The Role of Pharmacogenetics in the Treatment of Chronic Hepatitis C Infection

Authors

  • Marina Kawaguchi-Suzuki,

    1. Department of Pharmacotherapy and Translational Research, College of Pharmacy, University of Florida, Gainesville, Florida
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  • Reginald F. Frye

    Corresponding author
    1. Department of Pharmacotherapy and Translational Research, College of Pharmacy, University of Florida, Gainesville, Florida
    • Address for correspondence: Reginald F. Frye, Department of Pharmacotherapy and Translational Research, University of Florida College of Pharmacy, P.O. Box 100486, Gainesville, FL 32610-0486; e-mail: frye@cop.ufl.edu.

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Abstract

Hepatitis C virus (HCV) chronically infects 170 million people worldwide. Until recently, combination therapy with peginterferon-α (pegIFN) and ribavirin (RBV) has been the standard of care. However, for many patients, especially those infected with the most common HCV genotype 1 (HCV-1), this treatment has resulted in unsatisfactory treatment response rates. Many clinical factors, including pharmacogenetics, influence the treatment response rate. Genetic variation in the interleukin 28B (IL28B) gene is the major determinant of treatment response, a finding that has been replicated in multiple independent cohorts. This review focuses on the association between pharmacogenetics and conventional pegIFN/RBV therapy in patients infected with HCV non–genotype 1; patients reinfected with HCV after liver transplantation; and patients coinfected with HCV and human immunodeficiency virus. We also review the pharmacogenetic data for boceprevir and telaprevir triple therapy in patients with HCV-1 infection, as well as viral genomic polymorphisms and genetic variants that may protect against anemia. Pharmacogenetic information offers a personalized medicine approach to help clinicians and patients make better informed decisions to maximize response and minimize toxicity for the treatment of chronic HCV infection.

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