Drug Resistance to HIV-1 Integrase Inhibitors Among Treatment-Naive Patients in Beijing, China.
PMID: 35300056
2022
Pharmacogenomics and personalized medicine
Result: Additionally, the most common protease inhibitors associated mutation was Q58E (0.23%, 11/865), followed by M46I (4.05%, 5/865) and L33F (2.89%, 3/865)(as shown in Figure 2).
HIV-1 drug resistance profiling using amino acid sequence space cartography.
Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F
Result: In Class III, only the Gag mutation P453L positively correlated with some major mutations as follows: L33F (phi = 0.28, p = 0.004), M46I (phi = 0.30, p = 0.001), I54L (phi = 0.27, p = 0.022), I54V (phi = 0.38, p < 0.001), V82A (phi = 0.20, p = 0.031), V82T (phi = 0.27, p = 0.021), and I84V (phi = 0.38, p < 0.001), (Table 3).
Table: L33F
Prevalence of HIV-1 drug resistance in Eastern European and Central Asian countries.
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: L33F
Cantilever-centric mechanism of cooperative non-active site mutations in HIV protease: Implications for flap dynamics.
PMID: 34030114
2021
Journal of molecular graphics & modelling
Abstract: The HP3 PR contained the I13V, I62V, and V77I mutations while HP4 PR contained the same mutations with the addition of the L33F mutation.
Virological response and resistance profile in highly treatment-experienced HIV-1-infected patients switching to dolutegravir plus boosted darunavir in clinical practice.
Abstract: Among 13 non-responding patients for whom a genotypic resistance test result at failure was available, only two (15.4%) accumulated further resistance in integrase (Y143C/H/R; S147G and N155H) and protease (V32I, L33F, I54L).
Acquired HIV-1 Protease Conformational Flexibility Associated with Lopinavir Failure May Shape the Outcome of Darunavir Therapy after Antiretroviral Therapy Switch.
Abstract: The HIV-1 protease variants were from clinical isolates with a combination of drug resistance mutations; MUT-1 (M46I, I54V, V82A, and L10F), MUT-2 (M46I, I54V, L76V, V82A, L10F, and L33F), and MUT-3 (M46I, I54V, L76V, V82A, L90M, and F53L).
Introduction: Research shows that the emergence of V32I, L33F, I4
Multiple Molecular Dynamics Simulations and Free-Energy Predictions Uncover the Susceptibility of Variants of HIV-1 Protease against Inhibitors Darunavir and KNI-1657.
Abstract: Focused on the complexes of wild type (WT) PR and two mutant PRs (V32I/L33F/I54M/V82I and V32I/L33F/I54M/I84 V) with inhibitors Darunavir (DRV) and KNI-1657 (KNI), respectively, we have conducted research on the conformational dynamics and the resistance mechanism caused by residue mutations through multiple molecular dynamics (MD) simulations combined with an energy (MM-PBSA and solvated interaction energy (SIE)) prediction.
HIV-1 molecular transmission network among sexually transmitted populations in Liaoning Province, China.
Abstract: The L33F mutation at the HIV-1 resistance mutation site constitutes the interconnection in the largest transmission cluster in the network.
Result: Among them, 9 cases were protease inhibitor-related resistance, and the main resistance sites were L33F, V82A, Q58E, M46L, M46I; There were 4 cases of nucleoside reverse transcriptase inhibitor resistance, the main mutation sites were V75VI, K219Q, T215A, K65R; There were 5 cases of non-nucleoside reverse transcriptase inhibitor resistance, the main mutation sites were
ViMRT
HIV mutation literature information.
PMID: 
2022
Pharmacogenomics and personalized medicine
