Abstract: 97.9% of variants had the M46I/G73S/L90M pattern at XLF6.
Abstract: As therapy was prolonged, G73S was combined with M46I/L90M to form a resistance pattern M46I/G73S/L90M, which then became the dominant population.
Abstract: During the course of changing the regimen to incorporate Indinavir, the G73S mutation occurred and was combined with M46I/L90M.
Patients with discordant responses to antiretroviral therapy have impaired killing of HIV-infected T cells.
Result: By contrast, D30N, F53L, and L90M all produced Casp8p41:gag-pol cleavage ratios greater than WT protease (Figure 8B).
Result: Casp8p41 content was greatest in HXB2 WT infected cells and in the L90M non-DAM infected cells.
Result: Consistent with the premise that mutations in HIV protease will reduce the ability of HIV protease to kill infected cells, protease containing V82A or I54V induced less apoptosis in infected cells than either WT or L90M (Figure 10A).
Result: For this we chose the DAMs I54V,
Update of the drug resistance mutations in HIV-1: December 2010.
Abstract: The mutations I13V, K20M/R, E35G, and L90M were removed from the tipranavir/ritonavir bar, reflecting new understanding.
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
Abstract: Protease mutations with the highest rate of expression were L63P, M361 and L90M.
Result: As shown in Table III, the PI resistance-associated specific mutations with the highest degree of expression for 2
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.
Identification of human immunodeficiency virus type 1 non-B subtypes and antiretroviral drug-resistant strains in United States blood donors.
Abstract: Drug resistance profiles obtained for 18 donors identified one strain with protease mutation L90M that confers resistance to nelfinavir and one with RT mutation Y188H that confers resistance to nevirapine.
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
Abstract: In treated patients, K20M, D30N, G73S, I84V, and L90M, were more prevalent in subtype B, and K20T and N88S were more prevalent in subtype F1.
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
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: L90M did not reduce the susceptibility of subtype G to saquinavir, in contrast to subtype B.
Abstract: L90M was associated with a lower reduction in the susceptibility of subtype G to nelfinavir when compared with subtype B, and with no reduced susceptibility to saquinavir.
Abstract: Likewise, the pattern I54V/L-L90M did not reduce the susceptibility of subtype G to indinavir and saquinavir.
Emergence of multiclass drug-resistance in HIV-2 in antiretroviral-treated individuals in Senegal: implications for HIV-2 treatment in resouce-limited West Africa.
Abstract: Eight patients had HIV-2 with PI mutations associated with indinavir resistance, including K7R, I54M, V62A, I82F, L90M, L99F; 4 patients had strains with multiple PI resistance-associated mutations.
Discussion: However, the authors did find high treatment failure rates, RT mutations M184V/I and Q151M, and the PR mutation L90M in the virus strains from 7 patients who received NRTI- and nelfinavir-based regimens.
Discussion: Phenotypic resistance to indinavir has been reported with th
Analysis and characterization of dimerization inhibition of a multi-drug-resistant human immunodeficiency virus type 1 protease using a novel size-exclusion chromatographic approach.
Result: PRMDR contains multiple drug-resistant mutations (L10I, K45R, I54V, L63P, A71V, V82T, L90M and I93L) and is highly resistant to a number of active-site inhibitors, although it remains sensitive to the experimental active-site inhibitor JE-2147.
Proteochemometric modeling of drug resistance over the mutational space for multiple HIV protease variants and multiple protease inhibitors.
PMID: 19391634
2009
Journal of chemical information and modeling
Abstract: The model revealed the most deleterious mutations in the protease to be D30N, V32I, G48V, I50V, I54V, V82A, I84V, and L90M.
HIV mutation literature information.
PMID: 
2010
Virologica Sinica
Browser Board
Co-occurred Entities
Filtrator
ViMRT