The normal cell cycle activation program is exploited during the infection of quiescent B lymphocytes by Epstein-Barr virus

B lymphocytes in the peripheral circulation are maintained in a non-proliferative state. Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus (EBV) results in continual proliferation and the outgrowth of immortal cell lines. Because it is not clear at which...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1995-11, Vol.55 (21), p.4784-4787
Main Authors: HOLLYOAKE, M, STÜHLER, A, FARRELL, P, GORDON, J, SINCLAIR, A
Format: Article
Language:English
Subjects:
Adult
B-Lymphocytes - cytology
B-Lymphocytes - physiology
B-Lymphocytes - virology
Base Sequence
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Cell Cycle - physiology
Cell Cycle Proteins
Cells, Cultured
Cyclin D2
Cyclins - genetics
DNA-Binding Proteins - genetics
Gene Expression Regulation - physiology
Genes, cdc
Genes, myc
Herpesviridae Infections - blood
Herpesvirus 4, Human
Humans
Lymphocyte Activation
Medical sciences
Molecular Sequence Data
Polymerase Chain Reaction
RNA - blood
RNA - genetics
RNA, Messenger - blood
RNA, Messenger - genetics
Trans-Activators
Transcription Factors - genetics
Tumors
Up-Regulation - physiology
Viruses
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Summary:B lymphocytes in the peripheral circulation are maintained in a non-proliferative state. Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus (EBV) results in continual proliferation and the outgrowth of immortal cell lines. Because it is not clear at which point in cell cycle the peripheral B lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells. We show that the expression of four cell genes, cdc-2, cyclin E, CD23, and cyclin D2, are up-regulated approximately 100-fold as a result of EBV-mediated immortalization. Because these genes play a positive role in cell proliferation, we suggest that this regulatory switch contributes to controlling entry into the cell cycle. Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40, anti-IgM, and IL4, or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation.
ISSN:0008-5472
1538-7445