literature

HIV mutation literature information.

Azvudine, a novel nucleoside reverse transcriptase inhibitor showed good drug combination features and better inhibition on drug-resistant strains than lamivudine in vitro.

PMID: 25144636 2014 PloS one

Table: L10R

Does GSS still maintain relevance on HAART outcome after the introduction of newest active antiretroviral drugs? 48 weeks results.

PMID: 22211659 2011 Current HIV research

Abstract: About 60% of tests reported L10FIRVC, M36ILV, M46IL, I54VLAMTS, V82AFTSLI, and L90M mutations in the protease region.

Prevalence and clinical significance of HIV drug resistance mutations by ultra-deep sequencing in antiretroviral-naive subjects in the CASTLE study.

PMID: 20532178 2010 PloS one

Table: L10R

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

Result: The major protease mutations V32I and I47V/A and the minor mutations L10R, I54M, and G73C/T/A were not observed

Discussion: The mutations L10F/R, K20I, V32I, I47V/A, I50L/V, I54L/A/M/T/S, A71T, G73C/T/A, V77I, and V82F/T/S, either absent or observed in our subtype B and F1 viruses, were not statistically different in viruses isolated from treated or untreated patients.

A novel substrate-based HIV-1 protease inhibitor drug resistance mechanism.

PMID: 17227139 2007 PLoS medicine

Method: In addition, the model was also adjusted on use of nelfinavir at baseline and on the number of PI mutations (L10IRVF, K20RM, M36I, A71VT, G73SA, V82AFTS, L90M) found to be associated with the virological response in univariate analyses in this subset of patients.

Interpretation of genotype and pharmacokinetics for resistance to fosamprenavir-ritonavir-based regimens in antiretroviral-experienced patients.

PMID: 17296739 2007 Antimicrobial agents and chemotherapy

Abstract: The Zephir mutation score included 12 IAS protease mutations associated with poorer virological response: L10I/F/R/V, L33F, M36I, M46I/L, I54L/M/T/V, I62V, L63P, A71I/L/V/T, G73A/C/F/T, V82A/F/S/T, I84V, L90M, and polymorphism mutations I13V, L19I, K55R, and L89M.

HIV-1 subtype B protease and reverse transcriptase amino acid covariation.

PMID: 17500586 2007 PLoS computational biology

Method: PI-selected mutations included L10I/V/F/R, V11I, K20R/M/I/T, L23I, L24I, D30N, V32I, L33F/I, E34Q, E35G, M36I/V, K43T, M46I/L/V, G48V/M, I50V/L, F53L, I54V/M/L/T/A/S, K55R, Q58E, L63P,

Predictive factors for response to a boosted dual HIV-protease inhibitor therapy with saquinavir and lopinavir in extensively pre-treated patients.

PMID: 18240863 2007 Antiviral therapy

Abstract: Covariates for the decrease of HIV-1 RNA from baseline to week 48 were baseline HIV-1 RNA (P < 0.001), lopinavir C(min)GIQ(arch) (P = 0.013), presence/absence of mutations at V82T/A/F/I/S or 184A/V plus L10I/R/V/F, 154M/V/L or L63P (P = 0.018), and previously taken antiretrovirals (P = 0.034).

Virological responses to atazanavir-ritonavir-based regimens: resistance-substitutions score and pharmacokinetic parameters (Reyaphar study).

PMID: 16856615 2006 Antiviral therapy

Abstract: The Reyaphar score included 12 baseline protease substitutions from the International AIDS Society USA list that were associated with poorer VR: L10I/F/R/V, K20I/M/R, L241, M461/L, 154L/M/T/V, L63P, A71I/L/V/T, G73A/C/F/T, V771, V82A/F/S/T, 184V, L90M and the polymorphism substitution Q58E.

Human immunodeficiency virus type 1 (HIV-1) genotyping in Rio de Janeiro, Brazil: assessing subtype and drug-resistance associated mutations in HIV-1 infected individuals failing highly active antiretroviral therapy.

PMID: 15867968 2005 Memorias do Instituto Oswaldo Cruz

Abstract: The K103N mutation was the most prevalent to the non-nucleoside RT inhibitor and the resistance associated to protease inhibitor showed the minor mutations L63P, L10F/R, and A71V as the more prevalent.

Browser Board

Co-occurred Entities

Filtrator