scholarly journals Model of Epstein-Barr virus infection of human thymocytes: expression of viral genome and impact on cellular receptor expression in the T- lymphoblastic cell line, HPB-ALL

Blood ◽  
1995 ◽  
Vol 85 (2) ◽  
pp. 456-464 ◽  
Author(s):  
RL Paterson ◽  
C Kelleher ◽  
TD Amankonah ◽  
JE Streib ◽  
JW Xu ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Receptor Expression ◽  
Productive Infection ◽  
Epithelial Tissue ◽  
Cellular Receptor ◽  
Barr Virus ◽  
Epstein Barr

Abstract Infection of B lymphocytes and epithelial tissue by Epstein-Barr virus (EBV) is associated with malignancy and autoimmunity. The cellular receptor for EBV has been identified as CD21 (CR2). A molecule, which is biochemically and immunologically similar to B-cell CD21, has been identified on a subpopulation of immature thymocytes, suggesting a role for this molecule in the regulation of T-cell development and further suggesting that immature T cells might be susceptible to EBV infection. A growing body of literature now documents the presence of EBV in tumors of T-cell origin. We have evaluated the susceptibility of the human immature T cell line, HPB-ALL, to infection by EBV. Electron microscopy studies showed a rapid internalization of virus by HPB cells. Southern blotting showed the intracellular presence of linear EBV genomes, and components of the virus replicative cycle were identified. Expression of the BamHI Z region of the genome, encoding the nuclear protein, ZEBRA, which is strictly associated with productive infection in B cells, was detected in HPB-ALL cells. A spliced variant of Z, RAZ, was also identified. Cell surface expression of EBV late antigens was observed to occur transiently. Infection of HPB cells was also accompanied by altered expression of T-cell surface molecules involved in antigen recognition, a process critical to normal development of the T-cell repertoire. Delineation of the outcome of T- cell infection by EBV may lead to a better understanding of the role of this virus in autoimmune processes and malignancy.

scholarly journals Model of Epstein-Barr virus infection of human thymocytes: expression of viral genome and impact on cellular receptor expression in the T- lymphoblastic cell line, HPB-ALL

Blood ◽  
1995 ◽  
Vol 85 (2) ◽  
pp. 456-464 ◽  
Author(s):  
RL Paterson ◽  
C Kelleher ◽  
TD Amankonah ◽  
JE Streib ◽  
JW Xu ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Receptor Expression ◽  
Productive Infection ◽  
Epithelial Tissue ◽  
Cellular Receptor ◽  
Barr Virus ◽  
Epstein Barr

Infection of B lymphocytes and epithelial tissue by Epstein-Barr virus (EBV) is associated with malignancy and autoimmunity. The cellular receptor for EBV has been identified as CD21 (CR2). A molecule, which is biochemically and immunologically similar to B-cell CD21, has been identified on a subpopulation of immature thymocytes, suggesting a role for this molecule in the regulation of T-cell development and further suggesting that immature T cells might be susceptible to EBV infection. A growing body of literature now documents the presence of EBV in tumors of T-cell origin. We have evaluated the susceptibility of the human immature T cell line, HPB-ALL, to infection by EBV. Electron microscopy studies showed a rapid internalization of virus by HPB cells. Southern blotting showed the intracellular presence of linear EBV genomes, and components of the virus replicative cycle were identified. Expression of the BamHI Z region of the genome, encoding the nuclear protein, ZEBRA, which is strictly associated with productive infection in B cells, was detected in HPB-ALL cells. A spliced variant of Z, RAZ, was also identified. Cell surface expression of EBV late antigens was observed to occur transiently. Infection of HPB cells was also accompanied by altered expression of T-cell surface molecules involved in antigen recognition, a process critical to normal development of the T-cell repertoire. Delineation of the outcome of T- cell infection by EBV may lead to a better understanding of the role of this virus in autoimmune processes and malignancy.

scholarly journals Absence of allogeneic restriction in human T-cell-mediated cytotoxicity to Epstein-Barr virus-infected target cells. Demonstration of an HLA-linked control at the effector level.

1979 ◽  
Vol 150 (6) ◽  
pp. 1310-1322 ◽  
Author(s):  
M Lipinski ◽  
W H Fridman ◽  
T Tursz ◽  
C Vincent ◽  
D Pious ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Cell Surface ◽  
Target Cell ◽  
Epstein Barr Virus ◽  
Target Cells ◽  
Specific Lysis ◽  
Barr Virus ◽  
Positive Target ◽  
Epstein Barr

