Epigenetic dysregulation in Epstein-Barr virus-associated gastric carcinoma: Disease and treatments

Figure 1 Epstein-Barr virus infects host gastric epithelial cells through direct and indirect mechanisms. Epstein-Barr virus (EBV) preferentially infects B lymphocytes, which subsequently infects gastric epithelial cells through direct cell-to-cell contact. EBV infection causes expression of latency 1a and/or 1b proteins in gastric epithelial cells. EBV infection also up-regulates genes including EBNA1, EBER, LMP2A, and BART, altering expression of DNMTs and miRNAs. Collectively, the abnormal intracellular signals lead to carcinogenesis and tumour development.

Figure 2 Mechanism of Epstein-Barr virus infection in B lymphocytes. Epstein-Barr virus (EBV) envelope glycoproteins gp350/220 bind to B lymphocyte receptors CD21 and/or CD35. Simultaneously, viral glycoprotein gp42 interacts with HLA II on the B cell membrane to trigger the core fusion complex, enabling EBV entry into the B cell.