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

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.