Tumour Viruses - Virus-Host Cell Interactions

TUMOUR VIRUSES - VIRUS–HOST CELL INTERACTIONS

There is a suggestion that 20% of human cancers might have a viral origin. Virus infected cells change dramatically, acquiring the characteristics of tumour cells exhibiting uncontrolled growth. For example, the Epstein–Barr virus (EBV) has been associated with the formation of lymphomas and nasopharyngeal carcinomas, the hepatitis B and C viruses with hepatocellular carcinoma, human papilloma viruses with cervical cancer, human T-cell lymphotrophic virus type 1 with adult T-cell leukaemia/lymphoma syndrome and HIV with Kaposi’s sarcoma.

There are no identified single mechanisms by which viruses induce tumours. The acquisition of viral genes by the host must be followed by other events such as environmental or dietary exposures to chemical carcinogens for cancer to occur. For example, there might be an association between EBV and malaria to trigger Burkitt’s lymphoma in young children in Africa. EBV and consumption of smoked fish might trigger nasopharyngeal carcinoma in adults in China. The development of liver cancer following infection with hepatitis B virus (HVB) might be triggered by high alcohol consumption, smoking and exposure to fungal toxin (aflatoxins), events that damage the liver.

It is known that the viral genome of oncogenic viruses can integrate the host DNA. Indeed, viral DNA has been recovered from infected cells. Following integration of the provirus, the regulation of cell growth and division can be affected. There is no means of eradicating proviruses. However, progress in the prevention of papillomavirus has been made by designing an effective vaccine combined to a successful vaccination programme that is responsible for an important decrease in cervical cancer cases.