Abstract
Hepatitis C virus (HCV) is one of the most epidemic viral infections in the world. Three-quarters of individuals infected with HCV become chronic. As a consequence of persistent inflammation, a considerable percentage of chronic patients progress to liver fibrosis, cirrhosis, and finally hepatocellular carcinoma. Cytokines, which are particularly produced from T-helper cells, play a crucial role in immune protection against HCV and the progression of the disease as well. In this study, the role of interleukins IL-33, IL-17, and IL-25 in HCV patients and progression of disease from chronicity to hepatocellular carcinoma will be characterized in order to use them as biomarkers of disease progression. The serum levels of the tested interleukins were measured in patients suffering from chronic hepatitis C (CHC), hepatocellular carcinoma (HCC), and healthy controls (C), and their levels were correlated to the degree of liver fibrosis, liver fibrosis markers and viral load. In contrast to the IL-25 serum level, which increased in patients suffering from HCC only, the serum levels of both IL-33 and IL-17 increased significantly in those patients suffering from CHC and HCC. In addition, IL-33 serum level was found to increase by liver fibrosis progression and viral load, in contrast to both IL-17 and IL-25. Current results indicate a significant role of IL-33 in liver inflammation and fibrosis progress in CHC, whereas IL-17 and IL-25 may be used as biomarkers for the development of hepatocellular carcinoma.
Highlights
The positive single-stranded RNA Hepatitis C virus (HCV) is a member of the familyFlaviviridae [1]
A total of 146 patients with chronic hepatitis C (CHC) and 45 patients diagnosed with hepatocellular carcinoma (HCC) in addition to 60 healthy controls were recruited in the current study
It is worthy of note that the results indicate that there was no correlation between IL-17 serum level and either viral load or liver fibrosis degree
Summary
The positive single-stranded RNA Hepatitis C virus (HCV) is a member of the familyFlaviviridae [1]. The positive single-stranded RNA Hepatitis C virus (HCV) is a member of the family. About 60–80% of infected people are chronic patients (CHC) because of the failure of immune system to eradicate the virus. It has been shown that persistent hepatic inflammation in CHC could progress to liver fibrosis, cirrhosis and eventually to hepatocellular carcinoma in many infected patients [2]. Chronic inflammation is basically due to interaction between the virus and host hepatocytes, leading to both hepatocyte injury and immune system suppression [3,4]. The immune response to HCV is regulated by the T-helper (TH) cells that activate both humoral and cellular responses via the secretion of cytokines, which, in turn, regulate both Th1 and Th2 cells [5,6]
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