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Epstein-Barr virus (EBV) and lymphomagenesis.
1Department of Pathology, Weill Medical College of Cornell University, New York, NY 10021, USA. ecesarm@med.cornell.edu
Frontiers in Bioscience : a Journal and Virtual Library
|January 30, 2002
Summary
Epstein Barr virus (EBV) causes B-cell immortalization, contributing to lymphoid cancers. However, EBV infection alone is insufficient for lymphoma development, requiring co-factors like immune suppression.
Area of Science:
- Virology
- Oncology
- Immunology
Background:
- Epstein Barr virus (EBV), a gamma herpesvirus, is linked to lymphoid malignancies, particularly in immunocompromised individuals.
- EBV infection is widespread, complicating the establishment of its direct causal role in lymphomagenesis.
- EBV's oncogenic potential is supported by its ability to transform human B-cells in vitro into immortalized lymphoblastoid cell lines (LCLs).
Purpose of the Study:
- To explore the role of Epstein Barr virus (EBV) in lymphomagenesis.
- To identify viral proteins involved in EBV-mediated B-cell transformation.
- To understand the co-factors contributing to EBV-associated lymphomas.
Main Methods:
- In vitro transformation assays of human B-cells with EBV.
- Identification of viral proteins essential for B-cell immortalization.
- Analysis of EBV presence in neoplastic lymphoid cells.
Main Results:
- EBV successfully infects and transforms normal human B-cells into continuously growing LCLs.
- Specific viral proteins crucial for EBV-induced B-cell transformation have been identified.
- Consistent presence of EBV in neoplastic cells of certain lymphoid malignancies indicates its etiopathogenic role.
Conclusions:
- EBV plays a significant role in lymphomagenesis through B-cell immortalization.
- EBV infection is necessary but not sufficient for the development of EBV-associated lymphomas.
- Impaired immune surveillance is a critical co-factor in the pathogenesis of EBV-associated lymphomas.