HIV mutation literature information.


  Antiretroviral genotypic resistance mutations in HIV-1 infected Korean patients with virologic failure.
 PMID: 19949656       2009       Journal of Korean medical science
Result: M41L, I54V, D30N, and V82A/T/S were observed in more than 10 patients and K103N (10/41, 24.4%) was the most frequently observed NNRTI associated mutation.


  Population trends in the prevalence and patterns of protease resistance related to exposure to unboosted and boosted protease inhibitors.
 PMID: 18839778       2008       Antiviral therapy
Abstract: Individual mutations L33F, M461/L, V82A/F/T/S/L and 184V became relatively more frequent over the period of study.


  The HIV-1 protease substitution K55R: a protease-inhibitor-associated substitution involved in restoring viral replication.
 PMID: 18252693       2008       The Journal of antimicrobial chemotherapy
Abstract: RESULTS: The K55R mutation, which is not a natural polymorphism, was identified to be strongly associated with protease mutations M46I/L and to a lesser extent L24I, I54V and V82A/T/S/F.


  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


  Genotypic drug resistance and long-term mortality in patients with triple-class antiretroviral drug failure.
 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]).


  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.


  Compensatory mutations at the HIV cleavage sites p7/p1 and p1/p6-gag in therapy-naive and therapy-experienced patients.
 PMID: 17302250       2006       Antiviral therapy
Abstract: The analysis of CS and PR mutations in therapy-experienced viruses revealed several positive correlations--A431V with L24I-M46I/L-I54V-V82A; I437V with I54V-V82F/T/S; L449V with I54M/L/S/T/A; and L449F/R452S/P453L: with D30N-I84V--whereas P453L and V82A were negatively correlated.


  Evidence of differential selection of HIV-1 variants carrying drug-resistant mutations in seroconverters.
 PMID: 16759049       2006       Antiviral therapy
Abstract: Among the mutations not detected in viruses from SCs, the RT E44D, V1081, Q151M and Y188C/H/L, and the protease D30N, G48V and V82A/F/S/T substitutions appeared to be negatively selected.


  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.



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