Department of Microbiology, Shimane University Faculty of Medicine, Izumo 693-8501, Shimane, Japan.
Faculty of Medicine, Muslim University of Indonesia, Makassar 90231, Indonesia.
World J Gastroenterol. 2022 Nov 28;28(44):6249-6257. doi: 10.3748/wjg.v28.i44.6249.
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.
EB 病毒（EBV）相关胃癌（EBVaGC）细胞来源于单个被 EBV 感染的细胞克隆。然而，超过 95%的胃癌患者有（）感染史，（）是胃癌的主要致病因子。因此，长期以来一直认为（）感染可能会影响 EBVaGC 的发展，EBVaGC 是胃癌的一个亚型。在 EBVaGC 的胃黏膜中观察到（）感染的萎缩性胃肠炎症这一症状。因此，目前尚不清楚（）感染是否是 EBV 感染引起的胃癌发生的协同因子，还是（）和 EBV 感染独立作用于胃癌的形成。有报道称 EBV 感染有助于（）感染引起的胃癌的致癌作用。相比之下，有几项研究报道称（）感染加速了 EBV 感染引发的肿瘤发生。通过回顾临床流行病学和实验数据，我们重新组织了（）和 EBV 感染在胃癌形成中的作用。
