The role of Epstein–Barr virus in cancer

Abstract

Epstein-Barr virus (EBV), discovered > 40 years ago from a Burkitt's lymphoma biopsy, was the first virus to be directly associated with human cancer. EBV has two distinct life cycles in the human host; a lytic form of infection that produces new infectious virions, and a latent form of infection that allows the virus to persist in a dormant state for the lifetime of the host. EBV has evolved a life cycle that mimics the natural differentiation pathway of antigen-activated B cells, giving the virus access to its site of latent infection, the resting memory B cell. By steering infected cells through the various stages of lymphocyte differentiation, EBV is able to enter a cell type suitable for long-term latent persistence and periodic reactivation. However, its presence in various stages of B-cell development, and its ability to infect certain epithelial cells, can have pathogenic consequences, and can contribute to the development of a diverse group of lymphomas and carcinomas. The presence of EBV in the tumour cells of EBV-associated cancers might provide a basis for specific therapy. This article focuses on the contributions that the virus may play in different types of human cancer, particularly Burkitt's lymphoma, Hodgkin's lymphoma, lymphomas and lymphoproliferative diseases in the immunocompromised, and nasopharyngeal and gastric carcinoma.

Expansion of Effector Memory TCR Vβ4+CD8+ T Cells Is Associated with Latent Infection-Mediated Resistance to Transplantation Tolerance

“…Furthermore, both ␥HV68 and EBV elicit a large T cell response resulting in an expanded T EM pool (50,67). Although EBV does not have a ␥HV68-M1 homolog, the fact that 1) the two ␥-herpesviruses have a large complex homologous genome that encodes a number of proteins in latently infected B cells (20,23,68), 2) both elicit a large T cell response that results in an effector memory pool (50,67), 3) the CD8 ϩ T cell response appears to be preferentially focused on only a few epitopes (46, 47, 49, 69 -71), 4) both are associated with tumor development (72)(73)(74), and that 5) EBV does not infect inbred strains of mice strongly suggest the utility of ␥HV68 infection of mice as a model to study the effects of latent infection on transplantation tolerance.…”

Trends in all-cause five-year mortality after head and neck cancers diagnosed over a period of 33 years. Focus on estimated degree of association with human papillomavirus

“…The most common histologic type is squamous cell carcinoma (HNSCC) in the oral and nasal cavity, pharynx (naso-, oro-, and hypopharynx), and larynx. The known risk factors for HNC include tobacco smoking, alcohol drinking, and certain viruses, such as the Epstein-Barr virus and human papillomavirus (HPV) [1,2]. Increase in exposure to HPV over the past few decades have been shown to influence the incidence of certain HNSCCs with significant increases of some HNSCCs, such as those of the oropharynx, especially the tonsil and base of the tongue [3][4][5].…”

Epigenetics of Nasopharyngeal Carcinoma

“…EBV was implicated in a variety of human malignancies, such as post-transplant lymphoma, AIDS-associated lymphomas, Burkitt lymohoma, Hodgkin's disease, T-cell lymphoma, NPC, parotid gland carcinoma and gastric carcinoma (Young and Rickinson 2004;Pattle and Farrell 2006). The association between EBV infection and NPC was well documented by the fact that EBV genome presents in virtually all the NPC cells Lo, To, and Huang 2004).…”