scholarly journals Epstein–Barr Virus and Helicobacter Pylori Co-Infection in Non-Malignant Gastroduodenal Disorders

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 104 ◽  
Author(s):  
Ramsés Dávila-Collado ◽  
Oscar Jarquín-Durán ◽  
Le Thanh Dong ◽  
J. Luis Espinoza
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Infection Rate ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Pubmed Database ◽  
Epstein Barr ◽  
H Pylori ◽  
Gastroduodenal Disorders

Epstein–Barr virus (EBV) and Helicobacter pylori (H. pylori) are two pathogens associated with the development of various human cancers. The coexistence of both microorganisms in gastric cancer specimens has been increasingly reported, suggesting that crosstalk of both pathogens may be implicated in the carcinogenesis process. Considering that chronic inflammation is an initial step in the development of several cancers, including gastric cancer, we conducted a systematic review to comprehensively evaluate publications in which EBV and H. pylori co-infection has been documented in patients with non-malignant gastroduodenal disorders (NMGDs), including gastritis, peptic ulcer disease (PUD), and dyspepsia. We searched the PubMed database up to August 2019, as well as publication references and, among the nine studies that met the inclusion criteria, we identified six studies assessing EBV infection directly in gastric tissues (total 949 patients) and three studies in which EBV infection status was determined by serological methods (total 662 patients). Due to the substantial methodological and clinical heterogeneity among studies identified, we could not conduct a meta-analysis. The overall prevalence of EBV + H. pylori co-infection in NMGDs was 34% (range 1.8% to 60%). A higher co-infection rate (EBV + H. pylori) was reported in studies in which EBV was documented by serological methods in comparison with studies in which EBV infection was directly assessed in gastric specimens. The majority of these studies were conducted in Latin-America and India, with most of them comparing NMGDs with gastric cancer, but there were no studies comparing the co-infection rate in NMGDs with that in asymptomatic individuals. In comparison with gastritis caused by only one of these pathogens, EBV + H. pylori co-infection was associated with increased severity of gastric inflammation. In conclusion, only relatively small studies testing EBV and H. pylori co-infection in NMGDs have been published to date and the variable report results are likely influenced by geographic factors and detection methods.

scholarly journals Helicobacter pylori and Epstein-Barr Virus Coinfection Stimulates Aggressiveness in Gastric Cancer through the Regulation of Gankyrin

mSphere ◽  
2021 ◽  
Author(s):  
Dharmendra Kashyap ◽  
Budhadev Baral ◽  
Shweta Jakhmola ◽  
Anil Kumar Singh ◽  
Hem Chandra Jha
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Epstein Barr Virus ◽  
Synergistic Effects ◽  
Gastric Epithelial Cells ◽  
Content Type ◽  
Barr Virus ◽  
Epstein Barr ◽  
H Pylori

In the present study, we evaluated the synergistic effects of EBV and H. pylori infection on gastric epithelial cells in various coinfection models. These coinfection models were among the first to depict the exposures of gastric epithelial cells to EBV followed by H. pylori ; however, coinfection models exist that narrated the scenario upon exposure to H. pylori followed by that to EBV.

scholarly journals Gastric Cancer and Associated Pathogens: Is There Any Association in Moroccan Region?

2021 ◽  
Author(s):  
Samia Alaoui Boukhris ◽  
Mounia El khadir ◽  
Safae Karim ◽  
Tiatou Souho ◽  
Dafr-Allah Benajah ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Retrospective Study ◽  
Epstein Barr Virus ◽  
University Hospital ◽  
Cancer Development ◽  
Barr Virus ◽  
Epstein Barr ◽  
H Pylori

