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      Mechanisms of B-Cell Oncogenesis Induced by Epstein-Barr Virus

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          Abstract

          Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus which asymptomatically infects the majority of the world population. Under immunocompromised conditions, EBV can trigger human cancers of epithelial and lymphoid origin.

          ABSTRACT

          Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus which asymptomatically infects the majority of the world population. Under immunocompromised conditions, EBV can trigger human cancers of epithelial and lymphoid origin. The oncogenic potential of EBV is demonstrated by in vitro infection and transformation of quiescent B cells into lymphoblastoid cell lines (LCLs). These cell lines, along with primary infection using genetically engineered viral particles coupled with recent technological advancements, have elucidated the underlying mechanisms of EBV-induced B-cell lymphomagenesis.

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          The NCI60 human tumour cell line anticancer drug screen.

          Robert Shoemaker (2006)
          The US National Cancer Institute (NCI) 60 human tumour cell line anticancer drug screen (NCI60) was developed in the late 1980s as an in vitro drug-discovery tool intended to supplant the use of transplantable animal tumours in anticancer drug screening. This screening model was rapidly recognized as a rich source of information about the mechanisms of growth inhibition and tumour-cell kill. Recently, its role has changed to that of a service screen supporting the cancer research community. Here I review the development, use and productivity of the screen, highlighting several outcomes that have contributed to advances in cancer chemotherapy.
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            Endogenous MHC class II processing of a viral nuclear antigen after autophagy.

            Casper Paludan, Dorothee Schmid, Markus Landthaler … (2005)
            CD4+ T cells classically recognize antigens that are endocytosed and processed in lysosomes for presentation on major histocompatibility complex (MHC) class II molecules. Here, endogenous Epstein-Barr virus nuclear antigen 1 (EBNA1) was found to gain access to this pathway by autophagy. On inhibition of lysosomal acidification, EBNA1, the dominant CD4+ T cell antigen of latent Epstein-Barr virus infection, slowly accumulated in cytosolic autophagosomes. In addition, inhibition of autophagy decreased recognition by EBNA1-specific CD4+ T cell clones. Thus, lysosomal processing after autophagy may contribute to MHC class II-restricted surveillance of long-lived endogenous antigens including nuclear proteins relevant to disease.
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              Epstein–Barr virus latent genes

              Myung-Soo Kang, Elliott Kieff (2015)
              Latent Epstein–Barr virus (EBV) infection has a substantial role in causing many human disorders. The persistence of these viral genomes in all malignant cells, yet with the expression of limited latent genes, is consistent with the notion that EBV latent genes are important for malignant cell growth. While the EBV-encoded nuclear antigen-1 (EBNA-1) and latent membrane protein-2A (LMP-2A) are critical, the EBNA-leader proteins, EBNA-2, EBNA-3A, EBNA-3C and LMP-1, are individually essential for in vitro transformation of primary B cells to lymphoblastoid cell lines. EBV-encoded RNAs and EBNA-3Bs are dispensable. In this review, the roles of EBV latent genes are summarized.
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                Author and article information

                Contributors
                Felicia Goodrum: Role: Editor
                Journal
                Journal ID (nlm-ta): J Virol
                Journal ID (iso-abbrev): J. Virol
                Journal ID (hwp): jvi
                Journal ID (pmc): jvi
                Journal ID (publisher-id): JVI
                Title: Journal of Virology
                Publisher: American Society for Microbiology (1752 N St., N.W., Washington, DC )
                ISSN (Print): 0022-538X
                ISSN (Electronic): 1098-5514
                Publication date (Electronic preprint): 10 April 2019
                Publication date (Electronic): 14 June 2019
                Publication date Collection: 1 July 2019
                Publication date PMC-release: 14 June 2019
                Volume: 93
                Issue: 13
                Electronic Location Identifier: e00238-19
                Affiliations
                [a ]Department of Life Sciences, Presidency University, Kolkata, West Bengal, India
                [b ]Department of Otorhinolaryngology-Head and Neck Surgery, and the Tumor Virology Program, Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
                University of Arizona
                Author notes
                Address correspondence to Abhik Saha, abhik.dbs@ 123456presiuniv.ac.in , or Erle S. Robertson, erle@ 123456upenn.edu .

                Citation Saha A, Robertson ES. 2019. Mechanisms of B-cell oncogenesis induced by Epstein-Barr virus. J Virol 93:e00238-19. https://doi.org/10.1128/JVI.00238-19.

                Article
                Publisher ID: 00238-19
                DOI: 10.1128/JVI.00238-19
                PMC ID: 6580952
                PubMed ID: 30971472
                SO-VID: a6e50a35-b4ec-41f8-b2e5-3c1fb3b2148c
                Copyright © Copyright © 2019 Saha and Robertson.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

                History
                Date received : 11 February 2019
                Date accepted : 8 April 2019
                Page count
                Figures: 2, Tables: 2, Equations: 0, References: 113, Pages: 13, Words: 8992
                Funding
                Funded by: Wellcome Trust/DBT India Alliance;
                Award ID: IA/I/14/2/501537
                Award Recipient :
                Funded by: HHS | National Institutes of Health (NIH), https://doi.org/10.13039/100000002;
                Award ID: P01CA174439
                Award ID: R01177423
                Award ID: R01171979
                Award ID: P30DK050306
                Award ID: P30CA016520
                Award ID: U54CA190158
                Award Recipient :
                Categories
                Subject: Gem
                Custom metadata
                cover-date July 2019

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: b-cell lymphomas,epstein-barr virus,lymphoblastoid cell lines,tumor virology
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: b-cell lymphomas, epstein-barr virus, lymphoblastoid cell lines, tumor virology

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