Introduction: The DetMDRs differ from isolates previously studied by our group in that these contain the major drug resistance mutations L33F, I47V, I50V, I54M, L76V, V82I/F, and I84F not present in the previous cohort (Table 1).
Revealing origin of decrease in potency of darunavir and amprenavir against HIV-2 relative to HIV-1 protease by molecular dynamics simulations.
Abstract: The decrease in binding free energies for PR2 relative to PR1 is found to arise from the reduction of the van der Waals interactions induced by the structural adjustment of the triple mutant V32I, I47V and V82I.
Introduction: APV is a potent inhibitor and efficiently inhibits the activity of PR1 (Figure 1C and D), but some mutations (V32I, I47V and V82I) in PR2 produce natural resistance to APV.
Result: As shown from Figure 7B, the residues involving the increase of the van der Waals interaction in PR2 are V32I, V82I, D29', D
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 and time of treatment failure: I13V, K14R, K20I, E35Q, M36I, R41K, R57K, Q61N, C67E, H69K, V82I and L89M (Table S1).
Structures of darunavir-resistant HIV-1 protease mutant reveal atypical binding of darunavir to wide open flaps.
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 for SQV, a second molecule was found in a location adjacent to the usual active site location in PMID: 23888308
2013
Virus genes
Abstract: Approximately 70% polymorphisms as minor mutations were observed in protease gene, of which 14 distinct amino acids changes were linked to partial DR such as G16E, K20R, M36I, D60E, I62V, L63P, I64M, H69K, T74A/S, V77I, V82I, I85V, L89M, and I93L.
Molecular epidemiology of HIV in a cohort of men having sex with men from Istanbul.
PMID: 23296905
2013
Medical microbiology and immunology
Abstract: In these patients, the nucleoside reverse transcriptase inhibitor (NRTI)-associated resistance mutations M41L, T215C, V75I, T69N, the non-NRTI associated mutations V106I, E138A, K103N and the protease inhibitor associated mutations Q58E and V82I were detected.
Tenofovir-based regimens associated with less drug resistance in HIV-1-infected Nigerians failing first-line antiretroviral therapy.
Result: Secondary mutations related to polymorphisms (I13V (95%), M36I (83%), H69K (82%), V82I (43%) and L63P (28%)) also occurred among those genotyped.
Short communication: Drug resistance mutations in the HIV type 1 protease and reverse transcriptase genes in antiretroviral-naive Vietnamese children.
PMID: 22260721
2012
AIDS research and human retroviruses
Abstract: Minor mutations were found in the protease gene, including L10I, I13V, G16E, M36I, D60E, I62V, I64V, L63P, H69K, V82I, and I93L.
Critical differences in HIV-1 and HIV-2 protease specificity for clinical inhibitors.
Discussion: M36I occurred in 28 viruses (98%), T74S occurred in two viruses (7%), I93L occurred in 27 isolates with a prevalence of 93%, and V82I occurred in one virus (3.4%).
Discussion: However, that study reported 46% prevalence for K20R and 8% for V82I, which are higher than the findings in the current study.
HIV mutation literature information.
PMID: 
2014
Discoveries (Craiova, Romania)
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