Mechanistic study of interaction between IL-22 and HCV core protein in the development of hepatocellular carcinoma among liver transplant recipients.

Background: Hepatitis C virus (HCV) infects more than 170 million people worldwide that represents a major threat to global public health. Several viruses including HCV have developed mechanisms against the cellular responses essentially "hijacking" the antiviral responses generated against it. Interleukin 22 activated JAK-STAT pathways are responsible for several functions including liver regeneration, antiviral responses and cell cycle regulation.

IL-22 in hepatocyte's survival of Pakistani patients with end stage liver disease: an insight into IL 22 mediated hepato-regenerative pathway.

Hepatitis is the principal cause of hepatocellular carcinoma (HCC) and decompensated cirrhosis. HCC is amongst the leading causes of deaths worldwide. Current therapeutic options have proven to be unsuccessful in treating this disease due to multifactorial nature of the disease.

Purinoceptor expression in hepatocellular virus (HCV)-induced and non-HCV hepatocellular carcinoma: an insight into the proviral role of the P2X4 receptor.

The basic idea behind this study was to discover the association and prevalence of purinoceptors in hepatitis C virus (HCV) and non-HCV hepatocellular carcinoma (HCC). Immunohistochemistry was performed to study the expression of P2X4 and P2X7 receptors on ex-planted liver tissue samples that were collected from HCC patients. Antibodies specific for the P2X4 and P2X7 receptors were used to target the specific receptors and secondary antibody was used with 3,3'-diaminobenzidine (DAB) detection system to visualize the color change in case of any positive expression There was a substantial increase in P2X4 receptor expression in HCV induced HCC as compared to non-HCV HCC.