Abstract
Infection of human B cells with Epstein-Barr virus (EBV) was seen to result in activation-induced cytidine deaminase (AID) and polymerase-η (pol-η) gene expression. AID and pol-η are cellular gene products that play central roles in the DNA-modifying processes involved in immunoglobulin gene class switch recombination and somatic hypermutation. Errors in these processes can result in oncogene mutation/translocation, thereby contributing to lymphomagenesis. It was seen that EBV infected, AID, and pol-η expressing B cells accumulated mutations in cellular proto-oncogenes (BCL-6 and p53) that are known to be involved in the genesis of B cell lymphoma. The nature of the mutations seen in these oncogenes was consistent with the known activity of AID and pol-η. These findings indicate that EBV induced AID and pol-η expression, and that this was associated with oncogene mutation, providing a novel means by which EBV infection of B cells may contribute to lymphomagenesis.
Original language | English (US) |
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Pages (from-to) | 934-942 |
Number of pages | 9 |
Journal | Molecular Immunology |
Volume | 44 |
Issue number | 5 |
DOIs | |
State | Published - Feb 2007 |
Keywords
- AID
- B lymphocyte
- BCL-6
- EBV
- Error-prone DNA polymerases
- Lymphoma
- Oncogene
- Somatic hypermutation
- p53
ASJC Scopus subject areas
- Immunology
- Molecular Biology