The clinical implications of antiretroviral pharmacogenomics

被引:14
作者
Fox, Julie
Boffito, Marta
Winston, Alan
机构
[1] St Marys Hosp, Clin Trials Ctr, Div Med, Imperial Coll London, London W2 1NY, England
[2] St Marys Hosp, Dept HIV Med, London W2 1NY, England
[3] Chelsea & Westminster Hosp, Dept HIV Med, St Stephens Ctr, London SW10 9NH, England
关键词
antiretroviral therapy; HIV; pharmacogenomics; toxicity;
D O I
10.2217/14622416.7.4.587
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Heterogeneity exists in the effectiveness and toxic effects of antiretroviral agents between individuals and populations. Although patient-related clinical variables such as age, sex and ethnic origin have been associated with drug response, inherited predispositions may have a significant effect on treatment outcome. The role of host and pathogen pharmacogenomics is gaining increasing interest in the field of both antiretrovirals in development, such as the chemokine (C-C motif) receptor 5 (CCR5) inhibitors, and in established therapies where toxicity and efficacy may be predicted. Despite numerous studies available in the literature, the interpretation of the relationship between genetic polymorphisms and clinical outcomes is often posed with many confounding variables, making clinical interpretations of these results difficult. This review summarizes the key findings in the growing knowledge between human genetics and response to antiretroviral drugs and how these findings may be effectively applied in a clinical context.
引用
收藏
页码:587 / 596
页数:10
相关论文
共 71 条
  • [21] Gazzard BG, 1999, INT J CLIN PRACT, V53, P60
  • [22] P-glycoprotein and multidrug resistance
    Gottesman, MM
    Pastan, I
    Ambudkar, SV
    [J]. CURRENT OPINION IN GENETICS & DEVELOPMENT, 1996, 6 (05) : 610 - 617
  • [23] Pharmacogenomics and HIV therapeutics
    Haas, DW
    [J]. JOURNAL OF INFECTIOUS DISEASES, 2005, 191 (09) : 1397 - 1400
  • [24] Haas DW, 2004, AIDS, V18, P2391
  • [25] Ligand specificity of the genetic variants of human α1-acid glycoprotein:: Generation of a three-dimensional quantitative structure-activity relationship model for drug binding to the a variant
    Hervé, F
    Caron, G
    Duché, JC
    Gaillard, P
    Rahman, NA
    Tsantili-Kakoulidou, A
    Carrupt, PA
    d'Athis, P
    Tillement, JP
    Testa, B
    [J]. MOLECULAR PHARMACOLOGY, 1998, 54 (01) : 129 - 138
  • [26] Hypersensitivity reactions during therapy with the nucleoside reverse transcriptase inhibitor abacavir
    Hetherington, S
    McGuirk, S
    Powell, G
    Cutrell, A
    Naderer, O
    Spreen, B
    Lafon, S
    Pearce, G
    Steel, H
    [J]. CLINICAL THERAPEUTICS, 2001, 23 (10) : 1603 - 1614
  • [27] The C3435T mutation in the human MDR1 gene is associated with altered efflux of the P-glycoprotein substrate rhodamine 123 from CD56+ natural killer cells
    Hitzl, M
    Drescher, S
    van der Kuip, H
    Schäffeler, E
    Fischer, J
    Schwab, M
    Eichelbaum, M
    Fromm, MF
    [J]. PHARMACOGENETICS, 2001, 11 (04): : 293 - 298
  • [28] The mechanisms that control intracellular penetration of the HIV protease inhibitors
    Hoggard, PG
    Owen, A
    [J]. JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, 2003, 51 (03) : 493 - 496
  • [29] Cost-effectiveness analysis of HLA B*5701 genotyping in preventing abacavir hypersensitivity
    Hughes, DA
    Vilar, FJ
    Ward, CC
    Alfirevic, A
    Park, BK
    Pirmohamed, M
    [J]. PHARMACOGENETICS, 2004, 14 (06): : 335 - 342
  • [30] Mitochondrial haplogroups and peripheral neuropathy during antiretroviral therapy: an adult AIDS clinical trials group study
    Hulgan, T
    Haas, DW
    Haines, JL
    Ritchie, MD
    Robbins, GK
    Shafer, RW
    Clifford, D
    Kallianpur, AR
    Summar, M
    Canter, JA
    [J]. AIDS, 2005, 19 (13) : 1341 - 1349