Peripheral T lymphocytes from patients with infectious mononucleosis (IM) are sensitized in vivo against the Epstein-Barr virus (EBV). The expression of HLA-A, B, or C molecules at the target cell surface is necessary for the cytotoxic reaction because (a) EBV-positive Daudi cells lacking HLA-A, B, and C determinants are resistant to anti-EBV T-cell lysis, (b) cytolysis of EBV-positive target cells can be consistently inhibited by anti-HLA-A, B, and C and anti-beta 2 microglobulin antibodies. However, no evidence for allogeneic restriction in this system was apparent as (a) cytotoxic T lymphocytes (CTL) from one given individual could exert a cytotoxicity of a similar magnitude on different EBV-positive target cells, regardless of the number of HLA-A or B specificities shared by the effectors and targets; (b) CTL from IM patients were able to kill target cells without any HLA-A or B antigen in common; and (c) T5-1 variants lacking one or two HLA antigens at the A, B, or D locus are killed to the same extent as the parental cells. 7 of the 9 IM patients with detectable circulating anti-EBV CTL carried the HLA-A1 antigen, whereas none of the 16 IM patients lacking detectable peripheral CTL were HLA-A1 positive (mean specific lysis of T5-1 target cells by T cells from HLA-A1 positive patients: 29.3 vs. 0.6% in HLA-A1-negative patients) (P less than 10(-9)). These data suggest an HLA-A1-linked gene control of the magnitude of the anti-EBV CTL response. Thus, the HLA region appears to act at two different level sin the T-cell-mediated lysis of EBV-infected cells by controlling first, the development of anti-EBV and second, the expression of HLA-A, B, and C molecules involved as recognition structures at the target cell surface.

Early exposure to interleukin-21 limits rapidly generated anti–Epstein-Barr virus T-cell line differentiation

Cytotherapy ◽  
2015 ◽  
Vol 17 (4) ◽  
pp. 496-508 ◽  
Author(s):  
Julie Orio ◽  
Cédric Carli ◽  
Valérie Janelle ◽  
Martin Giroux ◽  
Julie Taillefer ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Early Exposure ◽  
Barr Virus ◽  
Interleukin 21 ◽  
Epstein Barr

Su.35. Epstein-Barr Virus Downregulates B Cell Surface CD1d to Evade Natural Killer T Cell Detection

2008 ◽  
Vol 127 ◽  
pp. S135-S136 ◽  
Author(s):  
Brian Chung ◽  
Lenka Allan ◽  
Dong Jun Zheng ◽  
John Priatel ◽  
Peter van den Elzen ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
B Cell ◽  
Natural Killer ◽  
Epstein Barr Virus ◽  
Cell Detection ◽  
Natural Killer T Cell ◽  
Barr Virus ◽  
Epstein Barr ◽  
Killer T Cell

Interaction between Epstein-Barr virus and a T cell line (HSB-2) via a receptor phenotypically distinct from complement receptor type 2

1992 ◽  
Vol 22 (5) ◽  
pp. 1123-1131 ◽  
Author(s):  
Joseph A. Hedrick ◽  
Debbie Watry ◽  
Catherine Speiser ◽  
Patrick O'Donnell ◽  
John D. Lambris ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Receptor Type ◽  
Complement Receptor ◽  
Complement Receptor Type ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Identification of a Novel Element Involved in Regulation of the Lytic Switch BZLF1 Gene Promoter of Epstein-Barr Virus

2001 ◽  
Vol 75 (2) ◽  
pp. 867-877 ◽  
Author(s):  
Richard J. Kraus ◽  
Sarah J. Mirocha ◽  
Heather M. Stephany ◽  
Joel R. Puchalski ◽  
Janet E. Mertz
Keyword(s):  
Cell Line ◽  
Epstein Barr Virus ◽  
Fold Increase ◽  
Productive Infection ◽  
Barr Virus ◽  
Lymphocytic Cell ◽  
Bzlf1 Gene ◽  
Epstein Barr ◽  
Bzlf1 Promoter ◽  
Mcf 7

ABSTRACT Epstein-Barr virus (EBV) is a human herpesvirus capable of establishing a latent state in B lymphocytes. EBV's BZLF1 gene product plays a central role in regulating the switch from latency to productive infection. Here, we identify a sequence element, 5′-CAGGTA-3′, called ZV, located at nucleotides −17 to −12 relative to the transcription initiation site of the BZLF1 promoter. ZV sequence-specifically binds a cellular nuclear factor(s), ZVR. ZVR DNA-binding activity was present in the EBV-negative B-lymphocytic cell line DG75, the EBV-positive B-lymphocytic cell lines GG68 and 721, the cervical cell line C33A, and the kidney cell line CV-1 but not in the breast carcinoma cell line MCF-7. Mutations in ZV that relieve binding of ZVR lead to a two- to fourfold increase in basal expression of the BZLF1 promoter in DG75, C33A, and CV-1 cells. The same mutants exhibited a 40- to 180-fold increase in tetradecanoyl phorbol acetate-ionomycin-induced expression in DG75 cells and a 22-fold increase in C33A cells. Thus, ZVR functions as a regulator of the BZLF1 promoter, repressing transcription when bound to the ZV site in the absence of inducers. No differences in basal or induced transcription between wild-type and ZV mutant BZLF1 promoters were observed in ZVR-negative MCF-7 cells. ZVR failed to bind any of the previously identified negative regulatory elements within the BZLF1 promoter. We conclude that ZV functions as an important regulatory element of the BZLF1 promoter, with ZVR likely playing important roles in the maintenance of latency and reactivation of EBV.

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