[1, 2] HCV recurrence after transplantation is universal and represents a major therapeutic challenge as current standard therapy against HCV infection is limited to the combination of pegylated interferon-α and ribavirin (IFN/RBV). However, the therapy has considerable side-effects, and the response rate is less than ideal.[3] Several cellular factors are known to be involved in the hepatocellular entry mechanism of HCV.[4] Tight-junction (TJ) proteins claudin-1 (CLDN1) and occludin (OCLN), CD81, scavenger receptor class B type 1 (SCARB1) have been reported to be part of the internalization complex and are essential for HCV entry both in Kinase Inhibitor Library vitro and in vivo.[2, 5-7] Previous studies have shown discrepancies

between messenger RNA (mRNA) and protein expression levels of these receptors in HCV infected patients, suggesting therefore the role of microRNAs (miRs) in the modulation of gene expression.[2, 4, 5] MiRs are small endogenous non-coding ∼22 nucleotide long RNAs that regulate gene expression at posttranscriptional level. MiRs induce degradation of the mRNA or suppression of protein translation upon binding to the 3′ untranslated regions (UTRs) of an mRNA.[8, 9] One microRNA sequence might interact with several mRNAs. selleck products Therefore, miRs exert negative regulation on mRNA and finally on protein expression. They are essential for maintenance of cellular homeostasis and normal function, serving as key regulators of

various biological processes including cellular stress, steatosis, proliferation, differentiation, and apoptosis.[9-11] Dysregulated expression of miRs might play role in the development of many diseases including viral infections and malignancies.[12-14] MiRs also participate in the control of selleck inhibitor HCV infection as well as in the IFN pathway via several mechanisms.[3, 15] The liver-specific microRNA, miR-122, is known

as a positive cofactor in HCV replication cycle[16] and has been found to be downregulated by α/β IFNs.[17] Besides, IFN-β has been described as modulator of the expression of several miRs having sequence-predicted targets within the HCV genomic RNA, and some of these miRs were shown to actively inhibit HCV replication.[17, 18] In addition, the hepatic microRNA expression pattern existing in chronic HCV-infected patients before antiviral therapy was shown to be associated with therapy response.[3] The aim of the current study was to evaluate the expression of miRs, which either have one of the HCV receptors among their target mRNAs according to target prediction software (such as miR-21, miR-34a, miR-96, miR-125b, miR-194, miR-195, and miR-224), or which may play role in HCV infection or in antiviral treatment response (such as miR-23a, miR-99a*, miR-122, miR-181a-2*, miR-217, and miR-221) in liver transplant recipients. A total of 28 liver needle biopsies of HCV-positive adult liver transplanted patients were included.