Epstein‐Barr virus receptors but not viral DMA are present in normal and malignant oral epithelium

Talacko, Anna; Teo, CG; Griffin, B. E.; Johnson, Newell W.

doi:10.1111/j.1600-0714.1991.tb00882.x

Cited by 41 publications

(32 citation statements)

References 28 publications

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“…Recently, the demonstration of the EBV/C3d receptor on cells from the stratified squamous epithelium of the oropharynx (Young et al, 1986;Talacko et al, 1991), which also covers the tonsils, has lead to the current hypothesis that this epithelium plays an important role in EBV persistence and the pathogenesis of B cell tumours (Allday & Crawford, 1988). In view of these findings, the observation of human palatine tonsils as a potential source of the EBVassociated lymphomas reported here is of particular importance.…”

Section: Discussionmentioning

confidence: 72%

Role of Epstein-Barr virus and interleukin 6 in the development of lymphomas of human origin in SCID mice engrafted with human tonsillar mononuclear cells

Nadal¹,

Albini²,

Schläpfer³

et al. 1992

Journal of General Virology

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Mice with severe combined immunodeficiency were inoculated intraperitoneally with 50x 106 human tonsillar mononuclear cells (hu-TMCs) from EpsteinBarr virus (EBV) antibody seropositive or seronegative human subjects. Between 5 and 11 weeks later, 29.4% (10/34) of mice injected with hu-TMCs from EBV seropositive donors, but none of 34 animals receiving hu-TMCs from EBV seronegative donors, developed intraabdominal and/or intrathoracic tumours (P, 0.002). By means of in situ hybridization using alpha satellite DNA from human chromosome 17, all tumours produced after cell transfer from EBV seropositive donors were identified to be of human origin. Histologically the tumours resembled large cell lymphomas; the EBV genome was detected by in situ hybridization and EBV nuclear antigen by immunofluorescence in these tumours. The tumours were polyor oligoclonal, and stained for human IgG and IgM, and less frequently IgA and IgD. Serum levels of human immunoglobulin in animals developing human tumours were significantly higher than in reconstituted mice without tumours and the sera exhibited polyoligo-or monoclonality in immunoelectrophoresis. Human interleukin 6 was detected in the serum of six of 10 animals with human lymphomas, but not in any animals without human lymphoma.

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Section: Discussionmentioning

confidence: 72%

Role of Epstein-Barr virus and interleukin 6 in the development of lymphomas of human origin in SCID mice engrafted with human tonsillar mononuclear cells

Nadal¹,

Albini²,

Schläpfer³

et al. 1992

Journal of General Virology

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“…Confirmation of simultaneous expression of protein was not possible since at least one monoclonal antibody to CD21 cross-reacts with an unrelated epithelial cell protein, 23 only a subset of antibodies that recognize CD21 on B cells is reactive with all epithelial cells and reports from different groups using the antibodies are not consistent. 24, 25, 26, 27 Even subclones of a single epithelial cell line were found to be recognized differently. 16 However, the good correlation between the expression of CD21 mRNA and infection with EBV suggests that CD21 protein itself is expressed.…”

Section: Discussionmentioning

confidence: 98%

Oral dysplasia and squamous cell carcinoma: Correlation between increased expression of CD21, Epstein-Barr virus and CK19

Jiang¹,

Gu²,

Moore-Medlin³

et al. 2012

Oral Oncology

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OBJECTIVES Epstein-Barr virus is an orally transmitted human gammaherpesvirus that infects B lymphocytes and epithelial cells. Although most primary infections are asymptomatic, long term carriage of the virus can be associated with either lymphoid or epithelial malignancies. The association of EBV with oral squamous cell carcinomas is sporadic and it is uncertain if the virus is involved in initiation of the tumor or, possibly, in its progression. Complement receptor type 2, CR2 or CD21, is a receptor for the major attachment protein of EBV, which significantly enhances epithelial cell infection, but its expression on normal tissues is restricted to tonsil and adenoid epithelium. As cells become dysplastic they are reported to express higher levels of CK19. We sought to evaluate whether CD21 and CK19 expression change as oral epithelial cells outside Waldeyer’s ring become dysplastic. MATERIALS AND METHODS Epithelial cells were isolated by laser capture microdissection and levels of CD21, CK19 and EBV RNA were measured by quantitative reverse transcriptase PCR. RESULTS We report that expression of CD21 increases in frequency and intensity as oral epithelial cells become more dysplastic and that expression correlates with an increase in infection by EBV. Tumors or dysplastic lesions that carry EBV also generally express higher levels of CK19 than those that do not. CONCLUSION The findings suggest that dysplasia may make cells more susceptible to infection by EBV and that infection by the virus may alter the phenotype of the infected cell in a manner which could affect prognosis.

