EBV and Cell Interactions in the Tumor Microenvironment

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 6339

Special Issue Editors


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Guest Editor
Translational Cell Therapy Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan
Interests: cancer biology; cancer therapy, virology; antiviral therapy; phytochemicals; genomic instability; DNA repair; immunotherapy

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Guest Editor
National Institute of Cancer Research, National Health Research Institutes, Miaoli County, Taiwan
Interests: virology; cancer biology; epigenetics; molecular biology; cancer immunotherapy

Special Issue Information

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

Manuscript Submission Information

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Keywords

  • Epstein–Barr virus
  • tumorigenesis
  • tumor metastasis
  • virus–host interaction
  • EBV-associated malignancies
  • tumor microenvironment
  • immune response
  • immune evasion

Published Papers (1 paper)

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Review

25 pages, 1196 KiB  
Review
Immunosuppressive Tumor Microenvironment and Immunotherapy of Epstein–Barr Virus-Associated Malignancies
by Xueyi Zheng, Yuhua Huang, Kai Li, Rongzhen Luo, Muyan Cai and Jingping Yun
Viruses 2022, 14(5), 1017; https://0-doi-org.brum.beds.ac.uk/10.3390/v14051017 - 10 May 2022
Cited by 13 | Viewed by 5915
Abstract
The Epstein–Barr virus (EBV) can cause different types of cancer in human beings when the virus infects different cell types with various latent patterns. EBV shapes a distinct and immunosuppressive tumor microenvironment (TME) to its benefit by influencing and interacting with different components [...] Read more.
The Epstein–Barr virus (EBV) can cause different types of cancer in human beings when the virus infects different cell types with various latent patterns. EBV shapes a distinct and immunosuppressive tumor microenvironment (TME) to its benefit by influencing and interacting with different components in the TME. Different EBV-associated malignancies adopt similar but slightly specific immunosuppressive mechanisms by encoding different EBV products to escape both innate and adaptive immune responses. Strategies reversing the immunosuppressive TME of EBV-associated malignancies have been under evaluation in clinical practice. As the interactions among EBV, tumor cells, and TME are intricate, in this review, we mainly discuss the epidemiology of EBV, the life cycle of EBV, the cellular and molecular composition of TME, and a landscape of different EBV-associated malignancies and immunotherapy by targeting the TME. Full article
(This article belongs to the Special Issue EBV and Cell Interactions in the Tumor Microenvironment)
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