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Blood, 1 February 2008, Vol. 111, No. 3, pp. 1420-1427. Prepublished online as a Blood First Edition Paper on November 8, 2007; DOI 10.1182/blood-2007-06-093278. This Article Full Text Full Text (PDF) Supplemental Methods, Table, and Figures Erratum (v111,p4421) All Versions of this Article: blood-2007-06-093278v1 111/3/1420    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hadinoto, V. Articles by Thorley-Lawson, D. A. Search for Related Content PubMed PubMed Citation Articles by Hadinoto, V. Articles by Thorley-Lawson, D. A. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY On the dynamics of acute EBV infection and the pathogenesis of infectious mononucleosis Vey Hadinoto1, Michael Shapiro1, Thomas C. Greenough2, John L. Sullivan2, Katherine Luzuriaga2, and David A. Thorley-Lawson1 1 Department of Pathology, Tufts University School of Medicine, Boston, MA; and 2 Pediatrics and Molecular Medicine, University of Massachusetts Medical School, Worcester 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. L. Gulley and W. Tang Laboratory Assays for Epstein-Barr Virus-Related Disease J. Mol. Diagn., July 1, 2008; 10(4): 279 - 292. [Abstract] [Full Text] [PDF]

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