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 HIV mutation literature information.


  Conformational analysis of TMC114, a novel HIV-1 protease inhibitor.
 PMID: 18173253       2008       Journal of chemical information and modeling
Abstract: All 43 conformers were subject to both rigid and flexible ligand docking in the wild-type and a triple mutant (L63P/V82T/I84V) of HIV-1 protease.


  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.


  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.


  Food and Drug Administration analysis of tipranavir clinical resistance in HIV-1-infected treatment-experienced patients.
 PMID: 17197808       2007       AIDS (London, England)
Abstract: The most common protease mutations that developed in tipranavir-treated individuals who experienced virologic failure were L10I/V/S, I13V, L33V/I/F, M36V/I/L V82T, V82L, 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.


  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
Result: I54V was significantly associated with L10F, L24I, L33F, M46I/L, G48V, F53L, V82A/F/T, I84V, and L90M.
Result: However, M46I was uniquely associated with F53L, G73S/T, V82F/T, I84V, and N88S.
Result: The mutations included in this analysis were the 22 positively associated mutations in Table 1 and 13 additional clinically relevant PI-resistance mutations ( PMID: 17926645       2007       Antiviral therapy
Abstract: In a regression model adjusted for CD4+ T-cell count, HIV RNA, year of TCF, age, gender and previous inferior antiretroviral therapy, harbouring > or =9 versus < or =8 mutations was associated with increased mortality (mortality rate ratio [MRR] 2.3 [95% confidence interval (CI) 1.1-4.8]), as were the individual mutations T215Y (MRR 3.4 [95% CI 1.6-7.0]), G190A/S (MRR 3.2 [95% CI 1.6-6.6]) and V82F/A/T/S (MRR 2.5 [95% CI 1.2-5.3]).


  Impact of the number of failed therapeutic regimes on the development of resistance mutations to HIV-1 in northeast Brazil.
 PMID: 17962868       2007       The Brazilian journal of infectious diseases
Abstract: There was a significant increase in resistance mutations V82A/F/L/T, I84V, L90M, M41L, K70R, L210W, T215Y/F and K219Q/E in MF.


  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: CONCLUSIONS: Baseline HIV-1 RNA < 5.0 log10 and CD4+ T-cell count > 200 cells/microl, lopinavir C(min)GIQ(arch) > 2,000 ng/ml and the absence of viral resistance mutations at V82T/A/F/I/S and 154M/V/L are highly predictive for therapeutic success of a regimen of saquinavir/lopinavir/ ritonavir without RTI in a heterogenic cohort of patients with an extensive pre-treatment history and highly variable pharmacokinetics.
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).
Abstract: RESULTS: The analyses de



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