Autoradiographic Detection of the Epstein-Barr Virus (EBV)-Associated Early Antigen (EA) in Lymphoblastoid Cell Lines

  • M. H. Moar
  • W. Siegert
  • G. Klein
Conference paper
Part of the Haematology and Blood Transfusion / Hämatologie und Bluttransfusion book series (HAEMATOLOGY, volume 20)

Abstract

Epstein-Barr Virus (EBV) is considered to be a strong candidate as the causative agent in certain human malignancies, particularly African Burkitt’s Lymphoma and Nasopharyngeal Carcinoma (5). Good circumstantial evidence supports this view: in patients suffering from these diseases there are anti-viral antibody titers which are much higher than those found in normal individuals (e.g. 3), and although the virus has never been detected in tumor biopsies directly the tumor cells consistently possess EBV-DNA and express a virus-determined nuclear antigen, EBNA, and in some cases, an EBV-associated membrane antigen as well (5). Moreover, the EBV-DNA in these tumor cells must posses a large coding potential since the synthesis of other EBV antigens can be induced in the cells by 1) explantation of biopsy material in culture, 2) by treatment of in vitro-established tumor cell lines under a variety of physiological conditions, 3) by somatic cell fusion and 4) by the use of DNA synthesis inhibitors (1, 5, 9). Further, in some such induction experiments frequently virus DNA synthesis and virus particles can be demonstrated indicating that the virus DNA coding potential in the original tumor cell is complete. More direct evidence for an oncogenic potential for the virus comes from observations such as the virus’s ability to cause tumors in heterologous hosts (as do some in vitro-established EBV-DNA containing cell lines) (7), and the ability of the virus to “immortalize” blood lymphocytes which have an otherwise limited lifespan in culture (6) and which, after EBV infection, express a variety of transformation characteristics in addition to “immortalization”.

Keywords

Acetone Lymphoma Leukemia Fluorescein FITC 

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References

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Copyright information

© Springer-Verlag Berlin Heidelberg 1977

Authors and Affiliations

  • M. H. Moar
    • 1
  • W. Siegert
    • 1
  • G. Klein
    • 1
  1. 1.Department of Tumor BiologyKarolinska InstituteStockholmSweden

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