The critical role of ferroptosis in virus-associated hematologic malignancies and its potential value in antiviral-antitumor therapy.

Epstein-Barr Virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human T-cell leukemia virus type 1 (HTLV-1) are key infectious agents linked to the development of various hematological malignancies, including Hodgkin's lymphoma, non-Hodgkin's lymphoma, and adult T-cell leukemia/lymphoma. This review highlights the critical knowledge gaps in understanding the role of ferroptosis, a novel form of cell death, in virus-related tumors. We focus on how ferroptosis influences the host cell response to these viral infections, revealing groundbreaking mechanisms by which the three viruses differentially regulate core pathways of ferroptosis, such as iron homeostasis, lipid peroxidation, and antioxidant systems, thereby promoting malignant transformation of host cells. Additionally, we explore the potential of antiviral drugs and ferroptosis modulators in the treatment of virus-associated hematological malignancies.