Abstract Purpose: Helicobacter pylori, Epstein-Barr virus and human papillomavirus are three pathogens associated with various human cancers. This study aimed to investigate the role of these pathogens in gastric cancer in Moroccan population Methods: For this, a retrospective study has been conducted on participants attending the gastroenterology department of Hassan II University Hospital of Fez. A total of 279 participants were enrolled. H. pylori, EBV and HPV were detected and genotyped by PCR.Results: A significant association has been established between H. pylori, EBV and gastric cancer. 93.4% and 43.3% of gastric cancer cases are related to H. pylori and EBV respectively (p≤0.01). H. pylori-EBV co-infection is responsible of 31.6% of gastric cancer cases (p<0.01). Correlation between pathogens genotypes and gastric cancer shows 55.6% of GC EBV positives are carrying the 30bp deletion in LMP1gene, while 16% of gastric cancers cases are carrying high-risk genotypes of HPV (p=0.21). Conclusion: The obtained results highlight the possible role of co-infection in gastric cancer development.

scholarly journals Helicobacter pylori and Epstein-Barr virus coinfection stimulates the aggressiveness in gastric cancer through the regulation of gankyrin

2020 ◽  
Author(s):  
Dharmendra Kashyap ◽  
Budhadev Baral ◽  
Nidhi Varshney ◽  
Anil Kumar Singh ◽  
Hem Chandra Jha
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Molecular Mechanism ◽  
Epstein Barr Virus ◽  
Gastric Epithelial Cells ◽  
Carcinogenic Activity ◽  
Barr Virus ◽  
Epstein Barr ◽  
H Pylori

AbstractPersistent coinfection of Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV) promotes aggressive gastric carcinoma. The molecular mechanisms underlying the aggressiveness in H. pylori and EBV coinfected gastric cancer is not well characterized. In the current study, we investigated the molecular mechanism involved in the cooperation of H. pylori and EBV-driven proliferation of gastric epithelial cells. Results showed that the coinfections are significantly more advantageous to the pathogens to create a microenvironment that favors the higher pathogen-associated gene expression. The EBV latent genes EBNA1 and EBNA3C are highly overexpressed in the coinfections compared to individual EBV infection at different time points (12 and 24 hrs). The H. pylori-associated genes 16s rRNA, CagA, and BabA has also been highly overexpressed in coinfections compared to H. pylori alone. Gankyrin is a small protein of 25 KDa involved in multiple biological and physiological processes. The upregulation of gankyrin modulates the various cell signaling pathways, leading to oncogenesis. The gankyrin shows a similar expression pattern as EBNA3C at both transcript and protein levels, suggesting a possible correlation. Further EBV and H. pylori create microenvironments that induce cell transformation and oncogenesis by dysregulation of the cell-cycle regulator, GC marker, cell migration, DNA response, and antiapoptotic genes in infected gastric epithelial cells by enhancing the expression of gankyrin. Our study provides new insights into the molecular mechanism where the interplay between two oncogenic agents (H. pylori and EBV) leads to the enhanced carcinogenic activity of gastric epithelial cells through overexpression of oncoprotein gankyrin.ImportanceIn the present study, we have evaluated the synergistic effect of EBV and H. pylori infection on gastric epithelial cells in various coinfection models. These coinfection models depict the first exposures of gastric epithelial cells with EBV and then the H. pylori. While other coinfection models narrated the first exposures of H. pylori followed by the infection of EBV. This led to an enhanced oncogenic phenotype in gastric epithelial cells. We determined the coinfection of EBV and H. pylori enhanced the expression of oncogenic protein gankyrin. The interplay between EBV and H. pylori promotes the oncogenic properties of AGS cells through the newly discovered oncoprotein gankyrin. EBV and H. pylori mediated upregulation of gankyrin further dysregulates various cancer-associated hallmarks of genes such as cell-migratory, gastric cancer marker, tumor suppressor, DNA damage response, and proapoptotic genes.

scholarly journals Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Charu Sonkar ◽  
Tarun Verma ◽  
Debi Chatterji ◽  
Ajay Kumar Jain ◽  
Hem Chandra Jha
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epstein Barr Virus ◽  
Morphological Changes ◽  
Ags Cells ◽  
Barr Virus ◽  
Apoptotic Genes ◽  
Epstein Barr ◽  
H Pylori

