Result: Regarding secondary PI RAM the strongest associations were found with the mutations K55R (covariation frequency 36.4%, phi = 0.32), I54V (covariation frequency 23.3%, phi = 0.27), and L33F (covariation frequency 27.2%, phi = 0.27).
Result: This cluster was linked to L24I, I54V, and V82A mutations.
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, A62V, K65RN, D67NG, T69D, T69 insertions, T69 deletion, K70REGQ, L74VI, V75MT, F77L, Y115F, F116Y, Q151M, M184VI, L210W, T215YFSDCIV, and Table: I54V
Increasing trends in primary NNRTI resistance among newly HIV-1-diagnosed individuals in Buenos Aires, Argentina.
PMID: 24093951
2013
Journal of the International AIDS Society
Table: I54V
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
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.
Introduction: Additionally, the effect of individual mutations I54V versus I54A on inhibitor binding is compared.
Introduction: Analysis of patient sequences in the Stanford HIV drug resistance database revealed that I54A also shares many of the mutations frequently observed together with I54V (detailed analysis in Supplementary Information).
Introduction: As mentioned previously, the binding of Flap+(I54V) to both APV and DRV was enthalpically unfavorable, and these reactions were entirely driven by the entropy of binding (Table 1).
Introduction: As with APV, only the Flap+(I54V) variant had an unfavorable binding enthalpy to DRV.
Introduction: Besides G48V or I54V, Flap+(
Persistence of HIV-1 transmitted drug resistance mutations.
PMID: 23904291
2013
The Journal of infectious diseases
Table: I54V
Energetic basis for drug resistance of HIV-1 protease mutants against amprenavir.
PMID: 22350569
2012
Journal of computer-aided molecular design
Abstract: Drug resistance arises from an increase in the energetic contribution from the van der Waals interactions between APV and PR (V32I, I50V, and I84V mutant) or a rise in the energetic contribution from the electrostatic interactions between the inhibitor and its target (I54M and I54V mutant).
Abstract: However, the affinities of the drug resistant protease variants V32I, I50V, I54V, I54M, I84V and L90M to amprenavir are decreased 3 to 30-fold compared to the wild-type.
HIV-1 integrase resistance among antiretroviral treatment naive and experienced patients from Northwestern Poland.
Result: It must be noted, that three of the patients with developed drug resistance were heavily experienced with reverse transcriptase (RT) and protease (PR) mutations (patient 1: RT: M41L, K103N, M184V, T215S; PR: L10I; patient 2: PR: M41L, V118I, K103N, M184V, L210W, T215S, RT: L10I,
HIV mutation literature information.
PMID: 
2013
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