Correlation between IL-35 and viral load in patients with liver hepatitis type B in Baghdad

Abstract

Hepatitis, including autoimmune hepatitis, alcoholic hepatitis, drug-induced hepatitis, bacterial hepatitis, viral hepatitis, and others, was a typical occurrence in clinical work. Hepatitis B virus (HBV) and hepatitis C virus (HCV), both non-cytopathic viruses, were shown to be frequent in liver damage. It has been observed that IL-35 is linked to a reduction in inflammation and can limit T-cell proliferation and the activity of its effector cells. The hepatitis B virus is a virus that causes liver disease. Serum IL-35 was shown to be higher in chronic hepatitis B virus patients. At the same time, research has discovered that Tregs and other cell types (such as activated myeloid, endothelial cells, and regulatory B cells) can secrete IL-35. The quantity of specific viral DNA or RNA in a blood sample is known as viral load count, and it is one of the potential biomarkers of hepatitis. A high viral load suggests that the immune system has failed to combat viruses. Real-time quantification of hepatitis B (HBV) DNA viral load is possible. Hepatic chronic, cirrhosis, and undetected patients are measured using polymerase chain reaction (PCR) and non-invasive methods. In the ordinary course of HBV infection, HBV DNA is the only thing that survives. HBV DNA levels represent viral levels and derive from mature infectious particles. Reproducibility. Various hospital-based and community-based case-control and cohort studies have repeatedly demonstrated substantial correlations between blood HBV DNA levels and the risk of liver cirrhosis and HCC. Chronic hepatitis B has a variable course in disease activity with a risk of clinical complications like liver cirrhosis and hepatocellular carcinoma. As clinical symptoms present in a late stage of the disease, identifying risk factors is important for early detection and, therefore, improving prognosis. Recently, two REVEAL-HBV studies from Iraq have shown a positive correlation between viral load at any point in time and the development of cirrhosis and hepatocellular carcinoma. Keywords: Hepatitis B virus HBV, Interleukin-35 IL-35, polymerase chain reaction PCR.