Virus-associated hematological malignancies have become a key focus in oncology research due to their complex pathological mechanisms and unique immune escape capabilities. In recent years, research in this area has increased with a deeper understanding of the role of viruses in tumorigenesis. However, the immune escape mechanisms in virus-associated hematological malignancies remain incompletely elucidated, posing challenges for the development and optimization of treatment strategies. This review summarizes the roles of various known viruses—particularly Epstein–Barr virus (EBV), human immunodeficiency virus (HIV), human T-cell leukemia virus type 1 (HTLV-1), Kaposi’s sarcoma-associated herpesvirus (KSHV), hepatitis B virus (HBV), and hepatitis C virus (HCV) in the pathogenesis of hematological malignancies. It focuses on elucidating how tumor cells utilize multiple immune escape mechanisms to evade host immune surveillance. Simultaneously, incorporating the latest research advances, it delves into cutting-edge therapeutic approaches, including targeting viral proteins, immune checkpoint inhibitors, chimeric antigen receptor T-cell (CAR-T) therapy, oncolytic viruses, virus-specific T-cell therapy (VST), and therapeutic vaccines. By integrating the molecular mechanisms of virus-associated hematological malignancies with clinical applications, this article aims to provide a theoretical basis and future research directions for precision therapy in this field.
Li et al. (Wed,) studied this question.