EBV and Cell Interactions in the Tumor Microenvironment

Dear Colleagues,

Epstein–Barr virus (EBV), a member of γ-herpesviridae, is one of the most popular infectious agents in the world, with over 90% of adults having been infected. EBV has been known to be associated with lymphatic and epithelial cell origins of human diseases. For lymphatic original diseases, EBV is reported to be involved in Hodgkin’s lymphoma, Burkitt’s lymphoma, and NK/T lymphoma. For epithelium original diseases, EBV is also associated with several human malignancies, including nasopharyngeal carcinoma (NPC) and gastric carcinoma (GC).

Through years of studies on EBV carcinogenesis, EBV infection contributes to the tumorigenic process through various pathways, including induction of oncogenic signaling, promotion of cell proliferation and invasion, and interference of genomic stability. In recent years, the study of the tumor microenvironment (TME) has made great progress. The TME consists of various non-transformed cells, including immune and stroma cells, and bioactive factors, including cytokines and chemokines, to help against the tumorigenesis of cancer cells. Through interaction with various factors in TME, EBV escapes from immune surveillance and establishes lifelong infection in the hosts and/or helps pre-malignant cells to develop cancers coincidentally. Understanding the role of the interaction between EBV and human cells in the tumor microenvironment is incredibly helpful in terms of developing therapeutic applications.

In this Special Issue, we focus on advances concerning the role of EBV–host interaction in oncogenesis, tumor invasion, epigenetic disorder, and genomic instability. Moreover, novel findings concerning the impact, mechanism, or application of interplay between EBV and components of the tumor microenvironment are also of interest. This Special Issue will collect all types of manuscripts (e.g., research articles, methodology development, perspectives, or reviews) to obtain novel knowledge on EBV oncology.

Dr. Chung-Chun Wu
Guest Editor

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