Prevalence of drug resistance and associated mutations in a population of Hiv-1+ Puerto Ricans in 2005.
PMID: 23875516
2010
Boletin de la Asociacion Medica de Puerto Rico
Result: There was a significant difference between men and woman for L90M (P= 0.0337) and M46I (P= 0.0424), two major mutations associated with resistance to PI inhibitors.
Discussion: In the case of the protease mutations, a statistically significant difference for L90M has been noticed since 2003 and the statistically significant difference observed for M46I in 2003 reappeared in 2005.
Discussion: The K103N RT mutation was more common in women while the protease mutations L90M and M46I were more prevalent in men.
GRL-02031, a novel nonpeptidic protease inhibitor (PI) containing a stereochemically defined fused cyclopentanyltetrahydrofuran potent against multi-PI-resistant human immunodeficiency virus type 1 in vitro.
PMID: 18955518
2009
Antimicrobial agents and chemotherapy
Abstract: GRL-02031 was potent against a variety of HIV-1(NL4-3)-based molecular infectious clones containing a single primary mutation reported previously or a combination of such mutations, although it was slightly less active against HIV-1 variants containing consecutive amino acid substitutions: M46I and I47V or I84V and I85V.
Abstract: Upon selection of HIV-1(NL4-3) in the presence of GRL-02031, mutants carrying L10F, L33F, M46I, I47V, Q58E, V82I, I84V, and I85V in the protease-encoding region and G62R (withi
Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.
PMID: 18992847
2009
Infection, genetics and evolution
Method: Mutations D30N (NFV), V32I (LPV), M46I/L (IDV/RTV), I47V/A (LPV/RTV), G48V (SQV), I50L/V (APV), V82A/F/T/S (LPV/IDV/RTV), I84V (APV/IDV/RTV) and L90M (SQV/NFV) were considered as major resistance mutations and were analyzed separately for each PI as well as quantitatively all together.
Result: Of note, M46I was more frequent than M46L in subtype B isolates, while M46L was more frequent than M46I in subtype F1 isolates (Ta
Table: M46I
Discordant genotypic interpretation and phenotypic role of protease mutations in HIV-1 subtypes B and G.
PMID: 19136678
2009
The Journal of antimicrobial chemotherapy
Abstract: Indinavir-associated mutations M46I/L, I84V and V82A/F/T developed earlier in subtype B across the time of exposure to that drug when compared with subtype G counterparts.
Emergence of multiclass drug-resistance in HIV-2 in antiretroviral-treated individuals in Senegal: implications for HIV-2 treatment in resouce-limited West Africa.
Result: Naturally occurring HIV-2 PR polymorphisms that are associated with PI resistance in HIV-1 were common; major (V32I/L, M46I/V, and I47V) and minor (L10V/I, E35G/R, Q58E, A71V/I, and G73A/T) PI resistance mutations were found in all 23 patients.
Result: The contribution of individual HIV-2 PR mutations that confer phenotypic resistance to PIs have not been delineated; however, the emergence of mutations (K7R, G17N, PMID: 19239356
2009
AIDS research and human retroviruses
Abstract: We found protease inhibitor-associated major resistance mutations in one of the 294 cases analyzed (0.3%; mutation M46I).
Gag mutations strongly contribute to HIV-1 resistance to protease inhibitors in highly drug-experienced patients besides compensating for fitness loss.
Introduction: Interestingly, some of these mutations appear to depend upon the presence of specific mutations in PR: Mutation A431V is mostly observed in PI-resistant viruses carrying mutations V82A and/or M46I in PR.
Protease inhibitor resistance analysis in the MONARK trial comparing first-line lopinavir-ritonavir monotherapy to lopinavir-ritonavir plus zidovudine and lamivudine triple therapy.
PMID: 19451297
2009
Antimicrobial agents and chemotherapy
Abstract: By week 96 (W96), virus samples from 18 of 33 patients in the monotherapy arm showed changes from baseline sequences, and 5 of these patients had viruses with major protease inhibitor (PI) resistance-associated mutations (M46I at W40, L76V at W48, M46I and L76V at W48, L10F and V82A at W72, and L76V at W84).
Molecular dynamics and free energy studies on the wild-type and mutated HIV-1 protease complexed with four approved drugs: mechanism of binding and drug resistance.
PMID: 19537723
2009
Journal of chemical information and modeling
Abstract: In agreement with virological and clinical data, the structural analysis showed that the single mutations V82A, I84V, and M46I are associated with higher energetic values for all analyzed complexes with respect to wild-type, indicating their decreased stability.
HIV type-1 clade C resistance genotypes in treatment-naive patients and after first virological failure in a large community antiretroviral therapy programme.
Discussion: Other mutations that are more likely to impact on the future use of a protease inhibitor, including D30N, M46I, I47V, I50V and V82A/F, were present, but in a minority of individuals, with only a single mutation noted per individual.
HIV mutation literature information.
PMID: 
2010
Boletin de la Asociacion Medica de Puerto Rico
Browser Board
Co-occurred Entities
Filtrator
ViMRT