Restriction fragment mass polymorphism (RFMP) analysis based on MALDI-TOF mass spectrometry for detecting antiretroviral resistance in HIV-1 infected patients.
PMID: 23480551
2013
Clinical microbiology and infection
Abstract: The concordance rates between the RFMP and direct sequencing assays for the examined codons were 97% (K65R), 97% (T69Ins/D), 97% (L74VI), 97% (K103N), 96% (V106AM), 97% (Q151M), 97% (Y181C), 97% (M184VI) and 94% (T215YF) in the reverse transcriptase coding region, and 100% (D30N), 100% (M46I), 100% (G48V), 100% (I50V), 100% (I54LS), 99% (V82A), 99% (I84V) and 100% (L90M) in th
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: However, I84V was also observed in 0.32% of control samples, indicating that it cannot necessarily be concluded that it was directly selected by atazanavir.
Result: Only 6 (1.9%) index patients experiencing virological failure had a major atazanavir-associated mutation, all in isolation:
Discussion: Our findings show that very few patients failing a therapy containing atazanavir are likely to have developed one of the major protease resistance mutations (I50L, I84V and N88S) that confer high-level phenotypic resistance to this drug.
Discussion: They described eight mutations that had an adverse effect on viral load reduction at 3 months, but only two of these (M46I and I84V) coincided with those identified in our analysis.
Importance of polar solvation and configurational entropy for design of antiretroviral drugs targeting HIV-1 protease.
PMID: 23614718
2013
The journal of physical chemistry. B
Abstract: On the other hand, we predict that the mutant I84V causes drug resistance against KNI-10075 while KNI-10033 is more potent against the I84V mutant compared to wild-type protease.
Extreme multidrug resistant HIV-1 protease with 20 mutations is resistant to novel protease inhibitors with P1'-pyrrolidinone or P2-tris-tetrahydrofuran.
PMID: 23590295
2013
Journal of medicinal chemistry
Result: Comparison with the PR/amprenavir structure reveals that mutations D30N, V32I, I47V and I84V in PR20 alter the size, shape and charge of the S2/S2' pocket in the PR20/amprenavir complex as described previously for the PR20/darunavir and PR20/saquinavir (3UFN) complexes.
Result: In addition, the smaller I84V mutation results in the loss of the van der Waals contact seen between the sulfonyl oxygen of amprenavir and Ile 84' of wild-type PR.
Result: The increase in size and the loss of charge in the S2 pocket of PR20 causes the THF ring of amprenavir to shift tow
Complex patterns of protease inhibitor resistance among antiretroviral treatment-experienced HIV-2 patients from Senegal: implications for second-line therapy.
PMID: 23571535
2013
Antimicrobial agents and chemotherapy
Abstract: Common protease substitutions included V10I, V47A, I54M, V71I, I82F, I84V, L90M, and L99F, and most patients harbored viruses containing multiple changes.
Abstract: In addition, the triple mutant that included I54M plus I84V plus L90M was resistant to all three PIs (31-, 10-, and 3.8-fold increases in the mean EC50 for darunavir, saquinavir, and lopinavir, respectively).
"Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."
Method: In our study, samples with at least one of the major PI RAM of the IAS-USA list as follows: D30N, V32I, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, L90M were considered as PI-resistant issued from PI-experienced patients.
Result: Among subtype B samples, the major
Tenofovir-based regimens associated with less drug resistance in HIV-1-infected Nigerians failing first-line antiretroviral therapy.
Result: Three patients had selected IAS PI major mutations (I50V, N83D, I84V and L90M).
Antiviral resistance and correlates of virologic failure in the first cohort of HIV-infected children gaining access to structured antiretroviral therapy in Lima, Peru: a cross-sectional analysis.
Method: The OLA was conducted according to the NIH protocol for mutations at HIV-1B protease positions D30N, I50V, V82A, V82S, V82T, I84V, N88D, and L90M as well as reverse transcriptase positions K103N, Y181C, K65R, T215F, T215Y, M184V, and Q151M.
A Comparative Insight into Amprenavir Resistance of Mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 Protease Based on Thermodynamic Integration and MM-PBSA Methods.
PMID: 26587633
2013
Journal of chemical theory and computation
Abstract: In this work, we examine L10I, G48V, L63P, A71V, G73S, V82A, and I84V single mutant HIV-1 PR strains in complexes with saquinavir to elucidate drug-protease interactions and dynamics.
Abstract: It was shown that mutations conferring major resistance (G48V, L63P, I84V) did not present these interactions.
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.
HIV mutation literature information.
PMID: 
2013
Clinical microbiology and infection
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