Development of Epstein-Barr virus-associated gastric cancer: Infection, inflammation, and oncogenesis.

Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC) cells originate from a single-cell clone infected with EBV. However, more than 95% of patients with gastric cancer have a history of () infection, and is a major causative agent of gastric cancer. Therefore, it has long been argued that infection may affect the development of EBVaGC, a subtype of gastric cancer. Atrophic gastrointestinal inflammation, a symptom of infection, is observed in the gastric mucosa of EBVaGC. Therefore, it remains unclear whether infection is a cofactor for gastric carcinogenesis caused by EBV infection or whether and EBV infections act independently on gastric cancer formation. It has been reported that EBV infection assists in the onco-genesis of gastric cancer caused by infection. In contrast, several studies have reported that infection accelerates tumorigenesis initiated by EBV infection. By reviewing both clinical epidemiological and experimental data, we reorganized the role of and EBV infections in gastric cancer formation.