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Abstract
The Epstein–Barr virus (EBV) is endemic in humans and can efficiently transform infected B cells under some circumstances. If an EBV carrier experiences immune suppression, EBV+ B cells can turn into lymphoblasts and exhibit growth expansion that may cause lymphoproliferative diseases which often develop into lymphoma. Our immune system conducts surveillance for EBV+ B cells in order to block spontaneous tumor formation. Here, we summarize the EBV products involved in tumorigenesis, EBV-associated lymphomas, and pathologically relevant mouse models. Preclinical mouse models for a range of EBV-associated diseases not only clear the path to new therapeutic approaches but also aid in our understanding of the nature of lymphomagenesis and immune surveillance.
Highlights
Epstein–Barr virus (EBV), an oncogenic γ herpes virus, is widespread in all human populations and persists in the vast majority of individuals throughout their lifetime
Genetic defects that lead to impaired T cell function predispose individuals to EBV-driven lymphoproliferative diseases or hematological diseases such as X-linked lymphoproliferative disease (XLP) or familial hemophagocytic lymphohistiocytosis (FHL) [6, 7]
Lymphomas associated with post-transplant lymphoproliferative diseases (PTLDs) arising in patients receiving immunosuppressive drug treatment after organ transplantation are usually positive for EBV
Summary
Epstein–Barr virus (EBV), an oncogenic γ herpes virus, is widespread in all human populations and persists in the vast majority of individuals throughout their lifetime. AIDS, Acquired immunodeficiency syndrome; BART, BamHI-A rightward reading frame transcript; BL, Burkitt lymphoma; CB, Centroblast; CTL, Cytotoxic T-lymphocyte; DLBCL, Diffuse large B-cell lymphoma; EBERs, EBV-encoded small RNAs; EBNA, EBV nuclear antigen; HL, Hodgkin’s lymphoma; IB, Immunoblast; LMP, Latent membrane protein; PCNSL, Primary central nervous system lymphoma; PEL, Primary effusion lymphoma; PTLD, Post-transplant lymphoproliferative disease. EBNA2 is expressed early after infection and has an important role in the immortalization of B cells through the induction of viral genes such as LMP1 and LMP2A.
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