Table 4.

Synergy between oncolytic viruses and chemotherapy agents

Virus	Agent (tumor model)	Putative Mechanisms
HSV (G207) *	Temozolamide (Glioma)†103 Taxane (docetaxel) (Prostate)75	Temozolamide induced increase in stress response genes, with ICP-34 homology102,103 Mitotic slippage with ↑apoptosis through combined G2-M and G1 arrest75
Reovirus (Reolysin)	Taxane (paclitaxel), cisplatin gemcitabine, vinblastine (Lung)79 Cisplatin, paclitaxel (Melanoma)78	Prolonged mitotic arrest, with ↑apoptosis78,79 ↑Caspase dependent apoptosis78
Vaccinia Virus	Taxane (paclitaxel) (Ovary, Colorectal)76	Chemosensitisation by: Post infection, type I interferon release Post-lysis, High-mobility group protein B1 release76
Adeno Virus (Onyx-015)	Taxane (paclitaxel), cisplatin, (Lung)‡101 Paclitaxel (Ovary)104	E1a induced cell cycle activation106 E1a sensitization to chemotherapy105 Mitotic slippage, and apoptosis104

Preclinical therapeutic synergy with OV is recognised across a range of tumor types and chemotherapies, and is ascribed when the Chou-Talalay combination index (CI) <1, (see main text). Underlying putative mechanisms of synergy are outlined.

^*Examples of clinically assessed oncolytic viruses are given in brackets

^†references in superscript

^‡this study used an alternative method to CI, to attribute synergy.