Abstract Background Helicobacter pylori (H. pylori) and Epstein - Barr virus (EBV) plays a significant role in aggressive gastric cancer (GC). The investigation of genes associated with these pathogens and host kinases may be essential to understand the early and dynamic progression of GC. Aim The study aimed to demonstrate the coinfection of EBV and H. pylori in the AGS cells through morphological changes, expression of the kinase and the probable apoptotic pathways. Methods Genomic DNA isolation of H. pylori and its characterization from clinical samples were performed. RT-qPCR of kinases was applied to scrutinize the gene expression of kinases in co-infected GC in a direct and indirect (separated through insert size 0.45 μm) H. pylori infection set up. Morphological changes in co-infected GC were quantified by measuring the tapering ends of gastric epithelial cells. Gene expression profiling of apoptotic genes was assessed through RT-qPCR. Results An interleukin-2-inducible T-cell kinase (ITK) showed significant upregulation with indirect H. pylori infection. Moreover, Ephrin type-B receptor six precursors (EPHB6) and Tyrosine-protein kinase Fyn (FYN) showed significant upregulation with direct coinfection. The tapering ends in AGS cells were found to be extended after 12 h. A total of 24 kinase genes were selected, out of which EPHB6, ITK, FYN, and TYK2 showed high expression as early as 12 h. These kinases may lead to rapid morphological changes in co-infected gastric cells. Likewise, apoptotic gene expression such as APAF-1 and Bcl2 family genes such as BAD, BID, BIK, BIM, BAX, AND BAK were significantly down-regulated in co-infected AGS cells. Conclusion All the experiments were performed with novel isolates of H. pylori isolated from central India, for the functional assessment of GC. The effect of coinfection with EBV was more profoundly observed on morphological changes in AGS cells at 12 h as quantified by measuring the tapering of ends. This study also identifies the kinase and apoptotic genes modulated in co-infected cells, through direct and indirect approaches. We report that ITK, EPHB6, TYK2, FYN kinase are enhanced, whereas apoptotic genes such as APAF-1, BIK, FASL, BAX are significantly down-regulated in AGS cells coinfected with EBV and H. pylori.

scholarly journals MicroRNA Changes in Gastric Carcinogenesis: Differential Dysregulation during Helicobacter pylori and EBV Infection

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 597
Author(s):  
Christian Prinz ◽  
Kemal Mese ◽  
David Weber
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Carcinogenesis ◽  
Barr Virus ◽  
Ebv Infection ◽  
Mrna Targets ◽  
Epstein Barr ◽  
Clinically Significant ◽  
C Complex ◽  
H Pylori

Despite medical advances, gastric-cancer (GC) mortality remains high in Europe. Bacterial infection with Helicobacter pylori (H. pylori) and viral infection with the Epstein–Barr virus (EBV) are associated with the development of both distal and proximal gastric cancer. Therefore, the detection of these infections and the prediction of further cancer development could be clinically significant. To this end, microRNAs (miRNAs) could serve as promising new tools. MiRNAs are highly conserved noncoding RNAs that play an important role in gene silencing, mainly acting via translational repression and the degradation of mRNA targets. Recent reports demonstrate the downregulation of numerous miRNAs in GC, especially miR-22, miR-145, miR-206, miR-375, and miR-490, and these changes seem to promote cancer-cell invasion and tumor spreading. The dysregulation of miR-106b, miR-146a, miR-155, and the Let-7b/c complex seems to be of particular importance during H. pylori infection or gastric carcinogenesis. In contrast, many reports describe changes in host miRNA expression and outline the effects of bamHI-A region rightward transcript (BART) miRNA in EBV-infected tissue. The differential regulation of these miRNA, acting alone or in close interaction when both infections coexist, may therefore enable us to detect cancer earlier. In this review, we focus on the two different etiologies of gastric cancer and outline the molecular pathways through which H. pylori- or EBV-induced changes might synergistically act via miR-155 dysregulation to potentiate cancer risk. The three markers, namely, H. pylori presence, EBV infection, and miR-155 expression, may be checked in routine biopsies to evaluate the risk of developing gastric cancer.

