DNA viruses and human cancer.

This review examines some of the evidence which aetiologically implicates various DNA viruses (primarily papillomavirus, hepatitis B virus and Epstein-Barr virus) in certain human cancers (cervical carcinoma, primary liver cell carcinoma, Burkitt's lymphoma and nasopharyngeal carcinoma, respectively). The evidence includes: presence of viral DNA, RNA and proteins in tumours (and cell lines derived from them); occurrence of viruses with apparently different oncogenic potential; their ability to transform cell lines in vitro or cause tumours in animals; epidemiological and serological data. Factors which affect the progression to cancer are briefly considered as they illustrate that there are several stages in tumorigenesis. These factors include the immune system, irradiation, presence of other viruses or carcinogens and treatment. The lack of a single unique characteristic which defines a transformed cell would be expected from the multistep hypothesis and is related to the possible virus-cell interactions that can occur. These form a continuous spectrum ranging from productive infection of a permissive cell, through infection of a non-permissive cell, to the inability of a virus to infect a cell. This spectrum may reflect the absence of increasing numbers of cellular functions necessary for productive virus infection, with cell transformation occurring as a rare type of abortive infection. The evidence, especially for human papillomavirus, indicates that it is quite probable that particular DNA viruses are the causative agents for certain human cancers. Even so other factors can play decisive roles in tumorigenesis. Final aetiological proof will only be obtained when an anti-virus vaccine eradicates one form of human cancer.