National Antivisection Society
Research projects 2001 - Hepatitis B
Analysis of cytokine-induced, non-cytotoxic inactivation of hepatitis B virus replication in human hepatocytes
Dr Nikolai Naoumov from the Institute of Hepatology, University College London has developed an in vitro model of human liver cells infected with the hepatitis B virus (HBV).
HBV is a DNA virus that causes acute and chronic liver diseases, including liver cancer, and this model allows the effects of cytokines (proteins involved in the immune response) upon the virus DNA to be studied.
In a preliminary study, human lymphocytes (white blood cells involved in the immune system) isolated from hepatitis B patients were co-cultured with a human cell line of liver tumour cells that are able to support full replication of HBV. Investigations using this model indicated that HBV replication could be inactivated using a cytokine known as IFNg. The model was validated and results confirmed by a parallel experiment using naturally infected human hepatocytes (liver cells) isolated from a liver biopsy taken from a hepatitis B patient.
The Lord Dowding Fund will support further research using the in vitro model to define in greater detail the mechanisms of cytokine-induced inactivation of HBV; the effect on different stages of the viral replication process and the use of nitric oxide as a mediator for this antiviral effect within the cells.
The question of whether certain cytokines can eliminate hepatitis B virus DNA is fundamental to understanding immune control of the disease. Cytokine use has great value as a potential therapy, because it is believed that they can inactivate the virus without destroying the liver cells. Similar studies have been carried out by others in animal models, particularly ducks, woodchucks and transgenic mice. Data from these experiments is not applicable to the human HBV infection because of the significant differences between human and animal hepatitis B viruses. This is the first time that human rather than animal liver cells will be used.
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