literature

HIV mutation literature information.

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

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.

Discussion: Moreover, despite the treatment history of B- and F1-infected adult patients was comparable, we could find subtype F1-specific treatment-related mutations, as K20T, L63P and N88S were more frequent only in treated than in untreated people infected with subtype F1, while L10V, K20M, D30N, L33F, M36I,

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: RESULTS: The analyses detected correlations between the primary outcome parameter and several factors: baseline CD4+ T-cell count (P = 0.001); absence of mutations at V82T/A/F/I/S plus 154M/V/L (P = 0.002) or K20M/R (P = 0.010); and lopinavir C(min)GIQ(arch) (P = 0.046).

Tipranavir: a new protease inhibitor for the treatment of antiretroviral-experienced HIV-infected patients.

PMID: 17425479 2007 Expert opinion on pharmacotherapy

Abstract: The TPV mutation score includes L10V, I13V, K20M/R/V, L33F, E35G, M36I, K43T, M46L, I47V, I54A/M/V, Q58E, H69K, T74P, V82L/T, N83D and I84V.

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.

Association of Gag cleavage sites to protease mutations and to virological response in HIV-1 treated patients.

PMID: 16875739 2007 The Journal of infection

Abstract: Two patterns of mutations in the protease were identified: (M46I/L, I54V, V82A/T/F) was associated to the A431V and (K20I/R/M, L89M/I) to the S373Q and L449P.

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.

Three-year clinical outcomes of resistance genotyping and expert advice: extended follow-up of the Argenta trial.

PMID: 16759048 2006 Antiviral therapy

Abstract: Independent predictors of new AIDS events/death were previous AIDS events, higher baseline viral load, less pronounced 3-month viral load drop and, in a separate model, baseline protease substitutions K20M/R and 184V.

Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.

PMID: 19825125 2005 Journal of the International AIDS Society

Table: K20M

Browser Board

Co-occurred Entities

Filtrator