Pathogenetic role of Epstein-Barr Virus in relation to tumour cell characteristics of nasal T/NK-cell lymphomas

1997 ◽  
Author(s):  
Kwok-shing, Alan Chiang
Keyword(s):  
Tumour Cell ◽  
Epstein Barr Virus ◽  
Nk Cell ◽  
Pathogenetic Role ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Initial Characterization of the Epstein–Barr Virus BSRF1 Gene Product

Viruses ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 285 ◽  
Author(s):  
Yusuke Yanagi ◽  
H. Masud ◽  
Takahiro Watanabe ◽  
Yoshitaka Sato ◽  
Fumi Goshima ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Nk Cell ◽  
Artificial Chromosome ◽  
Immunofluorescence Assay ◽  
Lytic Replication ◽  
Reading Frame ◽  
Barr Virus ◽  
Epstein Barr ◽  
Simplex Virus

Epstein–Barr virus (EBV) is a ubiquitous virus that causes infectious mononucleosis and several types of cancer, such as Burkitt lymphoma, T/NK-cell lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, it encodes more than 80 genes, many of which have not been characterized. EBV BamHI S rightward reading frame 1 (BSRF1) encodes a tegument protein that, unlike its homologs herpes simplex virus unique long 51 (UL51) and human cytomegalovirus UL71, has not been extensively investigated. To examine the role of BSRF1, we prepared knockout and revertant strains using the bacterial artificial chromosome system. Unexpectedly, the disruption of the gene had little or no effect on EBV lytic replication and the transformation of primary B cells. However, the knockdown of BSRF1 in B95-8 cells decreased progeny production. An immunofluorescence assay revealed that BSRF1 localized to the Golgi apparatus in the cytoplasm, as did its homologs. BSRF1 also associated with BamHI G leftward reading frame 3.5 (BGLF3.5), BamHI B rightward reading frame 2 (BBRF2), and BamHI A leftward reading frame 1 (BALF1), and BALF1 was incorporated into the tegument fraction with BSRF1. Taken together, our results indicate that BSRF1 plays a role in secondary envelopment or virion egress in the cytoplasm, as do its homolog genes.

scholarly journals Deciphering the role of Epstein-Barr virus in the pathogenesis of T and NK cell lymphoproliferations

Herpesviridae ◽  
2011 ◽  
Vol 2 (1) ◽  
pp. 8 ◽  
Author(s):  
Christopher P Fox ◽  
Claire Shannon-Lowe ◽  
Martin Rowe
Keyword(s):  
Epstein Barr Virus ◽  
Nk Cell ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Original paper Evaluation of the role of Epstein-Barr virus in cases of nodal or extranodal T- and NK-cell lymphoma using eber in situ hybridization

2015 ◽  
Vol 2 ◽  
pp. 161-169 ◽  
Author(s):  
Serap Karaarslan ◽  
Mine Hekimgil ◽  
Saliha Soydan ◽  
Yesim Ertan ◽  
Başak Doğanavşargil
Keyword(s):  
In Situ Hybridization ◽  
Epstein Barr Virus ◽  
Nk Cell ◽  
Cell Lymphoma ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Role of latent membrane protein 1 in chronic active Epstein–Barr virus infection‐derived T/NK‐cell proliferation

2014 ◽  
Vol 3 (4) ◽  
pp. 787-795 ◽  
Author(s):  
Takuto Ito ◽  
Hidetaka Kawazu ◽  
Takayuki Murata ◽  
Seiko Iwata ◽  
Saki Arakawa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epstein Barr Virus ◽  
Nk Cell ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Epstein Barr ◽  
Barr Virus Infection

Lack of Evidence of Pathogenetic Role of Epstein-Barr Virus in Thymic Lymphoid Hyperplasia and Thymomas in the Chinese Population of Hong Kong

1994 ◽  
Vol 2 (1) ◽  
pp. 17-22 ◽  
Author(s):  
John K. C. Chan ◽  
Timothy T. C. Yip ◽  
William Y. W. Tsang ◽  
S. Seneviratne ◽  
Y.F. Poon ◽  
...  
Keyword(s):  
Hong Kong ◽  
Chinese Population ◽  
Epstein Barr Virus ◽  
Lymphoid Hyperplasia ◽  
Pathogenetic Role ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Molecular Genetics in Epstein–Barr Virus-Associated Malignancies

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 593
Author(s):  
Srikanth Umakanthan ◽  
Maryann M Bukelo
Keyword(s):  
Epstein Barr Virus ◽  
Diagnostic Tools ◽  
Main Role ◽  
Genetic Changes ◽  
Barr Virus ◽  
Cancer Pathogenesis ◽  
Genomic Studies ◽  
Epstein Barr ◽  
Oncogenic Form

Global genomic studies have detected the role of genomic alterations in the pathogenesis of Epstein–Barr virus (EBV)-associated tumors. EBV oncoproteins cause a vital shift of EBV from an infectious virus to an oncogenic form during the latent and lytic phase within the lymphoid B cells and epithelial cells. This epigenetic alteration modulates the virus and host genomes and inactivates and disrupts numerous tumor suppressors and signaling pathways. Genomic profiling has played the main role in identifying EBV cancer pathogenesis and its related targeted therapies. This article reviews the role of genetic changes in EBV-associated lymphomas and carcinomas. This includes the prolific molecular genesis, key diagnostic tools, and target-specific drugs that have been in recent clinical use.

EBV load is associated with cfDNA fragmentation and renal damage in SLE patients

Lupus ◽  
2021 ◽  
pp. 096120332110103
Author(s):  
Anna Truszewska ◽  
Agnieszka Wirkowska ◽  
Kamila Gala ◽  
Piotr Truszewski ◽  
Łucja Krzemień-Ojak ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Renal Damage ◽  
Healthy Individuals ◽  
Pcr Assay ◽  
Barr Virus ◽  
Fragmentation Index ◽  
Epstein Barr

Background For long Epstein–Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. Methods Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. Results SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(–) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(–) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). Conclusions We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.

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