Hepatitis C virus (HCV) is presently the leading indication for liver transplantation in Western countries. Treatment for HCV infection includes a combination of pegylated interferon and ribavirin, which produces highly variable response rates. This reflects the lack of information regarding the roles of host and viral components during viral pathogenesis. Vital processes regulated by the liver, including metabolism, lipid homeostasis, cellular proliferation, and the immune response, are known to be systematically dysregulated as a result of persistent HCV infection. Nuclear receptors and their ligands are recognized as indispensable regulators of liver homeostasis. Pathways mediated by the nuclear receptor superfamily have been shown to be profoundly disrupted during HCV infection, leading to an increased importance in elucidating the exact nature of this complex relationship. Expanded understanding of the role of nuclear receptors in HCV infection may therefore be an essential step in the search for a more universally effective treatment.
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