HIV mutation literature information.


  Increasing proportions of HIV-1 non-B subtypes and of NNRTI resistance between 2013 and 2016 in Germany: Results from the national molecular surveillance of new HIV-diagnoses.
 PMID: 30408827       2018       PloS one
Table: M46I/L
Table: M46I
Figure: Three large clusters with M46I, V82L or T215S mutations are shown with blue branches and all sequences carrying the K103N mutation are depicted with dots at the tips.


  No impact of HIV-1 protease minority resistant variants on the virological response to a first-line PI-based regimen containing darunavir or atazanavir.
 PMID: 29077926       2018       The Journal of antimicrobial chemotherapy
Abstract: The most prevalent PI MRV were G73C (n = 5) and M46I (n = 3).


  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.
 PMID: 30409215       2018       AIDS research and therapy
Result: Most of the minority mutations in viruses from both groups of naive patients were observed in the RT, e.g., M41L, E44D, A62V, K65R, D67N, D67G, V75I, L100I, K103N, K103R, V188I, M184I, L210W, K219Q, Y318F, etc., although a number of minority mutations associated with resistance to PI (L10F, V11I, M46I/


  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.
 PMID: 29511083       2018       mBio
Result: 1) contained the V32I substitution, although other substitutions such as L10F, L33F, M46I, A71V, and I84V had been acquired in a subset of the six clones.
Result: Since the M46I substitution is often seen in various PI-resistant HIV-1 variants and that substitution was also seen in the present study.
Discussion: In contrast, a set of data compiled for NDA21-976/S003 and NDA21-976/S004 clearly indicates that 10 amino acid substitutions including L10F, V32I, L33F, S37N, M46I, I47V,


  Exploration of the effect of sequence variations located inside the binding pocket of HIV-1 and HIV-2 proteases.
 PMID: 29636521       2018       Scientific reports
Discussion: Therefore, our results suggest that the T31S, M46I, and V82I amino acid changes induce structural changes in PR2 that can affect PI binding.
Discussion: We demonstrated that the property changes between PR1 and PR2 structures are directly explained by the six substitutions (T31S, V32I, M46I, I47V, L76M, and V82I) located in PR pocket.
Discussion: We showed that PR2 pockets are more hydrophobic than PR1 pockets that it


  [Genetic analysis of the mutations in HIV-1 infected population in Ecuador].
 PMID: 29652972       2018       Revista chilena de infectologia
Abstract: Results The most frequent mutations were M184V/I, K101E/P/H, K103N/S, D30N, M46L/I, I54L/M, V82T/F/A/S/L and L90M in adults and F77L, K103N/S, M46L/I, V82T/F/A/S/L and L90M in children.


  HIV-1 transmitted drug resistance in Slovenia and its impact on predicted treatment effectiveness: 2011-2016 update.
 PMID: 29698470       2018       PloS one
Result: The first sequence is part of the largest Slovenian cluster (n = 53) and carries the T69D mutation, the second sequence is within a cluster of 20 Slovenian sequences and carries M46I, and the third is in a phylogenetic relationship with two other Slovenian sequences and is carries K103N (Fig 2).
Discussion: (2017) observed significantly less clustering of mutations T69D and M46I detected in the two sequences within large Slovenian clusters, which indicates that these two mutations are less fit to transmit than the wild type.


  Ultra-deep sequencing improves the detection of drug resistance in cellular DNA from HIV-infected patients on ART with suppressed viraemia.
 PMID: 30137335       2018       The Journal of antimicrobial chemotherapy
Abstract: However, the detection of RAMs by UDS with a 1% cut-off was significantly higher than that of bulk sequencing for RT codons D67N (65.4% versus 52.3%), M184V (66.2% versus 52.3%), L210W (48.9% versus 36.4%) and T215Y (57.9% versus 42.1%) and PR codons M46I (46% versus 26%), I54L (12.4% versus 3.9%), V82A (44.5% versus 29.9%) and L90M (57.7% versus 42.5%).


  HIV Reverse Transcriptase and Protease Genes Variability Can Be a Biomarker Associated with HIV and Hepatitis B or C Coinfection.
 PMID: 29844604       2018       Scientific reports
Result: The major mutations to PI were I54V (2.9%), V82A (11.7%), M46I (8.8%) and L90M (40.4%).


  Drug Resistance Mutation L76V Alters Nonpolar Interactions at the Flap-Core Interface of HIV-1 Protease.
 PMID: 30288468       2018       ACS omega
Discussion: Flap mutation M46I is strongly associated with L76V as shown by a large proportion of coprevalence in L76V-containing sequences.
Discussion: Impaired autoprocessing of precursor PR-containing L76V is partly rescued by addition of a second mutation of M46I and, although L76V reduces viral replication, viral fitness is partly rescued by combination with this mutation.



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