Epstein- Barr Virus: Clinical and Epidemiological Revisits and Genetic Basis of Oncogenesis



Abdelwahid Saeed Ali1, *, Mubarak Al-Shraim2, Ahmed Musa Al-Hakami1, Ian M Jones3
1 Department of Microbiology and Clinical Parasitology, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia
2 Department of Pathology, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia
3 Department of Biomedical Sciences, School of Biological Sciences, Faculty of Life Sciences, University of Reading, G37 AMS Wing, UK


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© Ali et al. ; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the (https://creativecommons.org/licenses/by/4.0/legalcode), which permits unrestricted, noncommercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to Professor Dr. Abdelwahid Saeed: Department of Microbiology and Clinical Parasitology, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia; Tel: +966-17241-8589(office); +966-561469977 (Cell phone) Fax: +966-72718194; E-mail: abumalaz2002@gmail.com


Abstract

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancies

Keywords: EBV, Epithelial tumors, Latency, Lymphoid tumors, Oncogenes, Oncogenesis.