Intact antigen presentation for Epstein-Barr virus (EBV)-specific CTL by a lymphoblastoid cell line established from a patient with severe chronic active EBV infection

1995 ◽  
Vol 184 (2) ◽  
Author(s):  
Hiroshi Kimura ◽  
Ikuya Tsuge ◽  
Shosuke Imai ◽  
Mitsuaki Yamamoto ◽  
Kiyotaka Kuzushima ◽  
...  
Keyword(s):  
Antigen Presentation ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

scholarly journals Signatures of B-cell receptor diversity in B lymphocytes following Epstein-Barr virus transformation

2019 ◽  
Vol 51 (6) ◽  
pp. 197-207
Author(s):  
Meimei Lai ◽  
Qiongdan Wang ◽  
Yutian Lu ◽  
Xi Xu ◽  
Ying Xia ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
High Throughput Sequencing ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Human Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Epstein-Barr virus (EBV) is a widespread human virus that establishes latent infection, potentially leading to tumors, hematological disorders, and other severe diseases. EBV infections are associated with diverse symptoms and affect various organs; therefore, early diagnosis and treatment are crucial. B cell receptor (BCR) repertoires of B cell surface immunoglobulins have been widely studied for their association with various infectious diseases. However, the specific genetic changes that modulate the BCR repertoires after an EBV infection are still poorly understood. In this study, we employed high-throughput sequencing (HTS) to investigate the diversity of BCR repertoires in an EBV-transformed lymphoblastic cell line (LCL). Compared with the noninfected control B cell line, the LCL exhibited a decrease in overall BCR diversity but displayed an increase in the expansion of some dominant rearrangements such as IGHV4-31/IGHJ4, IGHV4-59/IGHJ4, IGHV5-51/IGHJ3, and IGHV3-74/IGHJ3. A higher frequency of occurrence of these rearrangement types was confirmed in patients with EBV infection. Interestingly, the IGHV3-74 rearrangement was only detected in EBV-infected children, suggesting that our experimental observations were not coincidental. In addition, we identified a highly dominant consensus motif, CAR(xRx)YGSG(xYx)FD, in complementarity-determining region 3 (CDR3) sequences of the heavy chain in the LCL. Our findings demonstrated the utility of HTS technology for studying the variations in signature motifs of the BCR repertoires after EBV infection. We propose that the analysis of BCR repertoire sequences represents a promising method for diagnosing early EBV infections and developing novel antibody- and vaccine-based therapies against such infections.

scholarly journals A Positive Autoregulatory Loop of LMP1 Expression and STAT Activation in Epithelial Cells Latently Infected with Epstein-Barr Virus

2003 ◽  
Vol 77 (7) ◽  
pp. 4139-4148 ◽  
Author(s):  
Honglin Chen ◽  
Lindsey Hutt-Fletcher ◽  
Liang Cao ◽  
S. Diane Hayward
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Lmp1 Expression ◽  
Cell Line Hela ◽  
Epstein Barr ◽  
Phosphorylated Stat3

ABSTRACT STAT3 and STAT5 are constitutively activated and nuclear in nasopharyngeal carcinoma (NPC) cells. In normal signaling, STATs are only transiently activated. To investigate whether Epstein-Barr virus (EBV), and in particular the protein LMP1, contributes to sustained STAT phosphorylation and activation in epithelial cells, we examined STAT activity in two sets of paired cell lines, HeLa, an EBV-converted HeLa cell line, HeLa-Bx1, the NPC-derived cell line CNE2-LNSX, and an LMP1-expressing derivative, CNE2-LMP1. EBV infection was associated with a significant increase in the tyrosine-phosphorylated forms of STAT3 and STAT5 in HeLa-Bx1 cells. This effect correlated with LMP1 expression, since phosphorylated STAT3 and STAT5 levels were also increased in CNE2-LMP1 cells relative to the control CNE2-LNSX cells. No change was observed in STAT1 or STAT6 phosphorylation in these cell lines, nor was there a significant change in the levels of total STAT3, STAT5, STAT1, or STAT6 protein. Tyrosine phosphorylation allows the normally cytoplasmic STAT proteins to enter the nucleus and bind to their recognition sequences in responsive promoters. The ability of LMP1 to activate STAT3 was further established by immunofluorescence assays in which coexpression of LMP1 in transfected cells was sufficient to mediate nuclear relocalization of Flag-STAT3 and by an electrophoretic mobility shift assay which showed that LMP1 expression in CNE2-LNSX cells was associated with increased endogenous STAT3 DNA binding activity. In addition, the activity of a downstream target of STAT3, c-Myc, was upregulated in HeLa-Bx1 and CNE2-LMP1 cells. A linkage was established between interleukin-6 (IL-6)- and LMP1-mediated STAT3 activation. Treatment with IL-6 increased phosphorylated STAT3 levels in CNE2-LNSX cells, and conversely, treatment of CNE2-LMP1 cells with IL-6 neutralizing antibody ablated STAT3 activation and c-Myc upregulation. The previous observation that STAT3 activated the LMP1 terminal repeat promoter in reporter assays was extended to show upregulated expression of endogenous LMP1 mRNA and protein in HeLa-Bx1 cells transfected with a constitutively activated STAT3. A model is proposed in which EBV infection of an epithelial cell containing activated STATs would permit LMP1 expression. This in turn would establish a positive feedback loop of IL-6-induced STAT activation, LMP1 and Qp-EBNA1 expression, and viral genome persistence.

