Emergence of Resistance to Integrase Strand Transfer Inhibitors during Dolutegravir Containing Triple-Therapy in a Treatment-Experienced Patient with Pre-Existing M184V/I Mutation.
Result: This resistance test revealed infection with HIV-1 subtype B and the presence of the accessory mutations M36I, I62V, and V77I not causing any clinically relevant resistance to antiretroviral drugs.
First case of Dolutegravir and Darunavir/r multi drug-resistant HIV-1 in Cameroon following exposure to Raltegravir: lessons and implications in the era of transition to Dolutegravir-based regimens.
PMID: 32843050
2020
Antimicrobial resistance and infection control
Conclusion: Detected RAMs were M41L, K70Q, V75I, Q151M, M184V and T215F for NRTI; K103N and V108I for NNRTI; and L10F, K20I, M36I, M46I, I47V, I54L, L63H, L76V, V82S and L89I for PI/r.
HIV-1 Gag mutations alone are sufficient to reduce darunavir susceptibility during virological failure to boosted PI therapy.
PMID: 32556165
2020
The Journal of antimicrobial chemotherapy
Table: M36I
HIV-1 drug resistance mutations detection and HIV-1 subtype G report by using next-generation sequencing platform.
Abstract: In the present study polymorphic mutation in the position of K20R, M36I, H69K, L89 M were properly reported in CRF35AD that is dominant in Iranian HIV patients.
Abstract: The Protease inhibitor (PI) minor and major mutations were not reported but more than 95% of samples had polymorphisms mutation in K20R, M36I, H69K, L89 M positions.
Polymorphisms and drug resistance analysis of HIV-1 isolates from patients on first line antiretroviral therapy (ART) in South-eastern Nigeria.
Result: Polymorphisms at known secondary mutation sites (K20I, M36I/L, H69K/R and L89M) were found in all the samples while L63T/P/S/Q was found in 83.3% (10/12) and 31.3% (5/16) of subtypes G/UG and CRF02_AG respectively.
Table: M36I/L
Table: M36I
Discussion: I13V/A, K20I,
Discussion: A study on PI-naive Nigerian HIV-patients have earlier identified I13V, M36I and H69K as wild-type consensus mutations for HIV-1 subtypes G', G, CRF02_AG, CRF06_cpx, and A.
Highly drug-resistant HIV-1 protease reveals decreased intra-subunit interactions due to clusters of mutations.
Result: All three mutants utilize mutations in the hinge region at 35 and compensating M36I mutation to drive rearrangements of the hinge and alter its separation from the flap.
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: As shown in Figure 4C, the smaller M36I residue in PRS5B structures retains significant van der Waals contacts with Ile15' and Leu38' and the mutated I33L sidechain due to a shift in its main chain.
Result: By allowing a continuation of van der Waals contacts at the hinge-Loop 1 interface using a shorter side chain, M36I counterbalances the effects of
Detection of human immunodeficiency virus type 1 transmitted drug resistance among treatment-naive individuals residing in Jakarta, Indonesia.
Result: Despite no drug resistance-related major mutations were identified, several drug resistance-related minor mutations including M36I [amino acid substitution from methionine (M) to isoleucine (I) at position 36 in the PR gene] (85.71%), H69K (85.71%), L89M (76.19%), K20R (57.14%), and G16E (47.62%), were detected in the PR genes (Table 1).
Discussion: In the present study, no TDR against PIs was detected, while minor mutations, M36I (85.71%), H69K (85.71%), L89M (76.19%), K20R (57.14%), and G16E (47.62%), were frequently detected among 85.7
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 HIV genotype at this time reported the RT gene mutations M184V and L100L/F, conferring resistance to emtricitabine and lamivudine, and protease gene mutations L10V, M36I/M, K43R, L63P,
Conclusion: The genotype at this time demonstrated no reverse transcriptase (RT) gene mutations, but the following protease gene mutations: L10V, M36I, L63P, H69H/Y, A71T/A, and I93L.
Kinetic and thermodynamic characterisation of HIV-protease inhibitors against E35D upward arrowG upward arrowS mutant in the South African HIV-1 subtype C protease.
PMID: 31409143
2019
Journal of enzyme inhibition and medicinal chemistry
Discussion: M36I (present in the wild type) is reported to regulate the size of the binding cavity of the protease and influence the shape of the active site.
Discussion: The wild type contains only the M36I polymorphism.
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 mutation literature information.
PMID: 
2020
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