SEARCH:   Advanced

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 (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 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 Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 5, 2007 Accepted October 31, 2007 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-Lawson* Department of Pathology, Tufts University School of Medicine, Boston, MA, United States Pediatrics and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, United States * Corresponding author; email: david.thorley-lawson{at}tufts.edu. Memory B cells latently infected with EBV (mBLat) in the blood disappear rapidly upon 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 CTL response to immediate early (IE) lytic antigens (CTLIE) 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 CTLIE 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 mBLat in the circulation. Eventually the immune response arises and minimizes these cycles leaving the high levels of mBLat 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 CTLIE 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 co-factor in other AIM associated diseases CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Hoshino, H. Katano, P. Zou, P. Hohman, A. Marques, S. K. Tyring, D. Follmann, and J. I. Cohen Long-Term Administration of Valacyclovir Reduces the Number of Epstein-Barr Virus (EBV)-Infected B Cells but Not the Number of EBV DNA Copies per B Cell in Healthy Volunteers J. Virol., November 15, 2009; 83(22): 11857 - 11861. [Abstract] [Full Text] [PDF] P. G. Stevenson, J. P. Simas, and S. Efstathiou Immune control of mammalian gamma-herpesviruses: lessons from murid herpesvirus-4 J. Gen. Virol., October 1, 2009; 90(10): 2317 - 2330. [Abstract] [Full Text] [PDF] J. E. Roughan and D. A. Thorley-Lawson The Intersection of Epstein-Barr Virus with the Germinal Center J. Virol., April 15, 2009; 83(8): 3968 - 3976. [Abstract] [Full Text] [PDF] 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]

	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020