scholarly journals Prevalence of Gastric Cancer Associated with the Epstein-Barr Virus at Brazzaville Chu

2021 ◽  
Vol 11 (9) ◽  
pp. 137-141
Author(s):  
Fidele Mambouene ◽  
Anicet Boumba ◽  
Fabien Mouamba
Keyword(s):  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Key Words ◽  
Infection Rate ◽  
Epstein Barr Virus ◽  
Gastric Carcinomas ◽  
Barr Virus ◽  
Ebv Infection ◽  
Preliminary Study ◽  
Epstein Barr

Introduction: Several studies have shown an association between infection with Epstein-Barr virus (EBV) and the occurrence of many cancers in humans, including certain gastric carcinomas (GC). Indeed, recent studies have reported that 10% of CGs are associated with EBV. Materials and Methods: Samples of gastric carcinomatous tissues (biopsies and surgical specimens) were analyzed by PCR for the detection of EBV. Samples were collected retrospectively between January 2008 and December 2018. Results: during this period, 52 samples were analyzed. PCR results show the EBV infection rate to be 3.8%. Conclusion: The results obtained during this preliminary study confirm the association of EBV in 3.8% of CG cases, which is consistent with the data in the literature. Key words: EBV, gastric carcinoma, PCR.

scholarly journals Helicobacter pylori and Epstein–Barr Virus Infection in Gastric Diseases: Correlation with IL-10 and IL1RN Polymorphism

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Fasciana Teresa ◽  
Nicola Serra ◽  
Giuseppina Capra ◽  
Chiara Mascarella ◽  
Cesare Gagliardi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Epstein Barr Virus ◽  
Normal Gastric Mucosa ◽  
Gastric Diseases ◽  
Barr Virus ◽  
Genes Encoding ◽  
Epstein Barr

Introduction. Helicobacter pylori and Epstein–Barr virus (EBV) infection have recently been shown to be associated with gastric diseases. Polymorphisms in genes encoding cytokines such as interleukin 10 (IL-10) and interleukin 1 Receptor (IL-1RN) influence cytokine secretion levels and appear to contribute to the risk of developing gastroduodenal diseases. To our knowledge, this is the first preliminary study to address the association of coinfection with H. pylori and EBV and their correlation with genetic predisposition in the development of gastric diseases. Methods. Gastric biopsy samples of 96 patients with different gastric diseases were used. Results. Our results showed that the rate of coinfection was higher in patients with gastric cancer than in patients with normal gastric mucosa, active chronic gastritis, and MALT lymphoma. As regards the characterization of H. pilory strains, the polymorphism s1m1i1 of vacA gene was more frequent in patients with MALT Lymphoma in comparison to others, while the polymorphism s2m2i2 was most frequent in patients with normal gastric mucosa. In addition, patients who tested positive for the cagA gene were more frequently those affected with gastric cancer than those with inactive chronic gastritis. Similarly, the patients with oipA gene ON were more frequently those with gastric cancer than those with inactive chronic gastritis. Conclusion. According to our analysis, there was no correlation between coinfection and polymorphisms in genes encoding IL-10 and IL-1RN. We conclude that various factors can be involved in the development of gastric diseases.

scholarly journals Clinicopathologic Characteristics of Epstein–Barr Virus-Associated Gastric Cancer Over the Past Decade in Japan

2019 ◽  
Vol 7 (9) ◽  
pp. 305 ◽  
Author(s):  
Yanagi ◽  
Nishikawa ◽  
Shimokuri ◽  
Shuto ◽  
Takagi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Epstein Barr Virus ◽  
Clinicopathologic Characteristics ◽  
Barr Virus ◽  
Ebv Infection ◽  
The Past ◽  
Lymphoid Stroma ◽  
Human Herpes Virus ◽  
Epstein Barr

