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Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
Published on: September 28, 2022
Epstein-Barr virus LMP2A accelerates MYC-induced lymphomagenesis.
R Bultema1, R Longnecker, M Swanson-Mungerson
1Department of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Oncogene
|February 3, 2009
Summary
Epstein-Barr virus (EBV) protein LMP2A promotes Burkitt's lymphoma (BL) development by protecting B cells from MYC-induced apoptosis. This survival mechanism accelerates lymphoma formation in mice.
Area of Science:
- Oncology
- Virology
- Immunology
Background:
- Epstein-Barr virus (EBV) is linked to Burkitt's lymphoma (BL), but its role is unclear.
- EBV's latent membrane protein 2A (LMP2A) enhances B cell survival.
- Aberrant c-MYC expression, common in BL, induces B cell apoptosis.
Purpose of the Study:
- To investigate if EBV LMP2A protects B cells from apoptosis caused by c-MYC.
- To determine LMP2A's role in accelerating lymphoma development in a BL model.
Main Methods:
- Generated transgenic mice expressing LMP2A in B cells.
- Crossed LMP2A-transgenic mice with mice expressing a BL-associated c-MYC translocation.
- Analyzed B cell apoptosis, proliferation, lymphoma development, and Bcl-X(L) expression.
Main Results:
- LMP2A promoted B cell proliferation and protected against MYC-induced apoptosis in transgenic mice.
- LMP2A accelerated lymphoma development in LMP2A/lambda-MYC double-transgenic mice.
- LMP2A increased Bcl-X(L) expression in pre-tumor and tumor B cells.
Conclusions:
- EBV LMP2A promotes B cell survival in the presence of MYC.
- LMP2A may drive BL tumor development by preventing apoptosis of B cells with c-MYC translocations.
- LMP2A's anti-apoptotic function is a key mechanism in EBV-associated lymphomagenesis.
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