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Journal of Virology, July 2007, p. 7249-7268, Vol. 81, No. 13
0022-538X/07/$08.00+0     doi:10.1128/JVI.02754-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation{triangledown}

Dennis M. Walling,1,2* Autumn J. Ray,1 Joan E. Nichols,1,2 Catherine M. Flaitz,3 and C. Mark Nichols4

Division of Infectious Diseases, Department of Internal Medicine,1 Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, 301 University Boulevard, Galveston, Texas 77555-0435,2 Oral and Maxillofacial Pathology, Department of Diagnostic Sciences, University of Texas Health Science Center at Houston, Dental Branch, P.O. Box 20068, 6516 MD Anderson Boulevard, Houston, Texas 77225-0068,3 Bering-Omega Dental Clinic, 1427 Hawthorne, Houston, Texas 770064

Received 14 December 2006/ Accepted 12 March 2007

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with many malignant and nonmalignant human diseases. Life-long latent EBV persistence occurs in blood-borne B lymphocytes, while EBV intermittently productively replicates in mucosal epithelia. Although several models have previously been proposed, the mechanism of EBV transition between these two reservoirs of infection has not been determined. In this study, we present the first evidence demonstrating that EBV latently infects a unique subset of blood-borne mononuclear cells that are direct precursors to Langerhans cells and that EBV both latently and productively infects oral epithelium-resident cells that are likely Langerhans cells. These data form the basis of a proposed new model of EBV transition from blood to oral epithelium in which EBV-infected Langerhans cell precursors serve to transport EBV to the oral epithelium as they migrate and differentiate into oral Langerhans cells. This new model contributes fresh insight into the natural history of EBV infection and the pathogenesis of EBV-associated epithelial disease.

* Corresponding author. Mailing address: Division of Infectious Diseases, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0435. Phone: (409) 747-0236. Fax: (409) 772-6527. E-mail: dmwalling{at}comcast.net

{triangledown} Published ahead of print on 21 March 2007.

Journal of Virology, July 2007, p. 7249-7268, Vol. 81, No. 13
0022-538X/07/$08.00+0     doi:10.1128/JVI.02754-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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