Abstract
The Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the tumor cells. In fact, latent EBV-infected tumor cells utilize several specific mechanisms to form and shape the TME to their own benefit. These mechanisms have been studied largely in the context of EBV+ Hodgkin lymphoma, undifferentiated nasopharyngeal carcinoma, and EBV+ gastric cancer. This review describes the composition, immune escape mechanisms, and tumor cell promoting properties of the TME in these three malignancies. Mechanisms of susceptibility which regularly involve genes related to immune system function are also discussed, as only a small proportion of EBV-infected individuals develops an EBV-associated malignancy.
Highlights
Epstein–Barr virus (EBV) is a causal factor in various malignant diseases which usually originate from B cells or epithelial cells
As only a small fraction of latent EBV-infected cells develop into a malignancy in a minority of EBV-infected individuals, it is likely that characteristics of the host immune system are associated with susceptibility, i.e., the likelihood of EBV-infected cells to develop into a malignancy
There is a large overlap in tumor cell-tumor microenvironment (TME) interactions between EBV+ and EBV-negative cancers in both Hodgkin lymphoma (HL) and gastric carcinoma (GC) and it is not always possible to indicate if certain characteristics are EBV specific
Summary
Epstein–Barr virus (EBV) is a causal factor in various malignant diseases which usually originate from B cells or epithelial cells. In addition to the possession of tumor cell-transforming properties, EBV can influence the composition and the properties of the cells present in the tumor microenvironment (TME). In some EBV-associated cancers, little data on the TME is available because of low incidence of the disease (e.g., NK/T cell lymphoma), a minor TME component (e.g., Burkitt lymphoma), or a heterogeneous immune deficiency (e.g., post-transplant lymphoproliferative disorder). We will discuss the composition and the function of the TME in the three most widely studied EBV-associated cancers, i.e., classical Hodgkin lymphoma (HL), undifferentiated nasopharyngeal carcinoma (NPC), and gastric carcinoma (GC). All undifferentiated nasopharyngeal carcinoma cases are positive for EBV [2], while only approximately 10% of gastric carcinoma cases are EBV+ [3].
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