The review investigated the complex functions of programmed cell death in Epstein-Barr virus (EBV)-associated malignancies, emphasizing the subtle interactions between viral strategies and the host immune system. The aim of this study was to elucidate how EBV manipulates various cell death pathways, including apoptosis, ferroptosis, and autophagy, to ensure its survival and promote cancer development. By analyzing these processes, this review aims to highlight potential therapeutic approaches that can interrupt EBV's influence on these pathways, thereby improving immune detection and creating new opportunities for targeted therapies. A deeper understanding of the molecular mechanisms by which EBV influences cell death will contribute to the field of viral oncology and identify new targets for drug innovation. Furthermore, the findings discussed in this review could inspire the development of vaccines designed to prevent EBV infection or reduce its carcinogenic effects. Furthermore, it integrates recent findings on the diverse roles of non-coding RNAs and cell signaling in influencing cell death during EBV infection. By integrating existing knowledge and identifying gaps in understanding, it lays the foundation for future research that could lead to meaningful progress in the development of vaccines and therapeutic options for EBV-associated cancers. This review revealed the critical importance of continuing research into the complex relationship between EBV and host cell death mechanisms, ultimately aiming to improve outcomes for patients with EBV-associated diseases.