Fig. 8

Oncogenic mechanisms of KSHV in Kaposi sarcoma. a Progression of KS caused by KSHV. b KSHV infection induces intracellular DNA damage, mitotic disruption, and chromosomal structural abnormalities. c KSHV maintains telomere length in host cells by reducing TRF1 degradation. d KSHV enhances cell proliferation via NF-κB and Notch signaling, while vBcl-2 and vPK inhibit apoptosis. e KSHV facilitates immune evasion by inhibiting cGAS activity, suppressing IFN-I transcription, downregulating Nectin-2, CD155, and I-selectin ligands, and fostering a Treg and TAM-rich immunosuppressive microenvironment. f KSHV induces chronic inflammation and oxidative stress via promoting inflammatory factor release, inhibiting GR signals, and upregulating HO-1 transcription. g KSHV promotes angiogenesis and metastasis by increasing angiogenic factors and matrix metalloproteinases (MMPs). h KSHV infection augments aerobic glycolysis, pyrimidine synthesis, amino acid metabolism, and lipid generation in host cells. Blue text: Components of KSHV; Black text: Components of host cell; Direct oncogenesis: b–d; Indirect oncogenesis: e–h. This figure was created with BioRender.com