literature

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: 20695887 2010 The FEBS journal

Abstract: Substitution of the larger side chains in PR(V32I) , PR(I54M) and PR(L90M) resulted in the formation of new hydrophobic contacts with flap residues, residues 79 and 80, and Asp25, respectively.

Abstract: The PR(I84V)-A

Abstract: The observed structural changes in PR(I84V)-APV, PR(V32I)-APV and PR(I50V)-APV were related to their reduced inhibition by APV of six-, 10- and 30-fold, respectively, relative to wild-type PR.

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), 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.

Emergence of multiclass drug-resistance in HIV-2 in antiretroviral-treated individuals in Senegal: implications for HIV-2 treatment in resouce-limited West Africa.

PMID: 19143530 2009 Clinical infectious diseases

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.

Darunavir: a review of its use in the management of HIV infection in adults.

PMID: 19323590 2009 Drugs

Abstract: In a 24-week analysis of pooled data from the POWER 1 and 2 studies in treatment-experienced patients, 11 protease mutations associated with a reduced response to boosted darunavir were identified (V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V and L89V).

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.

Role of atazanavir in the treatment of HIV infection.

PMID: 19436623 2009 Therapeutics and clinical risk management

Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and

Factors associated with the selection of mutations conferring resistance to protease inhibitors (PIs) in PI-experienced patients displaying treatment failure on darunavir.

PMID: 18039922 2008 Antimicrobial agents and chemotherapy

Abstract: The most common mutations that emerged at rebound included V32I (44%), I54M/L (24%), L33F (25%), I84V (21%), and L89V (12%).

Clinically validated mutation scores for HIV-1 resistance to fosamprenavir/ritonavir.

PMID: 18390885 2008 The Journal of antimicrobial chemotherapy

Abstract: The fosamprenavir/ritonavir score A was introduced in the 2006 ANRS algorithm along with isolated mutations I50V and V32I + I47V.

Virological response to darunavir/ritonavir-based regimens in antiretroviral-experienced patients (PREDIZISTA study).

PMID: 18505178 2008 Antiviral therapy

Abstract: We determined the genotypic score I13V+V32I+L33F/I/V+E35D+ M361/L/V+I47V+F53L+I62V.