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Open Access Research article

Different papillomaviruses have different repertoires of transcription factor binding sites: convergence and divergence in the upstream regulatory region

Santiago García-Vallvé1, José R Iglesias-Rozas2, Ángel Alonso3 and Ignacio G Bravo3*

Author Affiliations

1 Evolutionary Genomics Group. Biochemistry and Biotechnology Department. Rovira i Virgili University (URV), c/Marcel-li Domingo, s/n. Campus Sescelades, 43007, Tarragona, Spain

2 Klinikum Stuttgart. Katharinenhospital, Institut für Pathologie (Neuropathologie). Kriegsbergstr. 60, D-70174 Stuttgart, Germany

3 Deutsches Krebsforschungszentrum. F050. Im Neuenheimer Feld-242. 69120 Heidelberg. Germany

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BMC Evolutionary Biology 2006, 6:20  doi:10.1186/1471-2148-6-20

Published: 9 March 2006



Papillomaviruses (PVs) infect stratified squamous epithelia in warm-blooded vertebrates and have undergone a complex evolutionary process. The control of the expression of the early ORFs in PVs depends on the binding of cellular and viral transcription factors to the upstream regulatory region (URR) of the virus. It is believed that there is a core of transcription factor binding sites (TFBS) common to all PVs, with additional individual differences, although most of the available information focuses only on a handful of viruses.


We have studied the URR of sixty-one PVs, covering twenty different hosts. We have predicted the TFBS present in the URR and analysed these results by principal component analysis and genetic algorithms. The number and nature of TFBS in the URR might be much broader than thus far described, and different PVs have different repertoires of TFBS.


There are common fingerprints in the URR in PVs that infect primates, although the ancestors of these viruses diverged a long time ago. Additionally, there are obvious differences between the URR of alpha and beta PVs, despite these PVs infect similar histological cell types in the same host, i.e. human. A thorough analysis of the TFBS in the URR might provide crucial information about the differential biology of cancer-associated PVs.