Gene Expression Profiles Associated with Depression in Patients with Chronic Hepatitis C
Aybike Birerdinc, Maria Stepanova, Arian Afendi, V. Chandhoke, Ancha Baranova, Zobair M. Younossi
This is a collaborative project between
School of Systems Biology, College of Science,George Mason University, Fairfax, VA
Translational Reseach Institute, Inova Hospital, VA
Depression is common among HCV-infected patients. Treatment of hepatitis C (HCV) with pegylated interferon-alpha (IFNα) can cause depression in approximately 30% of patients. It points at the need for effective detection of depression prior to and during IFNα treatment. Elevated rates of depression in untreated HCV can be a barrier to initiating HCV therapy and can impact outcomes.
Recent studies support the concept that inflammatory mechanisms play a crucial role in the pathomechanisms of depression. Elevations in proinflammatory cytokines and other inflammation-related proteins were found in plasma and cerebrospinal fluid (CSF) of depressed patients. An increase in the levels of proinflammatory cytokines can also predict the onset of a depressive episode. Interferon treatment can lead to an elevation of the levels of pro-inflammatory cytokine levels and induce depression.
Methods: CH-C patients treated with PEG-IFN+RBV were enrolled. Of the entire study cohort, 22% had pre-existing depression, while another 37% developed new depression in course of the treatment. Pre-treatment blood samples were collected and their peripheral blood mononuclear cells (PBMCs) were used to extract total RNA for one step RT-PCR profiling of 160 mRNAs. Gene expression profiles are being analyzed in order to test hypothesis that TGF-β1 play an important role in the imbalance of Th1/Th2 in patients with CH-C and depression. With further validation, TGF-β1 and other components of Th1/Th2 regulation pathway may provide a future marker for CH-C patients predisposed to depression.
RESULTS: are to be published soon