scholarly journals An Epstein-Barr Virus Isolated from a Lymphoblastoid Cell Line Has a 16-Kilobase-Pair Deletion Which Includes gp350 and the Epstein-Barr Virus Nuclear Antigen 3A

2001 ◽  
Vol 75 (18) ◽  
pp. 8556-8568 ◽  
Author(s):  
Wonkeun Lee ◽  
Yoon-Ha Hwang ◽  
Suk-Kyeong Lee ◽  
Chitra Subramanian ◽  
Erle S. Robertson
Keyword(s):  
Cell Line ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Phorbol Esters ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Amino Terminal ◽  
Epstein Barr

ABSTRACT Epstein-Barr virus (EBV) is associated with human cancers, including nasopharyngeal carcinoma, Burkitt's lymphoma, gastric carcinoma and, somewhat controversially, breast carcinoma. EBV infects and efficiently transforms human primary B lymphocytes in vitro. A number of EBV-encoded genes are critical for EBV-mediated transformation of human B lymphocytes. In this study we show that an EBV-infected lymphoblastoid cell line obtained from the spontaneous outgrowth of B cells from a leukemia patient contains a deletion, which involves a region of approximately 16 kbp. This deletion encodes major EBV genes involved in both infection and transformation of human primary B lymphocytes and includes the glycoprotein gp350, the entire open reading frame of EBNA3A, and the amino-terminal region of EBNA3B. A fusion protein created by this deletion, which lies between the BMRF1 early antigen and the EBNA3B latent antigen, is truncated immediately downstream of the junction 21 amino acids into the region of the EBNA3B sequence, which is out of frame with respect to the EBNA3B protein sequence, and indicates that EBNA3B is not expressed. The fusion is from EBV coordinate 80299 within the BMRF1 sequence to coordinate 90998 in the EBNA3B sequence. Additionally, we have shown that there is no detectable induction in viral replication observed when SNU-265 is treated with phorbol esters, and no transformants were detected when supernatant is used to infect primary B lymphocytes after 8 weeks in culture. Therefore, we have identified an EBV genome with a major deletion in critical genes involved in mediating EBV infection and the transformation of human primary B lymphocytes that is incompetent for replication of this naturally occurring EBV isolate.

Epstein-Barr Virus (EBV) Infection by Cocultivation of Fibroblast-Dominant Cell Line and EBV-Transformed Lymphocytes

ORL ◽  
1989 ◽  
Vol 51 (2) ◽  
pp. 69-76
Author(s):  
M. Furukawa ◽  
M. Kamide ◽  
T. Miwa ◽  
M. Sakumoto ◽  
R. Umeda
Keyword(s):  
Cell Line ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

scholarly journals Downregulation of RUNX1 by RUNX3 Requires the RUNX3 VWRPY Sequence and Is Essential for Epstein-Barr Virus-Driven B-Cell Proliferation

2009 ◽  
Vol 83 (13) ◽  
pp. 6909-6916 ◽  
Author(s):  
Gareth Brady ◽  
Hannah J. Whiteman ◽  
Lindsay C. Spender ◽  
Paul J. Farrell
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Critical Role ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT Cross-regulation of RUNX1 expression by RUNX3 plays a critical role in regulating proliferation of human B cells infected with Epstein-Barr virus (EBV). When EBV infection induces RUNX3, the consequent reduction in RUNX1 levels is required for the ensuing cell proliferation because forced expression of RUNX1 in an EBV lymphoblastoid cell line prevented cell proliferation. The TEL-RUNX1 fusion gene from acute B-lymphocytic leukemia retains almost all of the RUNX1 sequence but does not prevent B-cell proliferation in the same assay. B-cell maturation antigen (BCMA) was found to be induced by conditionally expressed RUNX3 in a lymphoma cell line. Chromatin immunoprecipitation assays confirmed that RUNX3 binds to the RUNX1 promoter in a lymphoblastoid cell line and a Burkitt's lymphoma cell line. The TLE binding VWRPY sequence from the C terminus of RUNX3 was found to be required for repression of the RUNX1 P1 promoter in a B-lymphoma cell line. The mechanism of repression in B-cell lines most likely involves recruitment of corepressor TLE3 or TLE4 to the RUNX1 promoter. The results demonstrate the importance of RUNX3-mediated repression of RUNX1 for EBV-driven B-cell proliferation and identify functional differences between human RUNX family proteins.

scholarly journals A Single Amino Acid in EBNA-2 Determines Superior B Lymphoblastoid Cell Line Growth Maintenance by Epstein-Barr Virus Type 1 EBNA-2

2014 ◽  
Vol 88 (16) ◽  
pp. 8743-8753 ◽  
Author(s):  
S. Tzellos ◽  
P. B. Correia ◽  
C. E. Karstegl ◽  
L. Cancian ◽  
J. Cano-Flanagan ◽  
...  
Keyword(s):  
Amino Acid ◽  
Cell Line ◽  
Virus Type ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Single Amino Acid ◽  
Barr Virus ◽  
Epstein Barr
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