Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation
Autor: | Dennis M. Walling, Catherine M. Flaitz, Joan E. Nichols, Autumn J. Ray, C. Mark Nichols |
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Rok vydání: | 2007 |
Předmět: |
Adult
Male Epstein-Barr Virus Infections Herpesvirus 4 Human Langerhans cell Immunology Biology Virus Replication medicine.disease_cause Models Biological Microbiology Herpesviridae Virus Cell Movement hemic and lymphatic diseases Virology Virus latency medicine Humans Gammaherpesvirinae Epstein–Barr virus infection Cells Cultured B-Lymphocytes Stem Cells Mouth Mucosa Cell Differentiation Epithelial Cells medicine.disease biology.organism_classification Epstein–Barr virus Virus Latency medicine.anatomical_structure Langerhans Cells Insect Science Pathogenesis and Immunity Female Virus Activation Stem cell |
Zdroj: | Journal of Virology. 81:7249-7268 |
ISSN: | 1098-5514 0022-538X |
DOI: | 10.1128/jvi.02754-06 |
Popis: | 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. |
Databáze: | OpenAIRE |
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