Expression of VCA (viral capsid antigen) and EBNA1 (Epstein–Barr-virus-encoded nuclear antigen 1) genes of Epstein–Barr virus in Pichia pastoris and application of the products in a screening test for patients with nasopharyngeal carcinoma

2007 ◽  
Vol 47 (1) ◽  
pp. 59 ◽  
Author(s):  
Guoqiang Hong ◽  
Bo Hu ◽  
Zhaoxia Li ◽  
Jue Xu ◽  
Zhenyu Zhu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Pichia Pastoris ◽  
Screening Test ◽  
Epstein Barr Virus ◽  
Nuclear Antigen ◽  
Viral Capsid ◽  
Viral Capsid Antigen ◽  
Barr Virus ◽  
Epstein Barr

Evaluation of the abbot Architect™ epstein-barr virus viral capsid antigen IgM, viral capsid antigen IgG and nuclear antigen IgG assays in a pediatric and adult population

2016 ◽  
Vol 81 ◽  
pp. 1-5 ◽  
Author(s):  
Simon Grandjean Lapierre ◽  
Emilie Vallières ◽  
Leila Rabaamad ◽  
Manon Labrecque ◽  
Caroline Chartrand ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Adult Population ◽  
Nuclear Antigen ◽  
Viral Capsid ◽  
Viral Capsid Antigen ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Combination of Plasma MIF and VCA-IgA Improves the Diagnostic Specificity for Patients With Nasopharyngeal Carcinoma

2020 ◽  
Vol 19 ◽  
pp. 153303382093577
Author(s):  
Ning Xue ◽  
Shan Xing ◽  
Weiguo Ma ◽  
Jiahe Sheng ◽  
Zhiliang Huang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Epstein Barr Virus ◽  
Inhibitory Factor ◽  
Viral Capsid ◽  
Macrophage Migration ◽  
Viral Capsid Antigen ◽  
Barr Virus ◽  
Epstein Barr

Introduction: The purpose of this study is to evaluate the diagnostic value of macrophage migration inhibitory factor in patients with nasopharyngeal carcinoma. Materials and Methods: The expression levels of macrophage migration inhibitory factor in nasopharyngeal carcinoma cell lines, tumor tissues, and plasma were measured by real-time polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry. Plasma Epstein-Barr virus viral capsid antigen was determined by immunoenzymatic techniques. Results: Both the messenger RNA and protein expression levels of macrophage migration inhibitory factor were upregulated in nasopharyngeal carcinoma cell lines and nasopharyngeal carcinoma tissues. Macrophage migration inhibitory factor in plasma was significantly elevated in patients with nasopharyngeal carcinoma compared to Epstein-Barr virus viral capsid antigen–negative and Epstein-Barr virus viral capsid antigen–positive healthy donors. The combination of macrophage migration inhibitory factor and Epstein-Barr virus viral capsid antigen was better for diagnosing nasopharyngeal carcinoma (area under receiver operating characteristic curve = 0.925, 95% CI: 0.898-0.951) than macrophage migration inhibitory factor (area under receiver operating characteristic curve = 0.778, 95% CI: 0.732-0.824) and Epstein-Barr virus viral capsid antigen. Combining macrophage migration inhibitory factor and Epstein-Barr virus viral capsid antigen had higher specificity (82.40% vs 69.96%) and higher positive predictive value (79.17% vs 67.44%) without an obvious reduction in sensitivity (95.25%) compared to Epstein-Barr virus viral capsid antigen alone. Macrophage migration inhibitory factor was highly expressed in nasopharyngeal carcinoma cell lines, whereas it was not associated with Epstein-Barr virus infection. The level of macrophage migration inhibitory factor in plasma was not related to the titer of Epstein-Barr virus viral capsid antigen. Conclusion: The combination of macrophage migration inhibitory factor and Epstein-Barr virus viral capsid antigen increases the specificity and positive predictive value of detecting nasopharyngeal carcinoma and improves the diagnostic accuracy of nasopharyngeal carcinoma in high-risk individuals.

scholarly journals Epstein-Barr virus glycoprotein gH/gL antibodies complement IgA-viral capsid antigen for diagnosis of nasopharyngeal carcinoma

Oncotarget ◽  
2016 ◽  
Vol 7 (13) ◽  
pp. 16372-16383 ◽  
Author(s):  
Rui-Chen Li ◽  
Yong Du ◽  
Qiu-Yao Zeng ◽  
Lin-Quan Tang ◽  
Hua Zhang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Viral Capsid ◽  
Viral Capsid Antigen ◽  
Virus Glycoprotein ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Mechanisms of Epstein‐Barr virus nuclear antigen 1 favor Tregs accumulation in nasopharyngeal carcinoma

2020 ◽  
Vol 9 (15) ◽  
pp. 5598-5608
Author(s):  
Jie Wang ◽  
Yunfan Luo ◽  
Pei Bi ◽  
Juan Lu ◽  
Fan Wang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Curcumin Inhibits Proliferation of Epstein–Barr Virus-Associated Human Nasopharyngeal Carcinoma Cells by Inhibiting EBV Nuclear Antigen 1 Expression

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Limei Liu ◽  
Jiaomin Yang ◽  
Wuguang Ji ◽  
Chao Wang
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Lytic Replication ◽  
Nuclear Antigen ◽  
Mrna Levels ◽  
Curcumin Treatment ◽  
Antitumor Effects ◽  
Barr Virus ◽  
Cycle Arrest ◽  
Epstein Barr

This investigation aims to study the effect of curcumin on the proliferation, cycle arrest, and apoptosis of Epstein–Barr virus- (EBV-) positive nasopharyngeal carcinoma (NPC) cells. EBV+ NPC cells were subjected to curcumin treatment. The cell viability was evaluated with the CCK-8. Cell cycle and apoptosis were analyzed by flow cytometry analysis. Expression (protein and mRNA) levels were detected with western blotting and quantitative real-time PCR, respectively. Curcumin efficiently reduced the viability of EBV+ NPC cells. Curcumin induced the cycle arrest of the HONE1 and HK1-EBV cells positive for EBV. Moreover, curcumin treatment promoted the NPC cell apoptosis, via the mitochondria- and death receptor-mediated pathways. Furthermore, curcumin decreased the expression of EBNA1 in the HONE1 and HK1-EBV cells and inhibited the transcriptional level of EBNA1 in the HeLa cells. Curcumin induced EBNA1 degradation via the proteasome-ubiquitin pathway. In addition, curcumin inhibited the proliferation of HONE1 and HK1-EBV cells positive for EBV, probably by decreasing the expression level of EBNA1. In both the HONE1 and HK1-EBV cells, curcumin inhibited the EBV latent and lytic replication. Curcumin could reduce the EBNA1 expression and exert antitumor effects against NPC in vitro.

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