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 Blood, 18 June 2009, Vol. 113, No. 25, pp. 6372-6381.
Prepublished online as a Blood First Edition Paper on April 7, 2009; DOI 10.1182/blood-2008-08-175828.

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IMMUNOBIOLOGY

Epstein-Barr virus colonization of tonsillar and peripheral blood B-cell subsets in primary infection and persistence

Sridhar Chaganti1, Emily M. Heath1, Wolfgang Bergler2, Michael Kuo3, Maike Buettner4, Gerald Niedobitek5, Alan B. Rickinson1, and Andrew I. Bell1

1 Cancer Research UK Institute for Cancer Studies, University of Birmingham, Birmingham, United Kingdom; 2 Krankenhaus St Joseph-Stift Bremen, Bremen, Germany; 3 Birmingham Children's Hospital, Birmingham, United Kingdom; 4 Pathological Institute, University Hospital Erlangen, Erlangen, Germany; and 5 Institute for Pathology, Sana Klinikum Lichtenberg/Unfallkrankenhaus Berlin, Berlin, Germany

Epstein-Barr virus (EBV) persists in the immune host by preferentially colonizing the isotype-switched (IgD–CD27+) memory B-cell pool. In one scenario, this is achieved through virus infection of naive (IgD+CD27–) B cells and their differentiation into memory via germinal center (GC) transit; in another, EBV avoids GC transit and infects memory B cells directly. We report 2 findings consistent with this latter view. First, we examined circulating non–isotype-switched (IgD+CD27+) memory cells, a population that much evidence suggests is GC-independent in origin. Whereas isotype-switched memory had the highest viral loads by quantitative polymerase chain reaction, EBV was detectable in the nonswitched memory pool both in infectious mononucleosis (IM) patients undergoing primary infection and in most long-term virus carriers. Second, we examined colonization by EBV of B-cell subsets sorted from a unique collection of IM tonsillar cell suspensions. Here viral loads were concentrated in B cells with the CD38 marker of GC origin but lacking other GC markers CD10 and CD77. These findings, supported by histologic evidence, suggest that EBV infection in IM tonsils involves extrafollicular B cells expressing CD38 as an activation antigen and not as a marker of ectopic GC activity.


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