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Review Article
Mechanisms of Disease
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Volume 350:1328-1337 March 25, 2004 Number 13
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Persistence of the Epstein–Barr Virus and the Origins of Associated Lymphomas
David A. Thorley-Lawson, Ph.D., and Andrew Gross, M.D.

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Epstein–Barr virus (EBV) is perhaps best known for its ability to immortalize human B lymphocytes in culture.1 This property makes it a candidate for causing human disease, particularly cancer and autoimmune disease.2,3 Recent work, however, has shown that EBV has evolved strategies that reduce its potential to become pathogenic.4,5,6 These new findings have encouraged a reassessment of how and when EBV may cause human disease. In this article, we review current knowledge of the ways in which EBV establishes and maintains a persistent infection at the same time that it minimizes its pathogenicity; we also discuss how these characteristics influence . . . [Full Text of this Article]

EBV Infection

In Vitro and in Vivo Infection

The Persistence of EBV

Resolution of the Infection

Minimizing the Pathogenic Effect of EBV

Other Interpretations

EBV and Epithelium

EBV and Disease

Lymphoma in Immunosuppressed Patients

Hodgkin's Disease

Burkitt's Lymphoma

Conclusions


Source Information

From the Department of Pathology, Tufts University School of Medicine (D.A.T.-L.), and the Department of Rheumatology, Tufts–New England Medical Center (A.G.) — both in Boston.

Address reprint requests to Dr. Thorley-Lawson at the Department of Pathology, Jaharis Bldg., Tufts University School of Medicine, 150 Harrison Ave., Boston, MA 02111, or at david.thorley-lawson@tufts.edu.


Related Letters:

EBV and Burkitt's Lymphoma
Rossi G., Bonetti F., Thorley-Lawson D. A.
Extract | Full Text | PDF  
N Engl J Med 2004; 350:2621, Jun 17, 2004. Correspondence

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