Herpes simplex virus (HSV) and human cytomegalovirus (HCMV) are candidates for the induction of premalignant or malignant disease. Morphological transformation studies have failed to demonstrate a viral oncogene, a virus-coded transforming protein or any sequence of DNA that uniquely transforms cells according to one-hit kinetics. Thus the mechanism of transformation is complex. The transformed cells are, however, all oncogenic in the host animal and in immunocompetent mice. Direct evidence for the presence of these viruses in human genital tumours is the finding that a small proportion (about 10%) retain fragments of virus DNA from different regions of the virus genomes. In contrast human papillomavirus (HPV) is strongly associated with genital neoplasia, being present in over 80% of tumours. However, HPV can also be detected in histologically normal tissue.

The most persuasive roles for HSV and HCMV in human tumourigenesis are as mutagens, as activators of cellular transcription or in switching on the synthesis of host cell proteins not normally expressed in untransformed cells. In these roles the prospects of further defining roles for HSV and HCMV in the multistage process of oncogenic transformation are good.


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