Fig. 10.

Schematic representation of HSV-P10 antitumor activity: HSVQ (blue) infection (bottom cell) activates AKT/mTOR signaling, initiating the induction of cell surface PDL-1 that provides an immunosuppressive signal to immune cells in the tumor microenvironment. Upon infection with HSV-P10 (red), PTENα expression in infected cells reduces the ratio of Phosphatidyl inositol triphosphate to Phosphatidyl inositol bi phosphate (PIP3/PIP2), and thus consequently negatively regulates AKT/mTOR pathway. PTENα also homes to the mitochondria resulting in increased ATP release from the tumor cells infected with HSV-P10, which activates a robust antitumor immune response. The increased infiltration of activated macrophages, neutrophils, and CD8 + T-cells results in a more efficient tumor cell lysis, and translates to a better therapeutic efficacy