DNA tumor viruses have long been useful experimental models of
carcinogenesis and have elucidated several important mechanisms of cell
transformation. Re- search in recent years has shown that human tumors
have a multifactorial nature and that some DNA tumor viruses may playa
key role in their etiology. The aim of this book is to assess our
knowledge of DNA tumor viruses by reviewing animal models, mechanisms of
transformation, association with human tumors, and possi- bilities of
prevention and control by vaccination. Animal models of tumor virology
have contributed significantly to our under- standing of the
epidemiology and pathogenesis of virus-induced tumors. Bovine
papillomaviruses induce papillomas in the intestine of cattle. The
papillomas undergo a transition to carcinomas in cows feeding on bracken
fern, which pro- duces a toxin with radiomimetic and immunosuppressive
functions. This example of cooperation between a virus and chemical
carcinogens parallels the cooperative role of human papillomaviruses
(HPVs) and herpes simplex virus type 2 (HSV-2) with environmental
carcinogens in the pathogenesis of cervical cancer. Likewise,
hepatocarcinomas appearing in woodchucks chronically infected by
woodchuck hepatitis virus (WIN) provide strong support for the
relationship between hepatitis B virus (HBV) infection and human
hepatocellular carcinoma. Also, the fact that WIN DNA integrates closely
to cellular oncogenes suggests a possible molecular mechanism for the
tumorigenesis induced by HBV.