Oncogenicity And Role In Human Cancers

Fully permissive host cells are usually killed by polyomavirus infection. Infected cells that have the viral tumour antigen expressed, and survive, may become immortalized and malignantly transformed. Large T-antigen contributes to this by at least two sets of activities: as a host-cell transcription factor and by complexing with and inactivating the tumour suppressor p53 as well as the retinoblastoma gene product pRB, and probably also other host proteins that regulate cell cycle progression and growth. Small t-antigen also acts as a transactivating factor, most probably by complexing with and inactivating protein phosphatase 2A, a mechanism which keeps important intracellular signal transduction pathways active. The oncogenic potential of primate polyomaviruses is evident by infection of rodents, while in the authentic host systems the viruses seem to require cofactors to be transforming. Human polyomaviruses are certainly not the cause of any human cancer. To what extent some viral strains may be part of an arsenal of alternative initiating and maintaining aetiological factors behind some cancers of the brain, bones, pancreas, intestines and other organs, is still an open question.

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