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

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          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

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          Most cited references 232

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          Maintenance of serological memory by polyclonal activation of human memory B cells.

          Production of antibodies can last for a lifetime, through mechanisms that remain poorly understood. Here, we show that human memory B lymphocytes proliferate and differentiate into plasma cells in response to polyclonal stimuli, such as bystander T cell help and CpG DNA. Furthermore, plasma cells secreting antibodies to recall antigens are produced in vivo at levels proportional to the frequency of specific memory B cells, even several years after antigenic stimulation. Although antigen boosting leads to a transient increase in specific antibody levels, ongoing polyclonal activation of memory B cells offers a means to maintain serological memory for a human lifetime.
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            Epstein-Barr virus: exploiting the immune system.

            In vitro, Epstein-Barr virus (EBV) will infect any resting B cell, driving it out of the resting state to become an activated proliferating lymphoblast. Paradoxically, EBV persists in vivo in a quiescent state in resting memory B cells that circulate in the peripheral blood. How does the virus get there, and with such specificity for the memory compartment? An explanation comes from the idea that two genes encoded by the virus--LMP1 and LMP2A--allow EBV to exploit the normal pathways of B-cell differentiation so that the EBV-infected B blast can become a resting memory cell.
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              Epidemiology of nasopharyngeal carcinoma.

              Nasopharyngeal carcinoma (NPC) is a rare malignancy in most parts of the world, with an incidence well under 1 per 100,000 person-years. Exceptions are the Chinese, especially the Cantonese living in the central region of Guangdong Province in Southern China. Other populations with elevated rates include the natives of Southeast Asia, the natives of the Artic region, and the Arabs of North Africa and parts of the Middle East. Intake of preserved foods at an early age has been linked to NPC risk in all population groups with increased NPC rates. Other recognized risk factors for NPC are cigarette smoking, and occupational exposure to formaldehyde and wood dust. Copyright 2002 Elsevier Science Ltd.
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                Author and article information

                Journal
                Open Virol J
                Open Virol J
                TOVJ
                The Open Virology Journal
                Bentham Open
                1874-3579
                3 November 2015
                2015
                : 9
                : 7-28
                Affiliations
                [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
                Author notes
                [* ]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@ 123456gmail.com
                Article
                TOVJ-9-7
                10.2174/1874357901509010007
                4740969
                26862355
                © Ali et al. ; Licensee Bentham Open.

                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.

                Categories
                Article

                Microbiology & Virology

                ebv, epithelial tumors, latency, lymphoid tumors, oncogenes, oncogenesis

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