: Epstein–Barr virus (EBV) is a ubiquitous human herpes virus, but related with several types of malignancies. Among EBV-related malignancies, EBV-associated gastric carcinoma (EBVaGC) has the largest patient’s number. We screened for EBV infection in 1067 GC lesions of 1132 patients who underwent surgical resection from 2007 to 2017 in Japan and examined clinicopathological features of EBVaGC. EBV infection was detected by in situ hybridization with EBV-encoded small RNA 1(EBER-1 ISH). EBV was infected in 80 GC lesions (7.1%). Mean age was significantly lower in patients with EBVaGC than with EBV-negative GC. EBVaGC was more frequent in men than in women. EBVaGC was found twice as frequent in the upper or middle stomach as in the lower stomach. Early EBVaGC was more frequent, and submucosally invaded cases were dominant. The presence of lymphatic vessel invasion was less in EBVaGC, but frequency of lymph node metastasis was similar. Carcinoma with lymphoid stroma (CLS) was found in 3.8% (43/1132) of all lesions with 60.5% of EBV positivity. The synchronous or metachronous multiple GC was frequent in EBVaGC. We clarified clinicopathologic characteristics of EBVaGC over the past decade in Japan. EBV infection should be examined in gastric cancer cases showing these characteristics.

Epstein-Barr virus associated gastric carcinoma at the United States-Mexico border: A single institution study.

2020 ◽  
Vol 38 (4_suppl) ◽  
pp. 440-440
Author(s):  
Sumit Gaur ◽  
Ramadevi Subramani ◽  
Meghan Mcalice ◽  
Osvaldo Padilla ◽  
Brenda Sofia Castillo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
In Situ Hybridization ◽  
Epstein Barr Virus ◽  
El Paso ◽  
Safety Net ◽  
Routine Testing ◽  
Barr Virus ◽  
Epstein Barr ◽  
H Pylori

440 Background: Globally, gastric cancer (GC) is the fourth most prevalent cancer, and the second leading cause of cancer related deaths. Epstein-Barr virus is implicated in the pathogenesis of 5-10% of gastric cancers. Based upon the results obtained from of the cancer genome atlas, EBV related GC is characterized by promoter hypermethylation, PIK3CA mutations (80%) and increased expression of PD-1 and PD-L1, making it an attractive target for molecularly targeted therapy and immunotherapeutic options. As such, a case can be made for routine testing for EBV in all GC patients. University medical center, El Paso is a tax payer funded safety net health system in El Paso country, TX. We conducted a pilot study to characterize the prevalence of EBV associated gastric cancer seen at this facility. Methods: After obtaining institutional review board (IRB) approval, we identified cases of GC that were diagnosed between January 1, 2008- and December 31-2017. A total of 104 cases were identified of which 17 samples were randomly selected. Pathology specimens were reviewed to identify grade, subtype (intestinal vs diffuse), degree of lymphocytic infiltration and presence/absence of H. pylori. Representative sections from archived tumors were used to perform in-situ hybridization to look for the presence of Epstein-Barr virus. Samples were analyzed using the Rembrandt In situ Hybridization and Detection Universal RISH& HRP Detection Kit for Epstein-Barr early RNA. Results: The median age of the 17 patients is 63 years with 59% being males. 95% self identified as Hispanic. 41% were smokers, 18% used alcohol. The mean BMI was 27.3. Forty one percent of gastric cancer cases were found in the body, 29% in the antrum, 12% in the cardia, and 6% in the fundus. Forty one percent of cases were Stage IV, 24% stage II, 17% Stage III and 17% Stage I. 95% of cases were high grade, 53% of them had signet ring features. 18% of samples were H. pylori positive. None of the seventeen samples tested positive for EBV. Conclusions: EBV does not seem to contribute significantly to the pathogenesis of gastric cancer in our local population. As such routine testing for EBV in all gastric cancer patients may not be a cost effective utilization of resources at our hospital.

Sign in / Sign up

Export Citation Format

Share Document