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 HIV mutation literature information.


  Virologic response to nelfinavir-based regimens: pharmacokinetics and drug resistance mutations (VIRAPHAR study).
 PMID: 12131209       2002       AIDS (London, England)
Abstract: At failure, L10I, D30N, M36I, V77I, N88S/D or L90M protease mutations had emerged since baseline.


  Virologic rebound on HAART in the context of low treatment adherence is associated with a low prevalence of antiretroviral drug resistance.
 PMID: 12131564       2002       Journal of acquired immune deficiency syndromes (1999)
Abstract: In the viremic group, substitutions in HIV protease were detected most frequently in the following positions in subjects on indinavir (IDV): L10I/V (35.7%), M46I/L (35.7%), A71T/V (35.7%), V82A (42.9%); and for subjects on nelfinavir (NFV): D30N (50.0%), V77I (56.3%), N88D (37.5%).


  Prevalence of HIV protease mutations on failure of nelfinavir-containing HAART: a retrospective analysis of four clinical studies and two observational cohorts.
 PMID: 12187506       2002       HIV clinical trials
Abstract: D30N and
Abstract: Although D30N confers little or no cross-resistance to other protease inhibitors (PIs) and has been shown to allow effective substitution of a second PI, L90M with secondary mutations is involved in broad cross-resistance to the class.
Abstract: BACKGROUND: Both D30N and L90M in HIV-1 protease are primary resistance mutations that emerge under nelfinavir drug pressure.


  Impact of human immunodeficiency virus type 1 subtypes on virologic response and emergence of drug resistance among children in the Paediatric European Network for Treatment of AIDS (PENTA) 5 trial.
 PMID: 12195348       2002       The Journal of infectious diseases
Abstract: No differences were observed in the frequency of development of resistance mutations L90M (P=1.00) and D30N (P=.61) in B and non-B viruses.


  Resistance mutations in HIV-infected patients experiencing early failure with nelfinavir-containing triple combinations.
 PMID: 12218942       2002       Medical science monitor
Abstract: All six individuals harbored the D30N mutation, and none presented the L90M mutation.
Abstract: The D30N substitution, rather than L90M, is the most frequently recognized, which does not challenge the efficacy of further rescue interventions with other PIs.


  Rapid phenotypic assay for human immunodeficiency virus type 1 protease using in vitro translation.
 PMID: 12367727       2002       Journal of virological methods
Abstract: Three drug-resistant proteases carrying a single mutation, D30N, L90M, and V82F, were analyzed in the absence of the inhibitors.


  Evolution of antiretroviral phenotypic and genotypic drug resistance in antiretroviral-naive HIV-1-infected children treated with abacavir/lamivudine, zidovudine/lamivudine or abacavir/zidovudine, with or without nelfinavir (the PENTA 5 trial).
 PMID: 12553485       2002       Antiviral therapy
Abstract: NFV-resistant virus was selected slowly through D30N or L90M pathways, and selection of ZDV-resistant virus was rare.


  [HIV genotypic mutation selectively induced by the protease inhibitor nelfinavir at codon 30. Case series and consequences for antiretroviral management].
 PMID: 12704265       2002       Le infezioni in medicina
Abstract: In a survey of 247 HIV-infected patients which received at least six months of combined antiretroviral therapy including the protease inhibitor nelfinavir during the last two years (2000-2001), the specific primary genotypic mutation D30N (with or without the minor mutation N88D), was detected in only four of the 149 (2.7%) subjects who received genotypization after virological failure.


  Phenotypic cross-resistance to nelfinavir: the role of prior antiretroviral therapy and the number of mutations in the protease gene.
 PMID: 11177403       2001       AIDS research and human retroviruses
Abstract: The D30N mutation was detected in only 1 of 74 patients who failed.
Abstract: The presence of the D30N mutation was rare and not useful in identifying NFV-resistant isolates.


  Structural implications of drug-resistant mutants of HIV-1 protease: high-resolution crystal structures of the mutant protease/substrate analogue complexes.
 PMID: 11340661       2001       Proteins
Abstract: Polar interactions in D30N are maintained, in agreement with the observed urea sensitivity.
Abstract: The side-chain variations at residue 30 relative to wild-type are the largest in D30N and the changes are consistent with the altered activity observed with peptide substrates.
Abstract: The side-chains of D30N and N88D are linked through a water molecule suggesting correlated changes at the two sites, as seen with clinical inhibitors.



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