Discussion: Similarly, mutations L10V/I, L19P, E35D, I64L/M and K70R occurred in >= 25% of CRF02_AG patients at a proportion that is significantly greater than in subtype B in this study.
Highly drug-resistant HIV-1 protease reveals decreased intra-subunit interactions due to clusters of mutations.
Result: All three resistant proteases have mutations for Glu35 (E35N or E35D) that break the ion pair with flap residue Arg57' and a compensating M36I.
Result: In PRS17/DRV, the E35D side chain forms an ion pair with K20R and a hydrogen bond with the side chain of Asn83'.
Result: Within each hinge mutation cluster, E35N/D and M36I are shared, although each mutant contains different accessory mutations.
Kinetic and thermodynamic characterisation of HIV-protease inhibitors against E35D G S mutant in the South African HIV-1 subtype C protease.
PMID: 31409143
2019
Journal of enzyme inhibition and medicinal chemistry
Abstract: Herein, we report the effect of nine FDA approved protease inhibitor drugs against a new HIV-1 subtype C mutant protease, E35D G S.
Abstract: The mutant has five mutations, E35D, two insertions, position 36 (G and S), and D60E.
Introduction: The variant has the following mutations; E35D, I36G, two insertions at position 35 (G and S), and D60E and is referred to as E35D G S (Figure S1) with the upward arrows showing positions of insertions.
Method: Briefly, C-SA HIV protease and mutant E35D G S were cloned in pGEX-6P-1 and expressed in Escherichia coli BL21 (DE3) pLysS.
Result: The reorganization of the hinge loop by mutations E35D, M36I, and S37D that breaks the ion pair anchoring the flaps and thereby increases the flap flexibility as described in the previously determined complex of PRS17 with darunavir (DRV) is also observed in the current substrate analogue complexes.
HIV Viral Rebound Due to a Possible Drug-Drug Interaction between Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide and Calcium-Containing Products: Report of 2 Cases.
PMID: 30798679
2019
Journal of the International Association of Providers of AIDS Care
Conclusion: The genotype performed at this time showed the following protease inhibitor gene mutations: I13I/V, E35D, D60E, L63P, I64V, and V77I and RT mutation V106I/V/M conferring resistance to efavirenz and nevirapine.
HIV Reverse Transcriptase and Protease Genes Variability Can Be a Biomarker Associated with HIV and Hepatitis B or C Coinfection.
Result: Global sequence analysis showed that the most frequent amino acid substitutions in RT were S162C (29.4%), T200A (35.3%), M184V (32.3%), L214F (67.6%), I135T (55.9%), D177E (26.5%) and E122K (44.1%), and the most in PR were V15I (41.2%), M36I (38.2%) and E35D (23.5%).
Polymorphisms and Mutational Covariation Associated with Death in a Prospective Cohort of HIV/AIDS Patients Receiving Long-Term ART in China.
Abstract: Among them, 7 polymorphisms (L74I, K103N, V106A, Y181C, G190A, T215I and P225H) were known to be drug resistance mutations, 7 polymorphisms (E6D, E35D, S37N, I93L, E169D, T200V and T200E were considered to be potential drug resistance mutations, and 6 polymorphisms (T39A, K43E, S68N, Q197K, T200V and E22
Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.
Abstract: In PRS17, the hinge loop cluster of mutations, E35D, M36I and S37D, contributes to the altered flap dynamics by a mechanism similar to that of PR20.
Result: Comparison of PRS17/DRV with PR20/DRV complex, which has E35D, M36I, S37N and I62V mutations, reveals that the hinge loop conformation of PR20 in subunit A is similar to PRS17 except for absence of the K20R mutation and consequent absence of the ion pair interactions observed between Arg20 and Asp35 in
HIV mutation literature information.
PMID: 
2020
The Journal of antimicrobial chemotherapy
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