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Journal of Virology, September 2005, p. 11128-11134, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11128-11134.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus Can Establish Infection in the Absence of a Classical Memory B-Cell Population

Margaret Conacher,1 Robin Callard,2 Karen McAulay,1 Helen Chapel,3 David Webster,4 Dinakantha Kumararatne,5 Anita Chandra,5 Gavin Spickett,6 Paul A. Hopwood,1 and Dorothy H. Crawford1*

Basic and Clinical Virology, University of Edinburgh, Royal (Dick) School of Veterinary Studies, Summerhall, Edinburgh EH9 1QH, United Kingdom,1 Immunobiology Unit, Institute of Child Health, Guilford Street, London WC1N 1EH, United Kingdom,2 Department of Immunology, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom,3 Department of Immunology, Royal Free Hospital, Rowland Hill Street, London NW3 2PF, United Kingdom,4 Clinical Biochemistry and Immunology, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom,5 Regional Immunology Department, Royal Victoria Infirmary, Queen Victoria Road, Newcastle upon Tyne NE1 4LP, United Kingdom6

Received 7 February 2005/ Accepted 12 May 2005

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that persists in the body for life after primary infection. The primary site of EBV persistence is the memory B lymphocyte, but whether the virus initially infects naïve or memory B cells is still disputed. We have analyzed EBV infection in nine cases of X-linked hyper-immunoglobulin M (hyper-IgM) syndrome who, due to a mutation in CD40 ligand gene, do not have a classical, class-switched memory B-cell population (IgD– CD27+). We found evidence of EBV infection in 67% of cases, which is similar to the infection rate found in the general United Kingdom population (60 to 70% for the relevant age range). We detected EBV DNA in peripheral blood B cells and showed in one case that the infection was restricted to the small population of nonclassical, germinal center-independent memory B cells (IgD+ CD27+). Detection of EBV small RNAs, latent membrane protein 2, and EBV nuclear antigen 3C expression in peripheral blood suggests full latent viral gene expression in this population. Analysis of EBV DNA in serial samples showed variability over time, suggesting cycles of infection and loss. Our results demonstrate that short-term EBV persistence can occur in the absence of a germinal center reaction and a classical memory B-cell population.

* Corresponding author. Mailing address: SBCLS, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, United Kingdom. Phone: 44 (0)131 650 3142. Fax: 44 (0)131 650 3177. E-mail: D.Crawford{at}ed.ac.uk.

Journal of Virology, September 2005, p. 11128-11134, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11128-11134.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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