The Epstein-Barr virus (EBV) infects more than 90% of the human population,
and is the cause of several both serious and mild diseases. It is a
tumorivirus, and has been widely studied as a model system for gene
(de)regulation in human. A central feature of the EBV life cycle is its ability
to persist in human B cells in states denoted latency I, II and III. In latency
III the host cell is driven to cell proliferation and hence expansion of the
viral population, but does not enter the lytic pathway, and no new virions are
produced, while the latency I state is almost completely dormant. In this paper
we study a physico-chemical model of the switch between latency I and latency
III in EBV. We show that the unusually large number of binding sites of two
competing transcription factors, one viral and one from the host, serves to
make the switch sharper (higher Hill coefficient), either by cooperative
binding between molecules of the same species when they bind, or by competition
between the two species if there is sufficient steric hindrance.Comment: 7 pages, 6 figures, 1 tabl