Figure 2.

Schematic Depiction of OV-Based Gene Therapies

(A) Virus-based immunostimulatory cytokine and chemokine expression can recruit and activate T cells, antigen-presenting cells (APCs), and natural killer (NK) cells, and subsequently improve the therapeutic activity of OVs. (B) Combination of OV with agents targeting costimulatory and/or coinhibitory molecules on T cells could lead to a more effective antitumor response. (C) Tumor-associated antigen (TAA)-encoding OVs can give rise to virus-like particle (VLP) presentation, inducing a potent antitumor effect. (D) The enzyme encoded by suicide gene can convert nontoxic prodrugs into toxic products in tumor cells, inducing tumor cell death. In addition, suicide genes also have a unique “bystander” effect. They can diffuse the toxic metabolic products to peripheral uninfected tumor cells through intercellular contact, thereby killing peripheral tumor cells. (E) Encoding OVs with anti-angiogenic transgenes (such as vascular endothelial cell growth inhibitor [VEGI]) can enhance viral permeability and inhibit endothelial cell proliferation. (F) Encoding OVs with tumor-suppressor genes can promote tumor regression and apoptosis.