Epstein-Barr virus genome-positive T lymphocytes in a boy with chronic active EBV infection associated with Kawasaki-like disease

Nature ◽  
1988 ◽  
Vol 333 (6172) ◽  
pp. 455-457 ◽  
Author(s):  
Hideaki Kikuta ◽  
Yuichi Taguchi ◽  
Kazuhiro Tomizawa ◽  
Kimikazu Kojima ◽  
Nobuaki Kawamura ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Epstein Barr Virus ◽  
Virus Genome ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Defective activity of Epstein-Barr virus (EBV) specific cytotoxic T lymphocytes in children with chronic active EBV infection and in their parents

1993 ◽  
Vol 35 (5) ◽  
pp. 394-399 ◽  
Author(s):  
MIKIYA FUJIEDA ◽  
HIROSHI WAKIGUCHI ◽  
HIROAKI HISAKAWA ◽  
HARUO KUBOTA ◽  
TAKANOBU KURASHIGE
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

scholarly journals Do Epstein–Barr Virus Mutations and Natural Genome Sequence Variations Contribute to Disease?

Biomolecules ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 17
Author(s):  
Paul J. Farrell ◽  
Robert E. White
Keyword(s):  
Genome Sequence ◽  
Epstein Barr Virus ◽  
Sequence Variation ◽  
Virus Genome ◽  
Barr Virus ◽  
Ebv Infection ◽  
Sequence Variations ◽  
The World ◽  
Epstein Barr ◽  
Different Parts

Most of the world’s population is infected by the Epstein–Barr virus (EBV), but the incidence of the diseases associated with EBV infection differs greatly in different parts of the world. Many factors may determine those differences, but variation in the virus genome is likely to be a contributing factor for some of the diseases. Here, we describe the main forms of EBV genome sequence variation, and the mechanisms by which variations in the virus genome are likely to contribute to disease. EBV genome deletions or polymorphisms can also provide useful markers for monitoring disease. If some EBV strains prove to be more pathogenic than others, this suggests the possible value of immunising people against infection by those pathogenic strains.

Reconstitution of Epstein-Barr Virus-Specific T Lymphocytes at the Early Stage of Allogeneic Stem Cell Transplantation

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 5469-5469 ◽  
Author(s):  
Ren Lin ◽  
Zhiping Fan ◽  
Ke Zhao ◽  
Qianli Jiang ◽  
Jing Sun ◽  
...  
Keyword(s):  
Stem Cell ◽  
T Lymphocytes ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Allogeneic Stem Cell Transplantation ◽  
Epstein Barr Virus ◽  
Early Stage ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Abstract Backgroud: Epstein-Barr virus (EBV) infection/reactivation is an common complication following allogeneic stem cell transplantation (allo-HSCT) which usually occure at the early stage after transplantation. EBV-specific cytotoxic T lymphocytes (EBV-CTLs) are considered to provide protection from EBV infection/reactivation and associated diseases in recipients of allo-HSCT. Herein, we evaluated the levels of EBV-CTLs early after transplantion and investigated the associaton between the reconstitution of EBV-CTLs and EBV infection/reactivation after allo-HSCT. Methods: Thirty patients undergoing allo-HSCT between November 2013 to September 2014 were enrolled in this study. Of these patients, 16 received HLA-matched donor and 14 received HLA-mismatched transplantation. Antithymocyteglobulin was given in 20 patients. EBV-CTLs were tested using Enzyme-linked immunospot assay (ELISPOT) presenting 9 peptides derived from 3 EBV proteins in +30, +90 and +180 days after transplantation. Results: EBV-CTLs, although low levels, were detected in 90% (27/30) patients in +30 days after HSCT. In most patients, EBV-CTLs levels in +90 days was significantly higher than +30 days and returned to normal levels within +180 days after HSCT. Thirteen patients developed EBV infection/reactivation within the median time of 48 (range, 23-110) after transplantation. EBV-CTLs levels had no significant difference among the patients with or without infection/reactivation in +30 days while the patients with EBV infection/reactivation had higher EBV-CTLs levels than those without in +90d after HSCT. Conclusion: Reconstitution of EBV-CTLs seems rapid in both HLA-matched and -mismatched donor transplantation. The association between EBV infection/reactivation and EBV-CTLs levels at monthly intervels after HSCT should be studied further. Disclosures No relevant conflicts of interest to declare.

Stable expression of Epstein-Barr virus BZLF-1–encoded ZEBRA protein activates p53-dependent transcription in human Jurkat T-lymphoblastoid cells

Blood ◽  
2000 ◽  
Vol 96 (2) ◽  
pp. 625-634 ◽  
Author(s):  
David H. Dreyfus ◽  
Masayuki Nagasawa ◽  
Colm A. Kelleher ◽  
Erwin W. Gelfand
Keyword(s):  
T Lymphocytes ◽  
Epstein Barr Virus ◽  
Apoptotic Cell ◽  
Stable Expression ◽  
Common Mechanism ◽  
Lymphoblastoid Cells ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Interaction between viral proteins and tumor suppressor p53 is a common mechanism of viral pathogenesis. The Epstein-Barr virus (EBV) BZLF-1 ORF-encoded ZEBRA protein (also denoted EB1, Z, Zta) binds to p53 in vitro and has been associated with the altered transcription of p53-regulated genes in B lymphocytes and epithelial cells. In this work, Jurkat T-lymphoblastoid cells that express ZEBRA were characterized by the use of transiently transfected p53 and p53 reporter genes. Stable expression of ZEBRA was associated with the activation of p53-dependent transcription and increased p53 dependent apoptotic cell death. In Jurkat cell lines, stably expressed ZEBRA protein was apparently localized to the cell cytoplasm, in contrast to the typical nuclear localization of this protein in other cell types. Previous studies have suggested that EBV infection of T lymphocytes may contribute to the malignant transformation of T cells and the increased replication of human immunodeficiency virus. Our observations suggest a mechanism through which ZEBRA protein expressed in human T lymphocytes could alter T-cell proliferation and apoptosis during EBV infection.

