Figure 1.

(A) Upon administration of OV therapy, infected tumor cells are recognized and quickly eradicated by antiviral innate mediators, including NK cells, M1 macrophages, neutrophils, and virus-specific T-cells of the cellular compartment. (B) Host-conditioning with cyclophosphamide and gemcitabine chemotherapy can blunt antiviral immune mechanisms to provide a window of sufficient OV replication. OV-infected tumor cells eventually die through lytic mechanisms or by immune-cell recognition during the rebound phase after chemotherapy. Dying tumor cells may lead to an efflux of tumor-associated antigens (TAA) or damage-associated molecular pattern molecules (DAMPs), (C) which can be engulfed by immature dendritic cells (DCs) and later presented to naïve T cells in the local tumor-draining lymph node. Together, these mechanisms may act in concert to promote (D) a coordinated tumor-directed immune response comprising of OV-mediated cell lysis, anti-viral immunity against OV-infected cells, and adaptive immunity responding to TAA. Reproduced with permission from reference.¹⁰³