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
Method: MDR769 L33F is based on the previously studied multi-drug resistant variant 769, MDR769, which contains the mutations Q7K, L10I, M36V, M46L, I54V, I62V, L63P, A71V, V82T, I84V, L90M.
Structural studies on molecular mechanisms of Nelfinavir resistance caused by non-active site mutation V77I in HIV-1 protease.
Introduction: The other mutations which were co-occurring with DBM and TPM included major mutations like- M46IL, I54MV, I84V, L90M, N88S, V32I, I47V, V82AS, D30N, G48V; and accompanied by minor mutations like- L10I, I13V, L63P, A71V, L89M, I93L, E35DN, I15V, D60E, L24I etc.
Outcome of patients on second line antiretroviral therapy under programmatic condition in India.
Result: In the experienced subgroup, at least seven major (M46I, V82A, I54V, L90M, I84V, M46L, and L76V) and 15 accessory mutations (I62V, A71V, L10I, L10V, K20R, L33F, Q58E, K20T, L10F, T74S, F53L, K43T, G73S, I85V, and A71I) developed and were ass
Conformational variation of an extreme drug resistant mutant of HIV protease.
PMID: 26397743
2015
Journal of molecular graphics & modelling
Method: Plasmid DNA encoding PR (subtype B of group M) with 20 mutations Q7K; L10F; I13V; I15V; D30N; V32I; L33F; E35D; M36I; S37N; I47V; I54L; Q58E; I62V; L63P; A71V; I84V; N88D; L89T and L90M (termed PR20) cloned between the Nde1 and BamH1 sites
Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.
Epidemiological and molecular characteristics of HIV infection among money boys and general men who have sex with men in Shanghai, China.
PMID: 25653132
2015
Infection, genetics and evolution
Result: Several minor mutations were detected in the protease (PR) region of the pol gene: L10I (3.8%), V11I (1.9%), L33F (1.9%) and A71T/V (17.3%); and several others were detected in the reverse transcriptase (RT) region of the pol gene: T69A (1.9%), V118I (11.5%), L210M (1.9%), V179I (11.5%) and K101Q (1.9%).
Viral Genetic Diversity and Polymorphisms in a Cohort of HIV-1-Infected Patients Eligible for Initiation of Antiretroviral Therapy in Abuja, Nigeria.
PMID: 25582324
2015
AIDS research and human retroviruses
Result: In the PR region, one sample displayed the K43T mutation; another one had the M46L, while a third specimen had K53Y, A71V, and I85V.
Discussion: A rare treatment-associated mutation K53Y, the polymorphic mutation A71V, as well as the PI-selected mutation I85V were also found in one sample each.
Exploring the drug resistance of V32I and M46L mutant HIV-1 protease to inhibitor TMC114: flap dynamics and binding mechanism.
PMID: 25562662
2015
Journal of molecular graphics & modelling
Introduction: Our previous studies on binding Gibbs free energies for WT, I50V single mutant and I50L/A71V double mutant showed that I50V decreases the binding affinity for TMC114, while the double mutant I50L/A71V increases the binding affinity and may be well adapted to accommodate the TMC114 in the active site.
The prevalence of transmitted HIV drug resistance among MSM in Anhui province, China.
Result: However, some accessory mutations that did not affect susceptibility to ARV drugs were found in the protease gene, including L10I/L/V (3.0%; 4/133), V11I/V (3.0%; 4/133), L33F (2.3%; 3/133), and A71A/V/T (12.8%; 17/133).
Discussion: Other commonly observed mutations were T69A/N/S, V179E, L10I/L/V, V11I/V, L33F, and A71A/T/V; none of these mutations is known to confer drug resistance to NRTIs, NNRTIs, or PIs.
HIV mutation literature information.
PMID: 
2015
Biochemistry and biophysics reports
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