Control of cell cycle entry and apoptosis in B lymphocytes infected by Epstein-Barr virus

L C Spender, E J Cannell, M Hollyoake, B Wensing, J M Gawn, M Brimmell, G Packham, P J Farrell (Lead / Corresponding author)

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    59 Citations (Scopus)

    Abstract

    Infection of human B cells with Epstein-Barr virus (EBV) results in activation of the cell cycle and cell growth. To interpret the mechanisms by which EBV activates the cell, we have assayed many proteins involved in control of the G0 and G1 phases of the cell cycle and regulation of apoptosis. In EBV infection most of the changes, including the early induction of cyclin D2, are dependent on expression of EBV genes, but an alteration in the E2F-4 profile was partly independent of viral gene expression, presumably occurring in response to signal transduction activated when the virus binds to its receptor, CD21. By comparing the expression of genes controlling apoptosis, including those encoding several members of the BCL-2 family of proteins, the known relative resistance of EBV-immortalized B-cell lines to apoptosis induced by low serum was found to correlate with expression of both BCL-2 and A20. A20 can be regulated by the NF-kappaB transcription factor, which is known to be activated by the EBV LMP-1 protein. Quantitative assays demonstrated a direct temporal relationship between LMP-1 protein levels and active NF-kappaB during the time course of infection.

    Original languageEnglish
    Pages (from-to)4678-4688
    Number of pages11
    JournalJournal of Virology
    Volume73
    Issue number6
    Publication statusPublished - Jun 1999

    Keywords

    • Apoptosis
    • B-Lymphocytes
    • Cell Cycle
    • Cell Line
    • Cyclin D2
    • Cyclins
    • DNA-Binding Proteins
    • E2F4 Transcription Factor
    • Epstein-Barr Virus Nuclear Antigens
    • Herpesvirus 4, Human
    • Humans
    • NF-kappa B
    • Proto-Oncogene Proteins
    • Proto-Oncogene Proteins c-bcl-2
    • Transcription Factors
    • Viral Matrix Proteins
    • bcl-2-Associated X Protein
    • Journal Article

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