Interferon [IFN]-mediated antiviral activity against the hepatititis C [HCV] through microRNAs [microRNAs]

MicroRNAs are a class of small non-coding RNA molecules that function through post-transcriptional regulation of gene expression by a process termed RNA interference [RNAi], and that also have to prominence as critical regulators in a wide array of mechanisms of cell physiology. The study will attempt to evaluate the expression of several microRNAs in peripheral blood mononuclear cells [PBMCs] from patients with chronic hepatitis C [CHC] at 12 hours after the first injection of pegylated interferon in comparison with healthy controls. forty patients with chronic hepatitis C virus infection [CHCV], their age ranged between [20-56] years, selected from the National Hepatology and Tropical Medicine Research Institute were included in this study, after 12 hours of the first interferon injection, and twenty healthy individuals were included to serve as controls. All the patients and controls were subjected to the following history, clinical examination, abdominal ultrasonography and collection of samples for routine laboratory investigations. CBCs and Taqman quantitative RT-PCR for MicroRNAs expression analysis of miR- 128a, miR 196a, miR- 196b, miR 296. Our study revealed that the microRNAs had a higher levels of expression in cases of CHCV infection. Our study concluded that there's a highly significant increase in expression levels of IFN-induced microRNAs were observed in patients of microRNAs-128a, 196a, 196b, 296. The future use of miR inhibitors or mimics and / or siRNAs might be useful for the development of diagnostic and therapeutic strategies aimed at the recovering of protective innate responses in HCV infections

key regulator for iron homeostasis in chronic hepatitis C

Hepcidin is a small, cysteine-rich cationic peptide produced by hepatocytes. There is a single human hepcidin gene; whose essential role in iron homeostasis was confirmed by identifying homozygous frameshift or nonsense mutations in affected individuals with severe Juvenile hemochromatosis. IL-6 may be the mediator of hepcidin induction by inflammation. Hypoferremia is a common response to systemic infections or generalized inflammatory disorders, anemia of chronic disease occurs in patients with acute and chronic immune activation and represents an important clinical problem. The study will attempt to determine the hepatic hepcidin expression levels in patients with chronic hepatitis C virus infection. Fifty patients with chronic hepatitis C virus infection [CHCV], their age between [20- 55] years, selected from the National Hepatology and Tropical Medicine Research Institute were included in this study, before interferon and Ribavirin therapy, and ten healthy individuals were included to serve as controls. All the patients and controls were subjected to the following history, clinical examination, abdominal ultrasonography and collection of blood samples for routine laboratory investigations. CBCs and serological assay for serum ferritin, iron, transferrin [s-TFR] levels, Liver biopsy for hepcidin mRNA levels and iron deposits in liver by [PCR] polymerase chain reaction. All subjects gave written informed consent for enrolment in the study, which was approved by the Research Ethical Committee of the General Organization for Teaching Hospitals and Institutes. Liver biopsy was taken from healthy subjects during abdominal surgery. Our results revealed that hepatic hepcidin expression is considered highly valid marker in case of CHCV infection. Our study concluded that there's a highly significant inverse correlation between hepcidin versus liver iron, serum iron and serum transferrin but there's no significant correlation versus ferritin. Hepcidin measuring and manipulating hepcidin levels will, in the future, have a role in diagnosing and treating any number of iron related disorders. Hepcidin itself has antimicrobial properties of uncertain importance so that careful clinical trials will be required to define appropriate indications of hepcidin antagonists