literature

HIV mutation literature information.

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: 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 (within p17), L363M (p24-p2 cleavage site), R409K (within p7), and I437T (p7-p1 cleavage site) in the gag-encoding region emerged.

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).

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

Method: Mutations L10F/I/R/V, K20M/R, L24I, L33F, M36I, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73C/S/T/A, V77I and N88D/S were considered as minor resistance mutations and were also analyzed separately and together as a group.

Table: L10F

Discussion: The mutations L10F/R, K20I, V32I, I47V/A, I5

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

PMID: 18390885 2008 The Journal of antimicrobial chemotherapy

Abstract: Two fosamprenavir/ritonavir mutation scores were constructed: score A (L10F/I/V + L33F + M36I + I54L/M/V/A/T/S + I62V + V82A/F/C/G + I84V + L90M) was based only on mutations associated with a worse VR, whereas score B (L10FIV + L33F + M36I + I54L/M/V/A/T/S + A71V - V77I - N88S + L90M) also took into account favourable mutations.

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).

[Resistance to anti-retroviral therapy in Chilean patients with HIV-1 from 2002 to 2005].

PMID: 18180829 2007 Revista medica de Chile

Abstract: The most common mutations found were T215Y (46%), L10F (44%), Ml84V (3896), K103N (35%) and M41L (32%).

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,

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.

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.

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