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Review
. 2017:2017:3456264.
doi: 10.1155/2017/3456264. Epub 2017 Mar 21.

Status of Epstein-Barr Virus Coinfection with Helicobacter pylori in Gastric Cancer

Shyam Singh  1 , Hem Chandra Jha  1
Affiliations
Review

Status of Epstein-Barr Virus Coinfection with Helicobacter pylori in Gastric Cancer

Shyam Singh et al. J Oncol. 2017.

Abstract

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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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
EBV and H. pylori coinfection in stomach. Stomach infected with EBV and H. pylori. Some of gastric epithelial cells coinfected with EBV and H. pylori. Further this coinfection turns into aggressive development of carcinoma.
Figure 2
Figure 2
Mechanisms of EBV and H. pylori coinfection in gastric epithelial cells. A detailed illustrative mechanism demonstrated in gastric epithelial cells. H. pylori infection leads to oxidative stress, toxin, and necrosis in cells. These reactions further lead to chronic inflammation, epigenetic modification, and mutation. All these alterations led to genomic instability. EBV infection leads to the expression of lytic and latent genes of EBV. These viral genes regulated epigenetic modification and chronic inflammation. Further these EBV derived mechanisms lead to genomic instability. Finally, genomic instability is one of the potent sources of carcinogenesis.
See this image and copyright information in PMC

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