Disrupted dichotomous intracellular control of human papillomavirus infection in cancer of the cervix.

The role of specific human papillomaviruses (HPVs) in the aetiology of cancer of the cervix is firmly established. Progression of an HPV-infected cell clone to invasive growth involves consecutive modifications of a set of host cell genes. Some of these modifications suppress viral oncogene functions post-transcriptionally, and others suppress transcription via a signalling pathway stimulated by activated macrophages and possibly by additional cells. I describe a scheme that tries to unify available data by postulating the existence of two intracellular signalling pathways in the control of latent HPV infections.