Figure 1. EBV biological model.

A) Newly infected B-cell Blasts move into the follicle and enter the GC, where they continue to divide as EBV-infected GC B-cells before exiting into the periphery as latently infected memory B-cells. A small subset of these are induced to undergo lytic reactivation, progressing through the lytic stages Immediate early, Early and Late before finally bursting and releasing infectious virus that may be amplified through infection of the epithelium (not detailed in the model) but ultimately culminate in the infection of new naive B-cells which become Blasts, thus completing the cycle. Theoretically each stage has the capacity to generate a CTL response. The Blast, Immediate early and Early stages are always regulated, while the GC and Late stages may not always be regulated [7], [32], [33]. Memory is never regulated under normal biological conditions [4], [8], [11]. This model of EBV biology is used to generate the CPM framework presented in this paper. B) Infected populations as displayed as circles whose area is proportional to their frequency within all tonsils (1∶5∶1.5×10²∶10⁴∶10⁴∶0.5×10⁴, Late∶Early∶ImmEarly∶Memory∶GC∶Blast). This graphic highlights the very large range in the sizes of these populations.