Schematic drawing of the proposed model for the course of acute EBV infection leading to AIM. Acute EBV infection leads to ever-increasing rounds of production of mB_Lat reactivation and infection of new B cells resulting in high levels of mB_Lats and virus shedding. This stimulates strong CTL responses that drastically reduce this one-way circuit, leaving high levels of mB_Lats that simply decay through apoptosis according to the normal half-life of a memory B cells. Apoptosis triggers viral reactivation leading to the production of cells expressing viral IE proteins that are rapidly destroyed by CTL_IEs. Hence the levels of CTL_IEs fall in parallel with those of the mB_Lats. We hypothesize that this massive cell death causes the symptoms of AIM, leading patients to enter the clinic at a time when the levels of mB_Lats and CTL_IEs are rapidly falling but levels of CTLs against other viral target (EA and LAT) and saliva shedding are already leveling off toward the levels found in persistent infection (dashed lines indicating the first 6 weekly visits to the clinic in our study).