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Blood, 1 August 2008, Vol. 112, No. 3, pp. 672-679. Prepublished online as a Blood First Edition Paper on May 28, 2008; DOI 10.1182/blood-2007-10-116269. This Article Full Text (PDF) All Versions of this Article: blood-2007-10-116269v1 112/3/672    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 Chaganti, S. Articles by Rickinson, A. B Search for Related Content PubMed PubMed Citation Articles by Chaganti, S. Articles by Rickinson, A. B Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted October 18, 2007 Accepted April 21, 2008 Epstein-Barr virus persistence in the absence of conventional memory B cells: IgM+IgD+ CD27+ B cells harbour the virus in X-linked lymphoproliferative disease patients Sridhar Chaganti, Cindy S Ma, Andrew I Bell, Debbie Croom-Carter, Andrew D Hislop, Stuart G Tangye, and Alan B Rickinson* Institute for Cancer Studies, University of Birmingham, Birmingham, United Kingdom Immunology and Inflammation Program, Garvan Institute for Medical Research, Sydney, Australia * Corresponding author; email: a.b.rickinson{at}bham.ac.uk. Epstein-Barr virus (EBV) persists in healthy virus carriers within the immunoglobulin (Ig)D- CD27+ (class-switched) memory B cell compartment that normally arises through antigen stimulation and germinal centre transit. Patients with X-linked lymphoproliferative disease (XLP) lack such class-switched memory B cells but are highly susceptible to EBV infection, often developing fatal symptoms resembling those seen in EBV-associated haemophagocytosis (EBV-AHS), a disease caused by aberrant virus entry into the NK or T cell system. Here we show that XLP patients who survive primary EBV exposure carry relatively high virus loads in the B cell, but not the NK or T cell, compartment. Interestingly, in the absence of conventional class-switched memory B cells, the circulating EBV load was concentrated within a small population of IgM+ IgD+ CD27+ (non-switched) memory cells rather than within the numerically dominant naive (IgM+ IgD+ CD27-) or transitional (CD10+ CD27-) subsets. In two prospectively studied patients, the circulating EBV load was stable and markers of virus polymorphism detected the same resident strain over time. These results provide the first definitive evidence that EBV can establish persistence in the B cell system in the absence of fully-functional germinal centre activity and of a class-switched memory B cell compartment. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Chaganti, E. M. Heath, W. Bergler, M. Kuo, M. Buettner, G. Niedobitek, A. B. Rickinson, and A. I. Bell Epstein-Barr virus colonization of tonsillar and peripheral blood B-cell subsets in primary infection and persistence Blood, June 18, 2009; 113(25): 6372 - 6381. [Abstract] [Full Text] [PDF] J. Heather, K. Flower, S. Isaac, and A. J. Sinclair The Epstein-Barr virus lytic cycle activator Zta interacts with methylated ZRE in the promoter of host target gene egr1 J. Gen. Virol., June 1, 2009; 90(6): 1450 - 1454. [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]

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