Fig. 10

Oncogenic mechanisms of HTLV-1 in adult T-cell leukemia/lymphoma. a Progression of ATLL caused by HTLV-1. b HTLV-1 encoded proteins upregulate oncogenes and silence tumor suppressor genes via NF-κB-dependent and NF-κB-independent pathways, recruiting transcription factors to gene promoters. c The viral Tax protein increases genomic instability by promoting DNA damage and inhibiting DNA double-strand break repair. d HTLV-1 infection boosts cell proliferation through persistent activation of AKT/NF-κB and TGF-β/Smad pathways, and promotes YAP nuclear translocation. e HTLV-1 encoded proteins inhibit apoptosis by suppressing caspase signaling, activating the NF-κB pathway, and preventing FoxO3a nuclear translocation. f HTLV-1-infected host cells achieve immune escape by reducing Tax protein expression, generating Tax mutants, and suppressing Th1 cytokine production. g HTLV-1 mediates immune suppression by inducing inhibitory receptor expression on T cells and recruiting Treg cells. h HTLV-1 induces chronic inflammation by causing host cells to overproduce IL-10. i HTLV-1 infection enhances intracellular glycolysis, pyrimidine biosynthesis, and lipid synthesis. Fuchsia text: Components of HTLV-1; Black text: Components of host cell; Direct oncogenesis: b–e; Indirect oncogenesis: f–i. This figure was created with BioRender.com