Abstract

Epstein-Barr virus (EBV) is involved in various clinical disorders and many of the disease entities are lymphoid and epithelial malignancies. The exact mechanisms that determine the exact form of EBV-related disorder are not clear at present. Many of the clinical manifestations of these diseases are based on the biological characteristics of the target cells for EBV infection and the expression and function of EBV gene, which also perturb host immune functions. In this monograph, I propose a hypothesis regarding the mechanism involved in shaping the manifestation of EBV infection that genomic instability of EBV-infected cells and how a defective immune surveillance system against such cells plays a critical role in determining the clinical manifestation of EBV infection. Using EBV-infected B-cells from patients and carriers with ataxia telangiectasia as an example of EBV infection, I present and discuss evidence in support of the proposed hypothesis.

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