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The Viral Genes Hypothesis

Viruses and human cancer. There is convincing evidence that viruses cause a number of specific cancers in animals. The polyoma virus has been isolated from mice and the simian virus 40 (SV 40) from monkeys. Tumor-producing viruses are called oncoviruses. There is, however, no clear cut evidence of malignant tumors being caused in humans by viruses. No infective viruses have been isolated from cell cultures such as HeLa cells. This does not mean, however, that viruses can be eliminated as a cause of cancer in man. There are several difficulties in trying to determine a virus-cancer relationship in humans. These include: (i) the impossibility of injecting cancer causing viruses into human beings, (ii) the viruses concerned may not be transmissible, (iii) viruses if present may not have a separated identity, but their genetic material may be incorporated into the DNA of human chromosomes and (iv) the presence of harmless viruses in tumors may confuse the picture.

Incorporation of viral DNA into the genome of the host. A virus usually multiplies in specific cells derived from animals in which the virus normally grows. Such cells are called permissive cells. Cells in which viruses do not grow are called non permissive cells.

Viruses on entering host cells undergo one of the two types of behavior. (i) They enter the lytic phase and multiply within the host cells, ultimately killing them. This type of infection is called lytic infection or productive infection, e.g., in a adenoviruses. (ii) The viral DNA may be inserted into the DNA of host chromosomes, and becomes an integral part of host DNA. The virus is now said to become a provirus. Transformation of normal cells into cancerous cells is often due to integration of viral genes into the chromosomes of the host cell. The gene of a cancer-causing virus which is responsible for transformation is called and oncogene.

Carcinogens. Agents which cause cancers are called carcinogens. It is believed that carcinogens affect the natural genetic processes of cells and disturb the control mechanisms.

1. Accumulation of mutational defects brought about by carcinogens. Carcinogens may cause alterations in DNA (mutations). Several mutational defects may result in the cell becoming cancerous (multi-hit-initiation).

2. Repression of normal gene activities. Carcinogens or their reactive metabolic derivatives may bind with DNA and cause disorganization in the decoding of DNA information. This may bring about repression of certain normal gene activities in precancerous cells.

3. Derepression of ‘forbidden’ gene activities. Carcinogens may induce ‘forbidden’ gene transcription for enzyme that stimulates cell division. This is brought about by derepression of certain information in DNA that is normally repressed. Probably the most acceptable suggestion of how transformation occurs is that the products of viral genes derpepress extensive regions of the cellular genome.

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