scholarly journals Evidence of Epstein-Barr Virus Infection Association With Gastric Cancer and Gastroduodenal Diseases

Author(s):  
Arghavan Zebardast ◽  
Maryam Pazhoohan ◽  
Azadeh Yazdani Cherati ◽  
Saghar Saber Amoli ◽  
Yousef Yahyapour ◽  
...  

Abstract Background: Epstein-Barr virus (EBV) is detected in epithelial tumors, such as nasopharyngeal carcinoma and gastric cancer (GC). EBV-associated gastric cancer is a distinct molecular subtype of gastrointestinal carcinomas as defined by Cancer Genome Atlas. This gamma-Herpes virus is present in approximately 10% of gastric carcinomas.Methods: The present study aimed to investigate the presence of EBV genome in gastric cancer and other gastroduodenal diseases either alone or together with Helicobacter pylori (HP). We examined 237 samples from Iranian patients diagnosed with GC and gastroduodenal disease for EBV infection by quantitative Real-Time PCR.Results: Of the 237 samples tested, EBV DNA was detected in 37 samples (15.6%), in 13 of the 81 GC cases (16%), and 24 of the 156 non-cancerous samples (15.4%). All samples containing EBV were gastric cancer of the intestinal type. Of 37 EBV-positive samples, 20 (54.1%) were over 55 years old and 20 (54.1%) were male. The EBV-EBER (EBV-encoded small RNA) DNA copy number in the gastric cancer group (mean = 2.14×10-1 copies/cell) was higher than that in the gastroduodenal disease group (mean = 1.39×10-2 copies/cell), and this difference was statistically significant (P> 0.001). Moreover, the concurrent infections with EBV and HP were detected in 17 out of 35 EBER-positive samples (48.6%), 6 (17/1%) cases were in the gastric cancer group and 11 (31/4%) cases were in the gastroduodenal disease group.Conclusions: In the present study, a high incidence (16%) of EBVaGC was observed in Babol city, Northern Iran. Also, the higher number of copies of EBV EBER DNA in the GC group than in the non-cancer group confirmed the possible role of EBV in inducing cancer. EBVaGC is not endemic in any region and varies in different nations. Therefore, further studies are needed to determine the role of this virus in the development of GC and other gastroduodenal diseases.

2010 ◽  
Vol 138 (5) ◽  
pp. S-438
Author(s):  
Junhong Zhao ◽  
Hongchuan Jin ◽  
Kin-Fai Cheung ◽  
Sui Zhang ◽  
Xiaoxing Li ◽  
...  

Author(s):  
Bert A. ‘t Hart

Abstract Using a non-human primate model of the autoimmune neuroinflammatory disease multiple sclerosis (MS), we have unraveled the role of B cells in the making and breaking of immune tolerance against central nervous system myelin. It is discussed here that B cells prevent the activation of strongly pathogenic T cells present in the naïve repertoire, which are directed against the immunodominant myelin antigen MOG (myelin oligodendrocyte glycoprotein). Prevention occurs via destructive processing of a critical epitope (MOG34-56) through the lysosomal serine protease cathepsin G. This effective tolerance mechanism is abrogated when the B cells are infected with Epstein–Barr virus, a ubiquitous γ1-herpesvirus that entails the strongest non-genetic risk factor for MS.


2021 ◽  
Vol 75 (1) ◽  
pp. 611-619
Author(s):  
Magdalena Dzikowiec ◽  
Dorota Pastuszak-Lewandoska

Abstract It is well established that human body is an ecosystem for numerous microorganisms: bacteria, fungi, eukaryotic parasites, and viruses. They form a “microbiome” that under conditions of homeostasis remains in a friendly mutual relationship with the host. However, the composition and diversity of this microbe community is dynamic and can be changed under the influence of environmental factors, such as diet, antibiotic therapy, lifestyle, and the host’s genotype and immunity. The result of gut microbiome dysbiosis can lead even to cancer. The aim of this review is the description of the healthy gastrointestinal microbiome and the role of two infectious agents: Gram-negative bacteria Helicobacter pylori and Epstein-Barr virus in the development of gastric cancer in terms of gut dysbiosis. H. pylori is the most important pathogen of gastric microbiome with clear impact on its diversity. Coinfection with Epstein-Barr virus causes chronic gastritis, and the inflammatory process is significantly increased. The process of carcinogenesis begins with chronic inflammation that causes atrophic gastritis, intestinal metaplasia, dysplasia, and finally cancer. It has been proven that chronic inflammatory infection caused by infectious agents increases the risk of stomach cancer. Molecular methods that are progressively used to explore the human microbiome provide hope that this knowledge will be used for future diagnoses and therapy in the state of its dysbiosis and in cases of gastric cancer.


2018 ◽  
Vol 39 (2) ◽  
pp. 206 ◽  
Author(s):  
Abolghasem Allahyari ◽  
Sakineh Amoueian ◽  
Armin Attaranzadeh ◽  
Zeinab Gholamimoallem ◽  
Masoud Sadeghi ◽  
...  

