Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
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
Abstract: Recognized major atazanavir mutations were found in six atazanavir-experienced patients (P < 0.001), including I50L and N88S.
Introduction: Randomized controlled trials have shown that the key substitutions in patients failing atazanavir-containing regimens are I50L and N88S.
Result: Only 6 (1.9%) index patients experiencing virological failure had a major atazanavir-associated mutation, all in isolation: I50L (n = 3), I84V (n = 2) and N88S (n = 1) (Table 2).
Result: Specifically, none of the patients who were observed to have I15S, K43T, I50L, V82T, I84V,
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.
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.
Potent antiviral HIV-1 protease inhibitor GRL-02031 adapts to the structures of drug resistant mutants with its P1'-pyrrolidinone ring.
PMID: 22401672
2012
Journal of medicinal chemistry
Discussion: The dynamic side chain position of Asp30 has been observed in various D30N single mutants and double mutants such as D30N/N88D and D30N/N88S.
Virologic failures on initial boosted-PI regimen infrequently possess low-level variants with major PI resistance mutations by ultra-deep sequencing.
Abstract: Overall, 3/36(8.3%) subjects had DRMs identified with Stanford-HIVdb weights >12 for ATV or LPV: N88S (at 0.43% level-mutational load 1,828) in 1 subject on ATV; I50V (0.44%-mutational load 110) and L76V (0.52%-mutational load 20) in 1 subject each, both on LPV.
Abstract: The most common UDS-detected DRM were NRTI in 18 subjects: M184V/I (11), TAMs(7) & K65R(4); PI DRMs were detected in 9 subjects: M46I/V(5), F53L(2), I50V(1), D30N(1), and N88S(1).
Result: Nineteen of 24 (79.2%) had any PI,
The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?
2Conclusion: The strategy of combining mutation-selecting drugs with ""resensitized"" drugs has already been discussed for the reverse transcriptase mutation M184V in NRTI-containing therapies and has also been shown to be an adequate option for a couple of other mutations including the mutation N88 S."
In Vivo validation of a bioinformatics based tool to identify reduced replication capacity in HIV-1.
PMID: 21603285
2010
The open medical informatics journal
Discussion: N88D/S did not have a significant effect on fitness in the statistical model and was not tested.
Discussion: Similarly, patients with the D30N mutation often develop the N88D/S mutation.
HIV-1 protease mutations and protease inhibitor cross-resistance.
PMID: 20660676
2010
Antimicrobial agents and chemotherapy
Abstract: Of the mutations with the greatest effect on PI susceptibility, I84AV was associated with decreased susceptibility to eight PIs; V32I, G48V, I54ALMSTV, V82F, and L90M were associated with decreased susceptibility to six to seven PIs; I47A, G48M, I50V, L76V, V82ST, and N88S were associated with decreased susceptibility to four to five PIs; and D30N, PMID: 20660190
2010
Journal of virology
Abstract: AE protease has been observed to develop resistance through a nonactive-site N88S mutation in response to nelfinavir (NFV) therapy, whereas clade B protease develops both the active-site mutation D30N and the nonactive-site mutation N88D.
Abstract: This weaker affinity may lead to the nonactive-site N88S variant in AE, which exhibits significantly decreased affinity for both NFV and DRV.
HIV mutation literature information.
PMID: 
2013
PloS one
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