Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.
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
Discussion: L63P and A71T were associated with subtype B, whereas L10V, K20R, M36I, F53L, and L89M were linked to non-B subtypes.
Discussion: We think, however, that the Q58E mutation, together with other accessory mutations, L10V, L33F, and K43T, may have contributed to the higher prevalence of TPV/r resistance in relation to DRV/r observed in our study.
HIV-1 protease inhibitor drug resistance in Kenyan antiretroviral treatment-naive and -experienced injection drug users and non-drug users.
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+
Mutations in the reverse transcriptase and protease genes of human immunodeficiency virus-1 from antiretroviral naive and treated pediatric patients.
The use of dried blood spot specimens for HIV-1 drug resistance genotyping in young children initiating antiretroviral therapy.
PMID: 26192603
2015
Journal of virological methods
Introduction: Only one specimen was predicted to be resistant to protease inhibitors (PI) due to the presence of major and minor PI mutations (L10F, M46I, I54V, L76V and V82A) while 8 specimens had minor PI mutations (A71T (n=3), L10I/V (n=3) and M46L/T (n=2)).
Gag-Protease Sequence Evolution Following Protease Inhibitor Monotherapy Treatment Failure in HIV-1 Viruses Circulating in East Africa.
PMID: 26258548
2015
AIDS research and human retroviruses
Introduction: Of particular relevance to this study were mutations associated with resistance to boosted lopinavir: L10I (three subtype A patients), L10V (one subtype A), K20R (five subtype As and 1 subtype C), L33V (one subtype D), L63P (one subtype A, two subtype Cs, and three subtype Ds).
Introduction: Other common mutations included L10V (observed in four patients), G16E (four patients), and K20R (six patients), none of which was a consensus residue in subtype A, C, or D.
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.
Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.
HIV mutation literature information.
PMID: 
2016
Biochemistry
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