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      • Record: found
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      Epstein–Barr virus (EBV)-associated epithelial and non-epithelial lesions of the oral cavity

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          Summary

          Epstein–Barr virus (EBV) is known to be associated with the development of malignant lymphoma and lymphoproliferative disorders (LPDs) in immunocompromised patients. EBV, a B-lymphotropic gamma-herpesvirus, causes infectious mononucleosis and oral hairy leukoplakia, as well as various pathological types of lymphoid malignancy. Furthermore, EBV is associated with epithelial malignancies such as nasopharyngeal carcinoma (NPC), salivary gland tumor, gastric carcinoma and breast carcinoma. In terms of oral disease, there have been several reports of EBV-related oral squamous cell carcinoma (OSCC) worldwide. However, the role of EBV in tumorigenesis of human oral epithelial or lymphoid tissue is unclear. This review summarizes EBV-related epithelial and non-epithelial tumors or tumor-like lesions of the oral cavity. In addition, we describe EBV latent genes and their expression in normal epithelium, inflamed gingiva, epithelial dysplasia and SCC, as well as considering LPDs (MTX- and age-related) and DLBCLs of the oral cavity.

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          Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.

          M Muramatsu, K Kinoshita, S Fagarasan … (2000)
          Induced overexpression of AID in CH12F3-2 B lymphoma cells augmented class switching from IgM to IgA without cytokine stimulation. AID deficiency caused a complete defect in class switching and showed a hyper-IgM phenotype with enlarged germinal centers containing strongly activated B cells before or after immunization. AID-/- spleen cells stimulated in vitro with LPS and cytokines failed to undergo class switch recombination although they expressed germline transcripts. Immunization of AID-/- chimera with 4-hydroxy-3-nitrophenylacetyl (NP) chicken gamma-globulin induced neither accumulation of mutations in the NP-specific variable region gene nor class switching. These results suggest that AID may be involved in regulation or catalysis of the DNA modification step of both class switching and somatic hypermutation.
          Article 0 comments Cited 474 times – based on 0 reviews     Review now
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            Virus Entry: Open Sesame

            Mark Marsh, Ari Helenius (2006)
            Detailed information about the replication cycle of viruses and their interactions with host organisms is required to develop strategies to stop them. Cell biology studies, live-cell imaging, and systems biology have started to illuminate the multiple and subtly different pathways that animal viruses use to enter host cells. These insights are revolutionizing our understanding of endocytosis and the movement of vesicles within cells. In addition, such insights reveal new targets for attacking viruses before they can usurp the host-cell machinery for replication.
            Article 0 comments Cited 355 times – based on 0 reviews     Review now
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              EBV-driven LMP1 and IFN-γ up-regulate PD-L1 in nasopharyngeal carcinoma: Implications for oncotargeted therapy

              Wenfeng Fang, Jianwei Zhang, Shaodong Hong … (2014)
              PD-L1 expression is a feature of Epstein-Barr virus (EBV) associated malignancies such as nasopharyngeal carcinoma (NPC). Here, we found that EBV-induced latent membrane protein 1 (LMP1) and IFN-γ pathways cooperate to regulate programmed cell death protein 1 ligand (PD-L1). Expression of PD-L1 was higher in EBV positive NPC cell lines compared with EBV negative cell lines. PD-L1 expression could be increased by exogenous and endogenous induction of LMP1 induced PD-L1. In agreement, expression of PD-L1 was suppressed by knocking down LMP1 in EBV positive cell lines. We further demonstrated that LMP1 up-regulated PD-L1 through STAT3, AP-1, and NF-κB pathways. Besides, IFN-γ was independent of but synergetic with LMP1 in up-regulating PD-L1 in NPC. Furthermore, we showed that PD-L1 was associated with worse disease-free survival in NPC patients. These results imply that blocking both the LMP1 oncogenic pathway and PD-1/PD-L1 checkpoints may be a promising therapeutic approach for EBV positive NPC patients.
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                Author and article information

                Contributors
                Kentaro Kikuchi
                Journal
                Journal ID (nlm-ta): Jpn Dent Sci Rev
                Journal ID (iso-abbrev): Jpn Dent Sci Rev
                Title: The Japanese Dental Science Review
                Publisher: Elsevier
                ISSN (Print): 1882-7616
                ISSN (Electronic): 2213-6851
                Publication date PMC-release: 15 March 2017
                Publication date (Print): August 2017
                Publication date (Electronic): 15 March 2017
                Volume: 53
                Issue: 3
                Pages: 95-109
                Affiliations
                [a ]Division of Pathology, Department of Diagnostic and Therapeutic Sciences, Meikai University School of Dentistry, 1-1 Keyakidai, Sakado, Saitama 350-0283, Japan
                [b ]Department of Anatomic and Diagnostic Pathology, Dokkyo Medical University School of Medicine, 880 Oaza-kitakobayashi, Mibu-machi, Shimotsuga-gun, Tochigi 321-0293, Japan
                Author notes
                [* ]Corresponding author. Fax: +81 49 286 6101. k-kikuchi@ 123456dent.meikai.ac.jp
                Article
                Publisher ID: S1882-7616(17)30008-X
                DOI: 10.1016/j.jdsr.2017.01.002
                PMC ID: 5501733
                SO-VID: 8578e715-a22b-4df8-a4c0-11871d14a1c3
                Copyright © © 2017 The Author(s)
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 11 April 2016
                Date revision received : 28 December 2016
                Date accepted : 31 January 2017
                Categories
                Subject: Review Article

                Keywords: epstein–barr virus (ebv),oral squamous cell carcinoma (oscc),mtx- and age-related ebv + b-cell lpd,activation-induced cytidine deaminase (aid),early growth transcription response-1 (egr-1)
                Data availability:
                Keywords: epstein–barr virus (ebv), oral squamous cell carcinoma (oscc), mtx- and age-related ebv + b-cell lpd, activation-induced cytidine deaminase (aid), early growth transcription response-1 (egr-1)

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