<p>Epstein-Barr virus (EBV) is a complex human herpesvirus characterized by a protein core, a 162-capsomer nucleocapsid, and a glycoprotein-spiked envelope, which facilitates its transmission through bodily fluids. The virus primarily targets B cells and oropharyngeal epithelial cells, establishing infection through viral gp350/220 binds to the host CD21/CR2 receptor, followed by gp42 interacting with HLA class II molecules to trigger endocytosis. Once infection is established, EBV utilizes two main types of encoded microRNAs to regulate the host environment. The BHRF1 miRNAs are expressed early to promote rapid cell proliferation and prevent B-lymphocyte apoptosis by targeting pro-apoptotic proteins. Meanwhile, the BART miRNA cluster, including miR-BART1, miR-BART2, miR-BART3, miR-BART4, miR-BART7, miR-BART8, and miR-BART22, which are robustly expressed in epithelial malignancies like nasopharyngeal and gastric carcinomas, has been found to significantly suppress caspase-3, a central executioner of apoptosis and target host immune mediators like CXCL-11 to stifle antiviral responses. Moreover, Min et al. discovered that miR-BART1-3p inhibited the expression of Disabled homolog 2 (DAB2), a tumor suppressor gene linked to apoptosis, in EBVaGC cells, allowing them to evade programmed cell death. EBV’s ability to cycle between B cells and epithelial cells, along with its association with the modulation of host cell processes and immune responses, highlights the mechanisms by which EBV establishes infection and contributes to oncogenesis.</p> Graphical abstract <p></p>