Co-infection with<i>Helicobacter pylori</i>and Epstein–Barr virus in benign upper digestive diseases: An endoscopic and serologic pilot study

Buzás, György Miklós; Konderák, Judith

doi:10.1177/2050640615610265

Cited by 9 publications

(7 citation statements)

References 30 publications

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“…However, EBV coinfection causes methylation of host SHP 1 and prevents its dephosphorylation activity of CagA and thus may increase oncogenic potential of CagA [199]. Further, a study suggested that both EBV and H. pylori coinfection were ominously more dominant in intestinal ulcer patients compared to GERD and dyspepsia patients [291]. H. pylori positive patients show increased anti-EBV IgG titre which suggests H. pylori role in augmenting EBV DNA load and higher immune responses [291].…”

Section: Ebv and H Pylori Factors Contributing To The Developmentmentioning

confidence: 99%

“…Further, a study suggested that both EBV and H. pylori coinfection were ominously more dominant in intestinal ulcer patients compared to GERD and dyspepsia patients [291]. H. pylori positive patients show increased anti-EBV IgG titre which suggests H. pylori role in augmenting EBV DNA load and higher immune responses [291]. However, some study is also available which suggested that H. pylori attenuated TGF- β expression which reactivates EBV lytic phase and might play a role in preventing EBV lytic reactivation and preventing GC [292].…”

Section: Ebv and H Pylori Factors Contributing To The Developmentmentioning

confidence: 99%

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Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Singh

Jha

2017

Journal of Oncology

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Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett's lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.

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Section: Ebv and H Pylori Factors Contributing To The Developmentmentioning

confidence: 99%

Section: Ebv and H Pylori Factors Contributing To The Developmentmentioning

confidence: 99%

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Singh

Jha

2017

Journal of Oncology

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“…We identified three studies in which EBV infection status was assessed by serological methods ( Table 2). A prospective study conducted in Hungary assessed the prevalence of H. pylori and EBV co-infection in 104 patients aged between 18 and 80 years with benign upper digestive diseases, as confirmed by endoscopy [43]. EBV infection status was assessed by serology and H. pylori infection was determined by the modified Giemsa stain and by IgG-chemiluminescence.…”

Section: Studies Assessing Ebv By Serological Methodsmentioning

confidence: 99%

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

Dávila-Collado¹,

Jarquín-Durán²,

Dong

et al. 2020

Pathogens

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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.

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“…For example, the Epstein‐Barr virus (EBV) is another well‐known contributor to the development of gastric cancer 66 . Previous studies showed co‐infection with H pylori and EBV was commonly seen in the clinical scenario and that dual infection was associated with more severe gastric lesions 67‐69 . Mechanistically, previous in vitro experiments showed that persistent H pylori infection downregulated virus‐specific cytotoxic T‐cell responses, thereby assisting in viral infection 70 .…”

Section: Future Directionsmentioning

confidence: 99%

Helicobacter pylori infection and eradication: Exploring their impacts on the gastrointestinal microbiota

2020

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The rapid development of microbiota research has remolded our view of human physiological and pathological processes. Among all the gastrointestinal microorganisms, Helicobacter pylori (H pylori) is probably the most notorious constituent. Although half of the adults worldwide are infected with H pylori, their clinical manifestations vary widely, suggesting other microorganisms beyond H pylori may play a role in determining clinical outcomes. Recently, many studies have put effort into elucidating the crosstalk within the human microbiota, some of which specifically explored the interplay between H pylori and other gastrointestinal microbial members. In this work, we reviewed these potential interactions. Meanwhile, the impacts of H pylori eradication therapy on gastrointestinal microbial homeostasis were summarized in terms of diversity, composition, functional capacity, and antibiotic resistance.

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Co-infection withHelicobacter pyloriand Epstein–Barr virus in benign upper digestive diseases: An endoscopic and serologic pilot study

Abstract: Both Helicobacter pylori and Epstein-Barr virus, and co-infection with these agents, were significantly more prevalent in duodenal ulcer patients than in dyspeptic/reflux patients.

Cited by 9 publications

References 30 publications

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

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

Helicobacter pylori infection and eradication: Exploring their impacts on the gastrointestinal microbiota

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