Abstract
Papillomaviruses do not replicate in tissue culture. Most viral DNAs were therefore directly cloned from biopsy material and characterized by hybridization to known reference DNAs, and by sequencing. There seems to be only one sense strand. The genome can be subdivided into a 0.4 – 1 kb regulatory region (origin of replication, enhancer and promoter elements), an early region, comprising about 4 kb, and a late region, consisting of 3 kb. At least 42 human papillomavirus (HPV) types are differentiated on the basis of less than 50% crosshybridization. They show various degrees of homology among each other, sometimes in different areas of the genome. The viral DNA usually persists extrachromosomally in tumor cells. Only with HPV16 and 18 integration was consistently, observed when tumors became malignant. In transformed cells there are rather low levels of viral transcripts, although an active enhancer in front of the early transcription unit is stimulated by a trans-activating viral protein. These positive regulatory signals are counteracted by negative control elements. So far, there is no evidence that activation of cellular oncogenes is required for transformation by papillomaviruses.
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Pfister, H., Kleiner, E., Lang, G., Sagner, G., Dietrich, W., Fuchs, P.G. (1987). Molecular Biology of Papilloma Virus. In: Aloni, Y. (eds) Molecular Aspects of Papovaviruses. Developments in Molecular Virology, vol 9. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2087-6_13
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DOI: https://doi.org/10.1007/978-1-4613-2087-6_13
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