High risk HPV can induce cervical and oropharyngeal Iesions. HPV productive infection is strictly linked by differentiation-dependent control of the late promoter. This latter produces HPV transcripts at different epithelial layers through a complex post-transcriptional control. The aim of this study is to develop a novel mathematical model of the late promoter condensing the biological knowledge present in literature. The model describes the interaction among primary transcript, spliced transcripts and their proteins and includes the major splicing mechanisms. When used as an in silico tool it shows the crucial role of splicing regulation to explain the HPV gene expression. Novel testing hypothesis are then formulated to uncover this still elusive but pivotal promoter.
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