Published in 2008, I've never seen this one, very interesting. Full text is free. http://bloodjournal.hematologylibrary.org/cgi/content/long/111/3/1420 On the dynamics of acute EBV infection and the pathogenesis of infectious mononucleosis Vey Hadinoto, Michael Shapiro, Thomas C. Greenough, John L. Sullivan, Katherine Luzuriaga, and David A. Thorley-Lawson1 Abstract: Memory B cells latently infected with Epstein-Barr virus (mBLats) in the blood disappear rapidly on presentation with acute symptomatic primary infection (acute infectious mononucleosis [AIM]). They undergo a simple exponential decay (average half-life: 7.5 3.7 days) similar to that of normal memory B cells. The cytotoxic T lymphocyte (CTL) response to immediate early (IE) lytic antigens (CTLIEs) also decays over this time period, but no such correlation was observed for the CTL response to lytic or latent antigens or to the levels of virions shed into saliva. We have estimated the average half-life of CTLIEs to be 73 ( 23) days. We propose that cycles of infection and reactivation occur in the initial stages of infection that produce high levels of mBLats in the circulation. Eventually the immune response arises and minimizes these cycles leaving the high levels of mBLats in the blood to decay through simple memory B-cell homeostasis mechanisms. This triggers the cells to reactivate the virus whereupon most are killed by CTLIEs before they can release virus and infect new cells. The release of antigens caused by this large-scale destruction of infected cells may trigger the symptoms of AIM and be a cofactor in other AIM-associated diseases. Here are the parts I thought were interesting (this is not meant to be a comprehensive summary but to point out particular things that struck me): From Introduction: "[If] infection is delayed until adolescence, it results in acute infectious mononucleosis (AIM) in 20% to 50% of cases." "There is evidence that AIM itself rather than EBV infection, per se, is a key predisposing factor for at least some of the associated diseases." "During AIM, the level of latently infected memory B cells can rise to half, and perhaps even higher, of the peripheral memory B-cell compartment." From Results: "...acute infection had still not resolved to stable persistence even by 1 year later. These observations were subsequently confirmed" (a graph indicates that the number of infected B cells one year after infectious mononucleosis was still declining but more than 1 log, or 10 fold, higher than the number seen in healthy carriers of the virus). From Discussion: "Our data show conclusively that by the time the clinical symptoms of AIM arise, the level of mBLats is always rapidly decreasing. Therefore, the emergence of clinical symptoms coincides with the massive cell death associated with the exponential decay of mBLats, not with infection per se." "[Our data imply] that 50% of mBLats, constituting 25% of the entire memory B-cell compartment, may be destroyed in 1 week at the height of the infection. This constitutes a massive, continuous deposition of cellular and viral antigens into the system. This action could be what is responsible for the long-term damage inflicted on the immune system and the predisposing factor for the AIM-associated diseases."