FKBP51 levels negatively correlate with Depressive symptoms in Chronic Hepatitis C

Background and aimsPatients with chronic hepatitis C infection have high rates of major depressive disorder. The reasons for this are multifactorial, but social and demographic factors do not entirely explain the increased burden. Direct neuropathologic effect of the virus in the development of depression has been postulated but the mechanisms remain unclear. Single nucleotide polymorphisms (SNPs) in FKBP5 (protein product FKBP51), a co-chaperone of the glucocorticosteroid receptor, have been associated with greater severity of affective disorders. We examined the interaction between FKBP5 SNPs and chronic hepatitis C infection in patients with and without depressive symptoms. Methodsforty-one subjects completed quality of life and psychiatric questionnaires. Thirteen patients were classified as depressed on the Hospital Anxiety and Depression Scale depression sub-score (HADS-D [&ge;]11). FKBP51 protein expression, FKBP5 mRNA and FKBP5 SNP analysis was compared between those with and without depression. ResultsThere were no statistically significant differences between the groups in demographics, medical co-morbidities or substance use. A moderate negative correlation (Spearman rho -0.53, p<0.001) was found between HADS-D sub-score and FKBP51 protein levels in serum. Correspondingly, the average expression fold change in peripheral blood FKBP5 mRNA relative to a reference gene was lower in the depressed group at 0.76 compared to controls at 1.40. There was no differential expression of FKBP5 SNPs between the groups. ConclusionLevels of FKBP5 mRNA and FKBP51 are lower in hepatitis C patients with depression and further exploration of this interaction is required.