Method: The PRP51 construct contains 14 mutations (L10I, I15V, K20R, L24I, V32I, L33F, M36I, M46L, I54M, L63P, K70Q, V82I, I84V, and L89M) plus three other mutations Q7K to minimize autoproteolysis and C67A and C95A to prevent cysteine-induced aggregation.
Result: Also, the flap hinge region comprising residues 34 to 43 shares a very similar conformation in
Virological efficacy and immunological recovery among Ethiopian HIV-1 infected adults and children.
Result: In 3 patients, naturally occurring polymorphisms that may or may not have an impact on levels of drug resistance were found (mutations M36I, H69K and L89M) (Table 2).
Table: M36I
Zero prevalence of primary drug resistance-associated mutations to protease inhibitors in HIV-1 drug-naive patients in and around Aligarh, India.
PMID: 24423716
2014
Journal of infection in developing countries
Abstract: The most frequent mutations were H69K and I93L (52 of 52 strains), followed by I15V (80.7%), L19I (69.2%), M36I (67.3%), R41K (94.2%), L63P (61.5%), and L89M (82.7%).
Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.
Discussion: Results from the HIV-1 drug resistance mutation research by the International AIDS Society-USA (updated in March 2013) have revealed that PI resistance mutation sites are L10I, K20M, V32I, M36I, M46I/L, I47V/A, I50V, Q58E, A71V, G73S, V82A/F/T, I84V, L89V,L90M; NRTIs resistance mutations are M41L, A62V, PMID: 24629078
2014
BMC bioinformatics
Result: According to the IAS-USA, the mutations associated with drug resistance, with a p >10%, were L10I, M36I, I62V, L63P, I64V, A71V/T, V77I, L90M, and I93L.
Result: We modelled the proteins with unusual mutations (L5F, D29V, L63G, L63R, P79L and T91V), natural polymorphisms (L63H andL63S), and drug-resistant mutant PRs with single mutations or patterns of mutations (D30N
HIV-1 pol diversity among female bar and hotel workers in Northern Tanzania.
Result: The most frequent polymorphisms were seen at positions M36I (81%), H69K (86%), L89M (74%), and I93L (62%).
Discussion: H69K (86%), M36I (81%), L89M (74%), and I93L (62%) were considered to be subtype-specific natural polymorphisms since they occur at high frequency in HIV-1 subtypes A1, C or D.
Effects of PRE and POST therapy drug-pressure selected mutations on HIV-1 protease conformational sampling.
Result: Although PR20 does not show a predominant closed flap orientation in the absence of inhibitor, this construct also contains the following mutations considered to be within the hydrophobic core: L10F/I13V/I15V/I33F/M36I/-I62V/L90M.
Result: Interestingly, the POST sequence contains hydrophobic core mutations L10I/I15V/M36I, which are mutated positions shared by PR20.
Result: Recently, we showed by DEER studies that addition of M36I/D30N to A71V restores a predomin
Persistence of frequently transmitted drug-resistant HIV-1 variants can be explained by high viral replication capacity.
Phenotypic characterization of virological failure following lopinavir/ritonavir monotherapy using full-length Gag-protease genes.
PMID: 25096075
2014
The Journal of antimicrobial chemotherapy
Result: A number of protease polymorphisms were present both at baseline an
Discussion: M36I has been associated with PI exposure, though was not linked to reduced susceptibility in a commercial phenotypic susceptibility system incorporating only patient-derived protease sequences.
Discussion: The resistance pathway involving M36I could therefore involve the Gag positions in Table S2.
Discussion: We detected a second individual (Patient 3204) with an emergent reduction in PI susceptibility (13-fold to lopinavir), also on a background of reduced susceptibility and associated with amino acid changes in Gag and M36I in protease.
Impact of M36I polymorphism on the interaction of HIV-1 protease with its substrates: insights from molecular dynamics.
Abstract: CONCLUSIONS: With multiple approaches and analyses we identified structural and dynamical determinants associated with the changes found in the binding affinity of the M36I variant.
Abstract: The observed impact of M36I, suggest that combination with other non-B subtype polymorphisms, could lead to major effects on the interaction with the 12 known cleavage sites, which should impact the virion maturation.
Conclusion: By contrast, analysis of the RH-IN substrate showed that the interaction between the residue at the P4 and P5 positions and the M36I enzyme was considerably over that of the WT enzyme (Additional file 8).
Conclusion: In this study we systematically analyzed structural and dynamical features related to the impact of the M36I mutation on the interaction of
ViMRT
HIV mutation literature information.
PMID: 
2014
ACS chemical biology
