Abstract: Methods and kits for characterizing liver damage in an individual are provided. The methods employ the use of immune analytes as biomarkers for detecting liver damage and predicting the likelihood that an individual suffering from liver damage will experience life-threatening liver failure. Concentration values for serum albumin and other identified immune analytes are obtained or determined from a blood sample taken from the individual. The obtained concentration values are then compared to corresponding concentrations from individuals having a healthy liver. By comparing the concentrations, an individual's likelihood of developing life-threatening liver failure and needing a liver transplant within a given time period (e.g., 6 months) can be identified.

Abstract: Methods and kits for characterizing liver damage in an individual are provided. The methods employ the use of immune analytes as biomarkers for detecting liver damage and predicting the likelihood that an individual suffering from liver damage will experience life-threatening liver failure. Concentration values for serum albumin and other identified immune analytes are obtained or determined from a blood sample taken from the individual. The obtained concentration values are then compared to corresponding concentrations from individuals having a healthy liver. By comparing the concentrations, an individual's likelihood of developing life-threatening liver failure and needing a liver transplant within a given time period (e.g., 6 months) can be identified.

Abstract: The present invention is directed to methods of treating cells infected with HCV and mammals suffering from HCV infection by transfecting the infected cells with miRNA-196 mimic. miRNA-196 mimic significantly down-regulates Bach1 protein and HCV gene expression, while also up-regulating HMOX1 gene expression. miRNA-196 binds with the 3?-UTR of Bach1 mRNA to reduce the expression of Bach1. As such, miRNA-196 can play an important role in the regulation of HCV replication and HMOX1/Bach1 expression in hepatocytes. The present invention also provides a formulation for the treatment of cells expressing HCV comprising a therapeutically effective amount of miRNA-196 such that Bach1 and HCV gene expression are down-regulated while HMOX1 expression is increased. The formulations are adapted to enable the transfection of miRNA-196 mimic into hepatocytes expressing HCV proteins.

Abstract: The present invention is directed to the treatment of hepatitis C infection with a metalloporphyrin. In particular, the present invention is based on the discovery that the NS5A protein plays a key role in HCV RNA replication by participating in polyprotein cleavage, interferon response and cellular signaling pathways. It has been found that metalloporphyrins, such as zinc porphyrins, induce post-translational down-regulation of HCV NS5A protein in an ubquitin-proteasome degradation pathway. That is, metalloporphyrins can be used to activate the ubiquitin-proteasomal pathway of NS5A protein catabolism. As a result, metalloporphyrins can be used to significantly suppress HCV viral replication in HCV infected cells.