Pathogenesis of Oncoviral Infections
Finn Skou Pedersen and Annette Balle Sørensen
from: Retroviruses: Molecular Biology, Genomics and Pathogenesis (Edited by: Reinhard Kurth and Norbert Bannert). Caister Academic Press, U.K. (2010)
Abstract
Retroviruses cause cancer in natural or laboratory settings by a variety of mechanisms. The acutely transforming or transducing retroviruses induce tumours in animals within days to weeks. They harbour a host-cell derived gene, an oncogene, which infiltrate signalling cascades that regulate cell growth and survival. The oncoprotein encoded by the viral oncogene is activated to dominant signalling, either by deregulated expression or as a result of a modified protein structure that uncouples downstream signalling from upstream physiological signals. The cis-acting or non-acutely transforming viruses cause disease with latency periods of months. These viruses work as insertional mutagens to promote multi-step oncogenesis, and large-scale mapping of proviral insertions in tumour DNAs provides a rich source of candidate genes with a potential role in cancer of non-retroviral aetiology. Viral proteins may also stimulate target cells to proliferate. One example is the mouse mammary tumour virus which stimulates lymphocytes via a virus-encoded superantigen. Other examples are the mitogenic stimulation of erythrocyte precursor cells by the defective envelope protein of the mouse spleen focus-forming virus, and the direct oncogenic affect of the envelope protein of the Jaagsiekte sheep retrovirus read more ...
