scholarly journals Epstein-Barr Virus Latent Infection and BAFF Expression in B Cells in the Multiple Sclerosis Brain: Implications for Viral Persistence and Intrathecal B-Cell Activation

2010 ◽  
Vol 69 (7) ◽  
pp. 677-693 ◽  
Author(s):  
Barbara Serafini ◽  
Martina Severa ◽  
Sandra Columba-Cabezas ◽  
Barbara Rosicarelli ◽  
Caterina Veroni ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
B Cells ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Activation ◽  
Latent Infection ◽  
Viral Persistence ◽  
B Cell Activation ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Early events in Epstein-Barr virus infection provide a model for B cell activation.

1985 ◽  
Vol 162 (1) ◽  
pp. 45-59 ◽  
Author(s):  
D A Thorley-Lawson ◽  
K P Mann
Keyword(s):  
B Cells ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Rna Synthesis ◽  
Cell Activation ◽  
Nuclear Antigen ◽  
Epstein Barr Virus Infection ◽  
B Cell Activation ◽  
Barr Virus ◽  
Epstein Barr

We have used Epstein-Barr virus (EBV) infection in vitro to delineate two distinct stages in B cell activation. Previous studies have shown that the BLAST-2 (EBVCS) (EBV cell surface) activation antigen is expressed on a small fraction of B cells within 24 h of stimulation with a variety of agents, including mitogens and EBV. In this study, we have been able to isolate the BLAST-2 (EBVCS)+ cells early after activation/infection with EBV. These cells are small B cells that are actively synthesizing RNA but not DNA, and are, therefore, clearly distinct from large proliferating lymphoblasts. In addition, they contain multiple copies of the EBV genome, express the viral nuclear antigen (EBNA) and, most importantly, proceed to undergo transformation when placed back in culture. By comparison, the BLAST-2 (EBVCS)- population does not undergo transformation, even though a fraction of these cells are activated for RNA synthesis and express EBNA. Thus, using the EBV system, we have been able to show directly that an activated B cell first expresses the BLAST-2 (EBVCS) antigen concomitant with an increase in RNA synthesis, and then subsequently proceeds to differentiate into a proliferating lymphoblast.

scholarly journals Manipulation of the Toll-Like Receptor 7 Signaling Pathway by Epstein-Barr Virus

2007 ◽  
Vol 81 (18) ◽  
pp. 9748-9758 ◽  
Author(s):  
Heather J. Martin ◽  
Jae Myun Lee ◽  
Dermot Walls ◽  
S. Diane Hayward
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Activation ◽  
B Cell Activation ◽  
Toll Like Receptor ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

ABSTRACT Epstein-Barr virus (EBV) infection of primary B cells causes B-cell activation and proliferation. Activation of B cells requires binding of antigen to the B-cell receptor and a survival signal from ligand-bound CD40, signals that are provided by the EBV LMP1 and LMP2A latency proteins. Recently, Toll-like receptor (TLR) signaling has been reported to provide a third B-cell activation stimulus. The interaction between the EBV and TLR pathways was therefore investigated. Both UV-inactivated and untreated EBV upregulated the expression of TLR7 and downregulated the expression of TLR9 in naive B cells. UV-inactivated virus transiently stimulated naive B-cell proliferation in the presence of the TLR7 ligand R837, while addition of the TLR7 antagonist IRS 661 impaired cell growth induced by untreated EBV. Interferon regulatory factor 5 (IRF-5) is a downstream mediator of TLR7 signaling. IRF-5 was induced following EBV infection, and IRF-5 was expressed in B-cell lines with type III latency. Expression of IRF-5 in this setting is surprising since IRF-5 has tumor suppressor and antiviral properties. B-cell proliferation assays provided evidence that EBV modulates TLR7 signaling responses. Examination of IRF-5 transcripts identified a novel splice variant, V12, that was induced by EBV infection, was constitutively nuclear, and acted as a dominant negative form in IRF-5 reporter assays. IRF-4 negatively regulates IRF-5 activation, and IRF-4 was also present in type III latently infected cells. EBV therefore initially uses TLR7 signaling to enhance B-cell proliferation and subsequently modifies the pathway to regulate IRF-5 activity.

scholarly journals Limiting dilution analysis of Epstein-Barr virus-induced immunoglobulin production by human B cells.

