Helicobacter pylori-associated oxidant monochloramine induces reactivation of Epstein–Barr virus (EBV) in gastric epithelial cells latently infected with EBV

Minoura-Etoh, Junko; Gotoh, Kazuyo; Sato, Ryugo; Ogata, Masao; Kaku, Nobuhiro; Fujioka, Toshio; Nishizono, Akira

doi:10.1099/jmm.0.46580-0

Cited by 57 publications

(45 citation statements)

References 24 publications

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“…In fact, several studies that address the effect and interaction between them do not detected any association [20, 23, 46–49]. However, there are others publications showing synergism between EBV and H. pylori in the pathogenesis of gastric diseases [30, 50–53]. In point of fact, it is suggested two possible mechanisms, first an additional inflammatory response in co-infection and increased tissue damaging by both H. pylori and EBV.…”

Section: Discussionmentioning

confidence: 99%

Prevalence and characteristics of Epstein–Barr virus-associated gastric carcinomas in Portugal

Nogueira

Mota

Gradiz

et al. 2017

Infect Agents Cancer

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BackgroundGastric cancer (GC) is one of the most common malignant tumors of the digestive tract and is the third leading cause of cancer death worldwide. Epstein–Barr virus (EBV) has been associated with approximately 10% of the total cases of gastric carcinomas. No previous study has analyzed the prevalence of EBV infection in gastric cancer of the Portuguese population.MethodsIn the present study, we have analyzed 82 gastric carcinoma cases and 33 healthy individuals (control group) from Coimbra region for the presence of EBV by polymerase chain reaction (PCR) and by in situ hybridization (ISH) for EBV-encoded small RNAs (EBERs). The status of H. pylori infection was assessed by serology and by PCR.ResultsEBV was detected by PCR in 90.2% of stomach cancer cases, whereas EBERs were detected in 11%. In our series, EBV-associated gastric carcinoma (EBVaGC) were significantly associated with gender and the majority of them presented lymph node metastasis. These cases were generally graded in more advanced pTNM stages and, non-surprisingly, showed worse survival. H. pylori infection was detected in 62.2% of the gastric cancers and 64.7% of these patients were CagA+. On the other hand, the H. pylori prevalence was higher in the EBV-negative gastric carcinomas (64.4%) than in those carcinoma cases with EBV+ (44.4%).ConclusionsThe present study shows that prevalence of EBVaGC among Portuguese population is in accordance with the worldwide prevalence. EBV infection seems to be associated to poorer prognostic and no relation to H. pylori infection has been found. Conversely, the presence of H. pylori seems to have a favourable impact on patient’s survival. Our results emphasize that geographic variation can contribute with new epidemiological data on the association of EBV with gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Prevalence and characteristics of Epstein–Barr virus-associated gastric carcinomas in Portugal

Nogueira

Mota

Gradiz

et al. 2017

Infect Agents Cancer

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“…In this report, we identify, to our knowledge for the first time, a microbial protein from P. falciparum, that can drive a latently infected B cell into viral replication. Previous studies by Minoura-Etoh et al demonstrated that monochloramine (NH 2 Cl), a Helicobacter pylori–associated oxidant, induces viral production in epithelial cells [26]. …”

Section: Discussionmentioning

confidence: 99%

A Molecular Link between Malaria and Epstein–Barr Virus Reactivation

et al. 2007

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Although malaria and Epstein–Barr (EBV) infection are recognized cofactors in the genesis of endemic Burkitt lymphoma (BL), their relative contribution is not understood. BL, the most common paediatric cancer in equatorial Africa, is a high-grade B cell lymphoma characterized by c-myc translocation. EBV is a ubiquitous B lymphotropic virus that persists in a latent state after primary infection, and in Africa, most children have sero-converted by 3 y of age. Malaria infection profoundly affects the B cell compartment, inducing polyclonal activation and hyper-gammaglobulinemia. We recently identified the cystein-rich inter-domain region 1α (CIDR1α) of the Plasmodium falciparum membrane protein 1 as a polyclonal B cell activator that preferentially activates the memory compartment, where EBV is known to persist. Here, we have addressed the mechanisms of interaction between CIDR1α and EBV in the context of B cells. We show that CIDR1α binds to the EBV-positive B cell line Akata and increases the number of cells switching to the viral lytic cycle as measured by green fluorescent protein (GFP) expression driven by a lytic promoter. The virus production in CIDR1α-exposed cultures was directly proportional to the number of GFP-positive Akata cells (lytic EBV) and to the increased expression of the EBV lytic promoter BZLF1. Furthermore, CIDR1α stimulated the production of EBV in peripheral blood mononuclear cells derived from healthy donors and children with BL. Our results suggest that P. falciparum antigens such as CIDR1α can directly induce EBV reactivation during malaria infection that may increase the risk of BL development for children living in malaria-endemic areas. To our knowledge, this is the first report to show that a microbial protein can drive a latently infected B cell into EBV replication.

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“…These genes are commonly found altered in various cancer types including GC [270]. Further, H. pylori positive individuals show a significantly higher EBV DNA load which suggests H. pylori role in lytic phase conversion of EBV [271]. Also, EBV DNA load was more in H. pylori positive patients than those uninfected with GC [272].…”

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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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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Helicobacter pylori-associated oxidant monochloramine induces reactivation of Epstein–Barr virus (EBV) in gastric epithelial cells latently infected with EBV

Cited by 57 publications

References 24 publications

Prevalence and characteristics of Epstein–Barr virus-associated gastric carcinomas in Portugal

Prevalence and characteristics of Epstein–Barr virus-associated gastric carcinomas in Portugal

A Molecular Link between Malaria and Epstein–Barr Virus Reactivation

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

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