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“…In this study, transcription of EBV latent genes was clearly detected. Other reports have been unable to establish the presence of EBER (38) or any of the EBV gene expression (15). The EBV infected OSCC cell clones expressed EBER-1, BARF0, EBNA-1, EBNA-2, and LMP-1.…”

Section: Discussionmentioning

confidence: 82%

Expression Pattern of Epstein-Barr Virus Latent Genes in Cell Lines Derived from Oral Squamous Cell Carcinoma

et al. 2004

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IntroductionEBV is a ubiquitous human herpes virus which establishes life-long persistent infection of B-cells in over 90% of the adult population of the world (1). Upon primary infection, EBV occasionally causes infectious mononucleosis. After primary infection, irrespective of whether it is clinically overt or silent, EBV establishes a life-long carrier state. EBV is associated with Burkitt's lymphoma (BL), undifferentiated nasopharyngeal carcinoma (NPC) and opportunistic lymphomas in immunocompromised hosts. EBV is also implicated in Hodgkin's disease (HD), certain T-cell lymphomas and gastric carcinoma (2, 3).Several EBV genes are potentially expressed in latently infected cells: EBNA-1, -2, -3A, -3B, -3C and leader protein (LP); LMP-1, -2A, -2B; untranslated EBER 1 and 2; and a transcript containing the BARF0 (2). Depending on the latent gene expression pattern, three main types of EBV latency have been described so far. In type I latency, EBNA-1, EBER 1, 2 and BARF0 transcripts are expressed (e.g., in vivo BL cells and several BL cell lines like Akata cell line) (4, 5). In type II latency, in addition to the genes expressed in type I, LMP genes are expressed (e.g., NPC and HD) (6). All of the latent genes are expressed in type III latency (e.g., in vitro EBV-immortalized B lymphoblastoid cell lines (LCL) and some B lymphoproliferative disorders of immunosuppressed patients) (7,8). Activity of the BamHI-C, -W or Q promoter (Cp, Wp or Qp accordingly) determines which of the EBNA transcripts will be expressed. In type I and II latency, Qp mediates selective expression of EBNA-1 transcript. However in type III latency, active Cp or Wp results in expression of all of the six EBNA mRNAs (2).EBV replication was detected within the epithelial cells of AIDS-associated oral hairy leukoplakia (10). Sev- LMP-1 is an integral membrane protein and it aggregates in patches on the plasma membrane (16). LMP-1 is suggested to be essential for B-lymphocyte growth transformation (17) and transforms rodent fibroblast cell line, Rat-1 (18). The Rat-1 cells expressing LMP-1 are tumorigenic in nude mice. In B-lymphocytes, LMP-1 is able to upregulate a number of cellular genes, including the apoptosis inhibiting bcl-2 gene (19). LMP-1 is frequently expressed in NPC biopsies (20,21). Expression of LMP-1 was detected in 20% cases of oral leukoplakia (22). In our previous report, 6 of 7 (85.7%) cases of OSCC were LMP1 positive (14). Therefore, LMP-1 might be an important component of transformation in epithelial tumors.Although there are some reports concerning association of EBV with OSCC in vivo, there is contradiction among the researchers about transcription of EBV genes in oral epithelium, specially the latent genes. So far, there have been no reports about in vitro expression pattern of EBV in OSCC cell lines. We, therefore, introduced EBV into the OSCC cell lines and successfully isolated EBVpositive OSCC cell lines. We investigated the expression pattern of EBV latent genes in isolated OSCC cells. Materials and Methods Cell l...

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Epstein‐Barr virus receptors but not viral DMA are present in normal and malignant oral epithelium

Cited by 41 publications

References 28 publications

Role of Epstein-Barr virus and interleukin 6 in the development of lymphomas of human origin in SCID mice engrafted with human tonsillar mononuclear cells

Role of Epstein-Barr virus and interleukin 6 in the development of lymphomas of human origin in SCID mice engrafted with human tonsillar mononuclear cells

Oral dysplasia and squamous cell carcinoma: Correlation between increased expression of CD21, Epstein-Barr virus and CK19

Expression Pattern of Epstein-Barr Virus Latent Genes in Cell Lines Derived from Oral Squamous Cell Carcinoma

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