Modeling HPV early promoter regulation

In high risk forms, human papillomaviruses (HPV) can either induce or promote cancerous lesions, especially cervical cancer which is considered the second most common cancer in the women worldwide. HPV life cycle is tightly linked to the infected cell differentiation program and its evolution is strictly joined to the switch between the early and the late viral polycistronic promoters.The aim of this study is to develop a novel mathematical model which collects and structures the available biologic knowledge on the early promoter regulation for HPV in episomal form. The model includes the main regulation by E2 viral protein as well as a novel discovered co-regulation function mediated by the viral E1 protein. Only by including both E2 and E1 regulatory effect the model is able to correctly predict the temporal behaviour of the early promoter switching off. A possible use of the model as in silico tool to evaluate new antiviral therapies is discussed.