Abstract
Hepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pathogenic bacteria and viruses. The only effective strategy to prevent disease progression is eradication of the viral infection. Immune cells play a pivotal role during liver inflammation, triggering fibrogenesis. The present paper discusses the potential role of markers in cell death and the inflammatory cascade leading to the severity of liver damage. We aim to present the clinical parameters and laboratory data in a cohort of 88 HCV-infected non-cirrhotic and 25 HCV cirrhotic patients, to determine the characteristic light microscopic (LM) and transmission electron microscopic (TEM) changes in their liver biopsies and to present the link between the severity of liver damage and the serum levels of cytokines and caspases. A matched HCV non-infected cohort was used for the comparison of serum inflammatory markers. We compared the inflammation in HCV individuals with a control group of 280 healthy individuals. We correlated the changes in inflammatory markers in different stages of the disease and the histology. We concluded that the serum levels of cytokine, chemokine, and cleaved caspase markers reveal the inflammatory status in HCV. Based upon the information provided by the changes in biomarkers the clinician can monitor the severity of HCV-induced liver damage. New oral well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Therefore, using the noninvasive biomarkers to monitor the evolution of the liver damage is an effective personalized medicine procedure to establish the severity of liver injury and its repair.
Highlights
IntroductionChronic Hepatitis C virus (HCV) infection is a major cause of liver-related morbidity and mortality
This article emphasizes the increased need to focus on molecular biology markers of inflammation and repair in patients with Hepatitis C virus (HCV)
Due to our better understanding of the molecular biology of RNA viruses, such as HCV, we have been able to highlight the mechanism of inflammation and repair in HCV
Summary
Chronic HCV infection is a major cause of liver-related morbidity and mortality. HCV infection leads to chronic hepatitis, and progresses to liver cirrhosis and hepatocellular carcinoma [3]. HCV end-stage liver disease has become the leading indication for liver transplantation, accounting for approximately half of the transplants performed in European and. The link between hepatitis virus, alcohol consumption, and disease severity is demonstrated [9,10,11,12,13,14,15,16,17,18,19,20]. HCV is connected to an increase in cytokine and chemokine serum levels [21,22,23]. In HCV sera, there are higher levels of alanine aminotransferase (ALT) than aspartate aminotransferase (AST) [10]
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