2018 ◽  
Author(s):  
Romina C. Vargas-Ayala ◽  
Antonin Jay ◽  
Hector Hernandez-Vargas ◽  
Audrey Diederichs ◽  
Alexis Robitaille ◽  
...  

AbstractHistone modifier lysine (K)-specific demethylase 2B(KDM2B) plays a role in hematopoietic cells differentiation and its expression appears to be deregulated in certain cancers of hematological and lymphoid origins. We have previously found that KDM2B gene is differentially methylated in cell lines derived from the Epstein-Barr virus (EBV) associated endemic Burkitt’s lymphomas (eBL) compared to EBV negative sporadic BL cells. However, whether KDM2B plays a role in eBL development has never been previously demonstrated. Oncogenic viruses have been shown to hijack the host cell epigenome to complete their life cycle and to promote the transformation process by perturbing cell chromatin organization. Here we investigated whether EBV would alter KDM2B levels to enable its life cycle and promote B-cells transformation. We show that infection of B-cells with EBV leads to down-regulation of KDM2B levels. We also show that LMP1, one of the main EBV transforming proteins, induces increased DNMT1 recruitment to KDM2B gene and augments its methylation. By altering KDM2B levels and performing chromatin immunoprecipitation in EBV infected B-cells, we were able to show that KDM2B is recruited to the EBV gene promoters and inhibits their expression. Furthermore, forced KDM2B expression in immortalized B-cells led to altered mRNA levels of some differentiation-related genes. Our data show that EBV deregulates KDM2B levels through an epigenetic mechanism and provide evidence for a role of KDM2B in regulating virus and host cell gene expression, warranting further investigations to assess the role of KDM2B in the process of EBV-mediated lymphomagenesis.IMPORTANCE. In Africa, Epstein-Barr virus infection is associated with endemic Burkitt lymphoma, a pediatric cancer. The molecular events leading to its development are poorly understood compared to the sporadic Burkitt lymphoma. In a previous study, by analyzing the DNA methylation changes in endemic compared to sporadic Burkitt lymphomas cell lines, we identified several differential methylated genomic positions in proximity of genes with a potential role in cancer, among them the KDM2B gene. KDM2B encodes a histone H3 demethylase already shown to be involved in some hematological disorders. However, whether KDM2B plays a role in the development of Epstein-Barr virus-mediated lymphoma has never been investigated before. In this study we show that Epstein-Barr virus deregulates KDM2B expression and describe the underlying mechanisms. We also reveal a role of the demethylase in controlling viral and B-cells genes expression, thus highlighting a novel interaction between the virus and the cellular epigenome.


The prevalence of polymorphism -1486T/C of the TLR-9 gene was studied in 44 patients with chronic Epstein-Barr virus infection (CEBV). The control group for the study of the polymorphisms prevalence of -1486T/C of the TLR-9 gene was 40 healthy donors. Three main genotypes of -1486T/C of the TLR-9 gene were identified based on the obtained results – TT, TC, CC. Investigation of the occurrence frequency of individual genotypes revealed the dominance of the TC genotype, compared with the homozygous TT and CC genotypes. The study of -1486T/C of the TLR-9 gene polymorphism frequency distribution for different genotypes demonstrated the specificity of changes in the TC genotype in patients with CEBV and the absence of such for the TT and CC genotypes. These results confirm the important role of the TLR-mediated signaling in the pathogenesis of the disease, which is necessary to determine the genetic background associated with the course of the disease and its possible consequences. These are the aspects that will further enable the identification of risk groups among such patients and provide timely therapy. The analysis of the results of the -1486T/C polymorphism of the TLR-9 gene revealed three main genotypes –TT, TC, CC. Investigation of the occurrence frequency of individual genotypes revealed the dominance of the genotype TC, compared with the homozygous genotypes of TT and CC. The study of frequency distribution of the polymorphism -1486T/C of TLR-9 for different genotypes demonstrated the specificity of changes in the TC genotype and the absence of suchin the TT and CC genotypes in patients with CEBV.Our study for the purpose of determining the 1486T/C polymorphism of the TLR-9, that is associated with chronic forms of CEBV infection, confirms the important role of TLR-mediated signaling in the pathogenesis of this disease, which is necessary to determine the genetic background associated with the course of the disease and possible consequences of CEBV. These aspects will further enable the identification of risk groups among such patients and provide timely therapy.Analysis of the results allowed establishing the following:1. The 1486T/C polymorphism of the TLR-9 gene is significantly more frequent in patients with CEBV than in the control.2. The frequency distribution of the -1486T/C polymorphism ofthe TLR-9 gene allowed the establishment of the association of the genotype TC with chronic forms of the EBV infection, which is very specific for this group of patients.


2020 ◽  
Vol 47 (2-3) ◽  
pp. 127-137 ◽  
Author(s):  
Agnieszka Pikuła ◽  
Magdalena Kwietniewska ◽  
Karol Rawicz-Pruszyński ◽  
Bogumiła Ciseł ◽  
Magdalena Skórzewska ◽  
...  

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