Abstract
Epstein-Barr virus (EBV) infects most people and establishes life-long infection controlled by the host's immune system. The genetic stability of the virus, deep understanding of the viral antigens and immune epitopes recognized by the host's T-cell system and the fact that recent infection can be identified by the development of symptomatic infectious mononucleosis makes EBV a powerful system in which to study human immunology. The association between EBV and multiple cancers also means that the lessons learned have strong translational potential. Increasing evidence of a role for resident memory T-cells and non-conventional γδ T-cells in controlling EBV infection suggests new opportunities for research and means the virus will continue to provide exciting new insights into human biology and immunology into the future.
Highlights
Epstein-Barr virus (EBV) was first identified in 1964 in a biopsy from a patient with Burkitt Lymphoma [1]
A history of infectious mononucleosis (IM) is associated with a raised incidence of Hodgkin lymphoma (HL) in the decade following infection and an increased risk of developing multiple sclerosis [5, 6]
In IM patients EBV loads in the tonsils are high yet EBV-specific CD8+ and CD4+ T cells are markedly lower in frequency at this site than in the blood of the same individual [23, 34, 42]
Summary
Epstein-Barr virus (EBV) was first identified in 1964 in a biopsy from a patient with Burkitt Lymphoma [1]. Studies in IM patients using HLA tetramers report that CD8+ T-cells specific for individual EBV lytic and latent epitopes can account for 1–40 and 0.1–5% of total CD8+ T cells, respectively [25, 26, 28]. Observations of raised perforin expression within the total CD4+ T cells of IM patients suggested that cytotoxic CD4+ T cells are present during primary EBV infection [43].
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