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.
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.
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