Role of Viruses in the Causation of Human Cancer

To prove a causal relationship between a putative cancer-causing virus and human cancer is not a simple task. Such proof relies on evidence that is to a fair extent circumstantial. This evidence includes (1) epidemiological data showing a correlation between living in an area of endemic viral infection and a type ofcancer; (2) serological evidence of antibody titers to viral antigens in patients with a given cancer type; (3) evidence for insertion of viral DNA into a cancer-bearing host's cell genome; (4) evidence for a consistent chromosomal translocation, particularly those involving an oncogene, in virally infected patients; (5) data showing that viral infection of cells in culture or transfection of viral genes into cells causes cell transformation and the ability of such cells to produce tumors in nude mice; and (6) development of cancers of the suspected target organ in transgenic mice produced by embryonic gene transfer of viral genes.

On the basis of this sort of evidence, some human cancers are considered to be caused by viral infection either directly or indirectly. By "directly," I mean that the viral gene(s) can themselves cause cells to become malignant (sometimes also requiring the loss of a tumor suppressor gene). By "indirectly," I mean that viral infection may simply cause the progression of malignant cell growth by producing an immunodeficiency state (e.g., the occurrence of non-Hodgkin's lymphoma in HIV-infected patients) or by stimulating the proliferation of already transformed cells. Sometimes viral infection acts in concert with other infectious agents or chemical carcinogens. Such is the case for malarial infection of Epstein-Barr virus (EBV)-infected patients and for aflatoxin exposure of individuals bearing the hepatitis B viral genome in their liver cells (see below). The types of

Table 2-4. Examples of Oncogenic Viruses


Species of Isolation

I. Oncogenic RNA viruses

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