Figure 1.

OV restriction mechanisms of GBM tumors. Infiltration of NK cells and tumor-associated macrophages (TAMs) at the tumor site, activation status of autophagy, expression of viral entry molecules and viral sensors (e.g., cGAS-STING) that lead to constitutive active type I interferon pathways, all could hamper the OV replication and oncolysis. Furthermore, cathepsin B expression and expression of specific proteins that drive specific tumor replication (e.g., nestin) could determine the OV efficacy. Created with BioRender.com.