Abstract
Background: A persistent infection of hepatitis B virus (HBV) can cause liver cirrhosis and hepatocarcinoma even though the virus itself is non-cytopathic and does not cause cell injury. It has been asserted that liver injury in chronic HBV infection is attributed to the host immune system responding to HBV infection. Cytokines have a critical role in mediating immune responses to viral infection. This study aimed to determine the correlation between the levels of serum IFN-γ, IL-2, IL-17, and TNF- α with the progress of chronic HBV infection that was determined through provisional diagnosis, patient’s age, and the levels of serum transaminases.Method: Blood samples were collected from patients with chronic hepatitis B and the levels of serum IFN-γ, IL-2, IL-17, and TNF-α were measured by using ELISA. The correlation between each cytokine levels and the provisional diagnosis, patient’s age, and serum transaminases were analyzed by using the Spearman correlation test with a p value of 0.05 is considered as statistically significant.Results: A total of 47 samples were collected from patients with chronic hepatitis B (n=38), chronic hepatitis B with liver cirrhosis (n = 6), and chronic hepatitis B with hepatocellular carcinoma (nc = 3). A significant correlation was found between the levels of serum IFN-γ and aspartate aminotransferase (AST) (p = 0.04).Conclusion: The increase of serum IFN-γ and AST levels may highlight the importance of these particular cytokine and liver transaminase in the immune response to chronic HBV infection since IFN-γ is capable to induce apoptotic cell death which promotes AST release and facilitates liver injury.
Highlights
Hepatitis B is a liver disease caused by hepatitis B virus (HBV)
A total of 47 samples were collected from patients with chronic hepatitis B (n = 38), chronic hepatitis B with liver cirrhosis (n = 6), and chronic hepatitis B with hepatocellular carcinoma (n = 3)
There was no significant correlation between the levels of serum IFN-γ, IL-2, IL-17, and tumour necrosis factor (TNF)-α with liver fibrosis, which may indicate that those cytokines are not directly involved in liver fibrosis
Summary
Hepatitis B is a liver disease caused by hepatitis B virus (HBV). There are 257 million people that had been infected by HBV and caused more than a million deaths per year, mostly caused by cirrhosis and hepatocarcinoma (HCC).[1] HBV is known to be a non-cytopathic virus and does not damage the infected liver cells; i.e., hepatocytes. The damage of liver cells during HBV infection is mainly caused by specific immune responses against infected hepatocytes in order to eliminate the virus. A persistent HBV infection can cause chronic liver disease and liver injury, leading to liver cirrhosis, hepatocarcinoma and liver failure. A persistent infection of hepatitis B virus (HBV) can cause liver cirrhosis and hepatocarcinoma even though the virus itself is non-cytopathic and does not cause cell injury. This study aimed to determine the correlation between the levels of serum interferon gamma (IFN-γ), interleukin-2 (IL-2), interleukin-17 (IL-17), and tumour necrosis alpha (TNF- α) with the progression of liver fibrosis that was determined through aspartate aminotransferase/AST to platelet ratio index (APRI) score and FibroScan in patients with chronic HBV infection
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