1983 ◽  
Vol 157 (1) ◽  
pp. 1-14 ◽  
Author(s):  
R Yarchoan ◽  
G Tosato ◽  
R M Blaese ◽  
R M Simon ◽  
D L Nelson
Keyword(s):  
B Cells ◽  
B Cell ◽  
Peripheral Blood ◽  
Epstein Barr Virus ◽  
Cell Activation ◽  
B Cell Activation ◽  
Barr Virus ◽  
Human B Cells ◽  
Epstein Barr ◽  
Limiting Dilution

The Epstein-Barr virus (EBV) is a herpes virus that has the capacity to infect human B cells and to induce them to secrete immunoglobulin (Ig). In the current experiments, Poisson analysis of limiting dilution cultures has been used to study the activation of human peripheral B cells by the B95-8 strain of EBV. Under the culture conditions used, 0.2-1% of peripheral blood B cells were activated by EBV to secrete IgM or IgG. In addition, when multiple replicate cultures containing limited numbers of B cells were tested for IgM and for IgG production, the precursors for IgM and IgG segregated independently; thus, individual B cell precursors matured into cells secreting IgM or IgG but not both classes of Ig. Additional experiments using limiting dilutions of EBV were undertaken to study the viral requirements for B cell activation. These studies indicated that B cell activation by EBV to produce Ig was consistent with a "one-hit" model and inconsistent with a "two-hit" model. Taken together, these results indicate that infection by one EBV virion is sufficient to induce a precursor peripheral blood B cell to secrete Ig and that only one isotype of Ig is then secreted.

scholarly journals Rheumatoid Factors Induce Signaling from B Cells, Leading to Epstein-Barr Virus and B-Cell Activation

2004 ◽  
Vol 78 (18) ◽  
pp. 9918-9923 ◽  
Author(s):  
Lixin Yang ◽  
Masayuki Hakoda ◽  
Kazuya Iwabuchi ◽  
Tsuyoshi Takeda ◽  
Takao Koike ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Activation ◽  
Mononuclear Cells ◽  
Rheumatoid Factors ◽  
B Cell Activation ◽  
Barr Virus ◽  
Membrane Bound ◽  
Epstein Barr

ABSTRACT B-cell antigen receptor signaling is initiated upon binding of the antigen to membrane-bound immunoblobulin (Ig), and the anti-Ig antibody (Ab) mimics this signaling. In B cells latently infected with Epstein-Barr virus (EBV), the same signals induce virus activation. We examine here whether rheumatoid factors (RFs), autoantibodies directed against the Fc portion of IgG, induce EBV and B-cell activation. As a source of RFs, RF-producing lymphoblastoid cell line (LCL) clones were isolated from peripheral blood mononuclear cells (PBMC) and synovial cells from patients with rheumatoid arthritis (RA) by EBV transformation. Burkitt's lymphoma-derived Akata cells, which are highly responsive to EBV activation by anti-Ig Abs, were used for the assay of EBV activation. Akata cells expressed IgG3 as membrane-bound Ig. RFs from a synovium-derived LCL were directed to IgG3 and induced EBV activation in 16 to 18% of Akata cells, whereas RFs from another synovium-derived LCL were directed to IgG1 and did not induce EBV activation. Pretreatment of RFs with the purified Fc fragment of human IgG completely abolished EBV activation. Furthermore, B-cell activation was assessed by incorporation of [3H]thymidine. RFs from synovium-derived LCLs efficiently induced B-cell activation, and the addition of CD40 ligand had a synergistic effect. On the other hand, RFs from PBMC-derived LCLs were polyreactive, had a lower affinity to IgG, and did not induce EBV and B-cell activation. The present findings imply a possible role for RFs as EBV and B-cell activators.

Early events in Epstein-Barr virus genome expression after activation: Regulation by second messengers of B cell activation

Virology ◽  
1991 ◽  
Vol 185 (2) ◽  
pp. 922-928 ◽  
Author(s):  
Ingo Mellinghoff ◽  
Masanori Daibata ◽  
Robert E. Humphreys ◽  
Carel Mulder ◽  
Kenzo Takada ◽  
...  
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Activation ◽  
Second Messengers ◽  
Virus Genome ◽  
B Cell Activation ◽  
Barr Virus ◽  
Genome Expression ◽  
Epstein Barr

scholarly journals Epstein-Barr virus (EBV) induces expression of B-cell activation markers on in vitro infection of EBV-negative B-lymphoma cells.

1987 ◽  
Vol 84 (22) ◽  
pp. 8060-8064 ◽  
Author(s):  
A. Calender ◽  
M. Billaud ◽  
J. P. Aubry ◽  
J. Banchereau ◽  
M. Vuillaume ◽  
...  
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Activation ◽  
B Cell Activation ◽  
Activation Markers ◽  
B Lymphoma ◽  
Barr Virus ◽  
B Lymphoma Cells ◽  
Epstein Barr
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