Abstract: Minor PI mutations including A71T, G48E, G48R, I13V, K20I, K20R, L10I, L10V, L33F, L63P, T74S, V11I, and V32L were detected among the ART-experienced (36.2 vs.
Result: Fourteen (29.8 %) ART-experienced IDUs harboured only minor mutations comprising of 1(2.1 %) K20I, 7 (8.5 %) K20R, 3 (6.4 %) L10I, 1 (2.1 %) V32L and 2 (12.5 %) L10V+
The Evolving Genotypic Profile of HIV-1 Mutations Related to Antiretroviral Treatment in the North Region of Brazil.
Result: In contrast, several secondary mutations were found to differ between B and non-B subtypes: L63P (p < 0.001) and A71T (p = 0.021) were higher in subtype B, and M36I (p < 0.001), K20R (p < 0.001), L10V (p = 0.004), L89 M (p < 0.001), and F53L (p = 0.011) were higher in non-B subtypes.
Result: In the experienced subgroup, at least seven major (M46I, Discussion: L63P and A71T were associated with subtype B, whereas L10V, K20R, M36I, F53L, and L89M were linked to non-B subtypes.
The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.
PMID: 29124158
2015
Biochemistry and biophysics reports
Introduction: Clinical isolates previously obtained from the Wayne State University Infectious Disease Clinic in Detroit, MI contain major drug resistance mutations L33F, I47V, I50V, I54M, L76V, V82I/F, and I84F as well as nonpolymorphicaccessory mutations L10V/G, V11I, I13V, K20T/R, L33I/M, K43T, F53L, A71L, T74P, and L89V.
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: Mutation K20R alters a residue near the protein surface showing varied interacti
The role of mutations at codons 32, 47, 54, and 90 in HIV-1 protease flap dynamics.
Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
Discussion: A high frequency of minor PI resistance mutations (M36I, L63P, and K20R/I) has been reported in newly diagnosed immigrants from Spain, infected with non-B subtypes.
Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.
PMID: 23711895
2013
The Journal of antimicrobial chemotherapy
Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and I93M) or were not significantly associated with atazanavir exposure (L10I/F/V, G16E, K20R/M/I/T, L24I, V32I, L33I/F/V, M36L/V, M46L, G48V, I54V
HIV mutation literature information.
PMID: 
2015
PloS one
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