Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F, K43T, F53L, Q58E, A71IL, G73STCA, T74P, N83D, and L89V) are assumed to have ancillary roles such as compensation for lower efficiency of proteolysis caused by major mutations; major resistance mutations (V32I, M46IL, I47VA, G48VM, PMID: 31920003
2020
The FEBS journal
Introduction: Two mutations in PRS5B have a major association with drug-resistance (M46L and I84V), while nine are classified as minor drug resistance mutations (L10I, V11I, M36I, I54V, I62V, I63P, I64V, A71V, and G73T).
High resistance to reverse transcriptase inhibitors among persons infected with human immunodeficiency virus type 1 subtype circulating recombinant form 02_AG in Ghana and on antiretroviral therapy.
Introduction: Previous research in Ghana has shown low prevalence (5%) of drug resistance, with some studies reporting no transmitted drug resistance mutations, while others observed only minor mutations L10I, L10 V, V11I, and E35G in 4 patients and V179E in another.
Genetic diversity and antiretroviral resistance-associated mutation profile of treated and naive HIV-1 infected patients from the Northwest and Southwest regions of Cameroon.
Result: Minor PI mutations were present in 27.6% (66/239) of the sequences with L10I/V being the most prevalent (22.2%) mutation followed by V11I (4.6%) and E35G (2.5%).
Characterization of minority HIV-1 drug resistant variants in the United Kingdom following the verification of a deep sequencing-based HIV-1 genotyping and tropism assay.
Result: Most of these minority drug resistance mutations were detected in the 67 cART-experienced individuals, e.g., the HIV-1 genotype of the following patients consisted of a mixture of majority and minority drug resistance mutations: patient SG79 (PR V11I 99.9%, K20I 99.9%; RT E44D 1.3%, D67N 1.1%, L100I 1.7%, M184V 84.9%, M184I 14.8%, K219Q 2.1%, INT E157Q 99.8%), patient SG86 (RT M184V 99.8%, INT L74M 97.9%, L74I 1.9%, E92Q 86
Identification of a Structural Element in HIV-1 Gag Required for Virus Particle Assembly and Maturation.
Figure: All revertant mutations were selected in MT-4 cells, except for V11I (*), which arose upon propagation of T58A/P122A in Jurkat cells.
Discussion: T58A improved replication capacity only for I124A virus, but the addition of V11I was required to fully rescue replication kinetics of both T58A/P122A and T58A/I124A mutants.
Discussion: V11I alone did not rescue the replication ability of either P122A or I124A.
Mechanism of Darunavir (DRV)'s High Genetic Barrier to HIV-1 Resistance: A Key V32I Substitution in Protease Rarely Occurs, but Once It Occurs, It Predisposes HIV-1 To Develop DRV Resistance.
Discussion: reported that 11 amino acid substitutions, V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V, and L89V, which appear to be associated with HIV-1 resistance against DRV, were identified among HIV-1 variants isolated from patients treated with DRV-including regimens on POWER studies.
Gag P2/NC and pol genetic diversity, polymorphism, and drug resistance mutations in HIV-1 CRF02_AG- and non-CRF02_AG-infected patients in Yaounde, Cameroon.
Method: Most of the subjects with major resistance mutation to NRTIs and/or NNRTIs harbored viruses that also had secondary resistance mutations to PIs: L10I, V11I, K20V, and K20I (Table 2).
Table: V11I
Surveillance of HIV-1 pol transmitted drug resistance in acutely and recently infected antiretroviral drug-naive persons in rural western Kenya.
Virological response, HIV-1 drug resistance mutations and genetic diversity among patients on first-line antiretroviral therapy in N'Djamena, Chad: findings from a cross-sectional study.
HIV mutation literature information.
PMID: 
2022
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