Surveillance of Transmitted Drug Resistance.
Result: T74P and L89V were considered to be accessory mutations based on analyses of phenotypic and clinical data derived from the POWER studies that led the FDA approval of darunavir.
Result: Figure 3 shows the locations of the PI-SDRMs and the three candidate mutations (L10F, T74P, and L89V) within the three-dimensional structure of HIV-1 protease.
Result: Three of the mutations were on four expert lists including L10F, T74P, and L89V.
Discussion: Three candidate PI-SDRMs (L10F, T74P, and L89V
Virologic suppression in patients with a documented M184V/I mutation based on the number of active agents in the antiretroviral regimen.
HIV-1 acquired drug resistance to integrase inhibitors in a cohort of antiretroviral therapy multi-experienced Mexican patients failing to raltegravir: a cross-sectional study.
Method: Participants with a history of genotypic/phenotypic drug resistance to protease inhibitors (PIs) or with HIV-1 genotypic drug resistance to PIs at baseline (including D30N, M46I/L, I47V/A, G48V, I50L, I54M/L, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, or L90M) were excluded, despite any reported effects of PI resistance or resistance
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 PI-R substitutions were D30N, V32I, M46I/L, I47V/A, G48V, I50V/L, I54M/L, Q58E, T74P, L76V, V82A/F/L/S/T, N83D, I84V, N88S and L90M in PR.
HIV mutation literature information.
PMID: 
2022
Journal of medical case reports
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