Detection of Epstein-Barr virus Genome in Squamous Cell Carcinomas of the Larynx

1995 ◽  
Vol 10 (4) ◽  
pp. 211-215 ◽  
Author(s):  
H. Kiaris ◽  
M. Ergazaki ◽  
J. Segas ◽  
D.A. Spandidos
Keyword(s):  
Squamous Cell ◽  
Normal Tissue ◽  
Epstein Barr Virus ◽  
Tumor Tissue ◽  
Virus Genome ◽  
Squamous Cell Carcinomas ◽  
Adjacent Normal Tissue ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Epstein-Barr virus (EBV) is a B-lymphotropic virus with a tumorigenic potential. EBV infection has been recognized as the main cause of nasopharyngeal carcinoma and Burkitt's lymphoma. The aim of our study was to determine the incidence of EBV in squamous cell carcinomas of the larynx. We employed for our analysis a sensitive polymerase chain reaction (PCR) assay, followed by restriction fragment length polymorphism (RFLP) for further confirmation of the specificity of the PCR-amplification reaction. Our analysis revealed that 9 of 27 (33%) specimens harbored the EBV genome in the tumor tissue while only 4 (15%) specimens from adjacent normal tissue exhibited evidence of EBV infection. Three were EBV positive for both normal and tumor tissue. No association has been found with disease stage, histological differentiation and nodes at pathology. The relatively high incidence of EBV in the tumor tissue (33%) of patients with laryngeal cancer, as compared to the low (15%) incidence of the virus genome detected in the adjacent normal tissue of the patients, indicates a probable role of EBV in the development of the disease.

Stable expression of Epstein-Barr virus BZLF-1–encoded ZEBRA protein activates p53-dependent transcription in human Jurkat T-lymphoblastoid cells

Blood ◽  
2000 ◽  
Vol 96 (2) ◽  
pp. 625-634 ◽  
Author(s):  
David H. Dreyfus ◽  
Masayuki Nagasawa ◽  
Colm A. Kelleher ◽  
Erwin W. Gelfand
Keyword(s):  
T Lymphocytes ◽  
Epstein Barr Virus ◽  
Apoptotic Cell ◽  
Stable Expression ◽  
Common Mechanism ◽  
Lymphoblastoid Cells ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Abstract Interaction between viral proteins and tumor suppressor p53 is a common mechanism of viral pathogenesis. The Epstein-Barr virus (EBV) BZLF-1 ORF-encoded ZEBRA protein (also denoted EB1, Z, Zta) binds to p53 in vitro and has been associated with the altered transcription of p53-regulated genes in B lymphocytes and epithelial cells. In this work, Jurkat T-lymphoblastoid cells that express ZEBRA were characterized by the use of transiently transfected p53 and p53 reporter genes. Stable expression of ZEBRA was associated with the activation of p53-dependent transcription and increased p53 dependent apoptotic cell death. In Jurkat cell lines, stably expressed ZEBRA protein was apparently localized to the cell cytoplasm, in contrast to the typical nuclear localization of this protein in other cell types. Previous studies have suggested that EBV infection of T lymphocytes may contribute to the malignant transformation of T cells and the increased replication of human immunodeficiency virus. Our observations suggest a mechanism through which ZEBRA protein expressed in human T lymphocytes could alter T-cell proliferation and apoptosis during EBV infection.

scholarly journals Search for Anti-EA(D) Antibodies in Subjects with an “Isolated VCA IgG” Pattern

2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Massimo De Paschale ◽  
Debora Cagnin ◽  
Teresa Cerulli ◽  
Maria Teresa Manco ◽  
Carlo Agrappi ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Virus Genome ◽  
Screening Tests ◽  
Enzyme Linked Immunosorbent Assay ◽  
Early Antigen ◽  
Economic Problems ◽  
Barr Virus ◽  
Ebv Infection ◽  
Genome Search ◽  
Epstein Barr

The presence of an “isolated viral capsid antigen (VCA) IgG” pattern in serum is not easy to interpret without the aid of further tests, such as specific immunoblotting or a virus genome search, that often give rise to organisational and economic problems. However, one alternative is to use an enzyme-linked immunosorbent assay (ELISA) to detect anti-early antigen (EA) antibodies, which can be found in about 85% of subjects with acute Epstein-Barr virus (EBV) infections. The purpose of this work was to search for anti-EA(D) antibodies in 130 samples with an isolated VCA IgG pattern at ELISA screening and classified as being indicative of past (102 cases) or acute (28 cases) infection on the basis of the immunoblotting results. Thirty-seven samples (28.5%) were positive for anti-EA(D), of which 25 (89.3%) had been classified by immunoblotting as indicating acute and 12 (11.8%) past EBV infection. This difference was statistically significant (P<.01). The results of our search for anti-EA(D) antibodies correctly identified nearly 90% of acute (presence) or past EBV infections (absence). When other tests are not available, the search for anti-EA antibodies may therefore be helpful in diagnosing patients with an isolated VCA IgG pattern at screening tests.

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