Two large virion envelope glycoproteins mediate Epstein-Barr virus binding to receptor-positive cells.

Epstein-Barr virus (EBV), an oncogenic human herpesvirus, binds to and infects normal human B lymphocytes via CD21, the CR2 complement receptor. Studies of the mechanisms that enable EBV to infect nonactivated, noncycling B cells provide compelling evidence for a sequence of events in which EBV binding to CD21 on purified resting human B cells rapidly activates the NF-κB transcription factor, which, in turn, binds to and mediates transcriptional activation of Wp, the initial viral latent gene promoter. Thus, EBV binding to its cellular receptor on resting B cells triggers an NF-κB–dependent intracellular signaling pathway which is required for infection.

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Epstein--Barr Virus Binding to Virus-carrying Cell Lines is Enhanced in the Presence of C3 and C3d

Journal of General Virology ◽

10.1099/0022-1317-65-3-507 ◽

1984 ◽

Vol 65 (3) ◽

pp. 507-513 ◽

Cited By ~ 2

Author(s):

A. Wells ◽

N. Koide ◽

G. Eggertsen ◽

A. Lundwall ◽

T. Godal ◽

...

Keyword(s):

Cell Lines ◽

Epstein Barr Virus ◽

Virus Binding ◽

Barr Virus ◽

Epstein Barr

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Synthesis and processing of the three major envelope glycoproteins of Epstein-Barr virus.

Journal of Virology ◽

10.1128/jvi.46.2.547-556.1983 ◽

1983 ◽

Vol 46 (2) ◽

pp. 547-556 ◽

Cited By ~ 25

Author(s):

C M Edson ◽

D A Thorley-Lawson

Keyword(s):

Epstein Barr Virus ◽

Envelope Glycoproteins ◽

Barr Virus ◽

Synthesis And Processing ◽

Epstein Barr

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The Epstein–Barr virus‐binding site on CD21 is involved in CD23 binding and interleukin‐4‐induced IgE and IgG4 production by human B cells

Immunology ◽

10.1046/j.1365-2567.1996.d01-651.x ◽

1996 ◽

Vol 88 (1) ◽

pp. 35-39 ◽

Cited By ~ 16

Author(s):

S. HENCHOZ‐LECOANET ◽

P. JEANNIN ◽

J.‐P. AUBRY ◽

P. GRABER ◽

C. G. BRADSHAW ◽

...

Keyword(s):

B Cells ◽

Binding Site ◽

Epstein Barr Virus ◽

Interleukin 4 ◽

Virus Binding ◽

Barr Virus ◽

Human B Cells ◽

Epstein Barr

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Epstein–Barr virus-induced B-cell transformation: quantitating events from virus binding to cell outgrowth

Journal of General Virology ◽

10.1099/vir.0.81153-0 ◽

2005 ◽

Vol 86 (11) ◽

pp. 3009-3019 ◽

Cited By ~ 51

Author(s):

Claire Shannon-Lowe ◽

Gouri Baldwin ◽

Regina Feederle ◽

Andrew Bell ◽

Alan Rickinson ◽

...

Keyword(s):

B Cell ◽

Cell Nucleus ◽

Epstein Barr Virus ◽

Cell Activation ◽

Cell Transformation ◽

Nuclear Antigen ◽

Virus Binding ◽

Barr Virus ◽

Epstein Barr

Epstein–Barr virus (EBV) infection and growth activation of human B cells is central to virus biology and disease pathogenesis, but is poorly understood in quantitative terms. Here, using virus at defined m.o.i., the different stages of this process at the single-cell level are followed in vitro. Virus binding to the B-cell surface, assayed by quantitative PCR, is highly efficient, particularly at the low m.o.i. values that most likely reflect physiologic events in vivo. However, only 10–15 % of bound virus genomes reach the cell nucleus, as visualized by sensitive fluorescence in situ hybridization (FISH) assay; viral genomes acquired per cell nucleus range from 1 to >10, depending on the m.o.i. Thereafter, despite differences in initial genome load, almost all nuclear genome-positive cells then go on to express the virus-encoded nuclear antigen EBNA2, upregulate the cell activation antigen CD23 and transit the cell cycle. EBNA2-positive cells in the first cycle post-infection then grow out to lymphoblastoid cell lines (LCLs) just as efficiently as do cells limiting-diluted from already established LCLs. This study therefore identifies EBV genome delivery to the nucleus as a key rate-limiting step in B-cell transformation, and highlights the remarkable efficiency with which a single virus genome, having reached the nucleus, then drives the transformation programme.

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