Oncolytic viruses (OVs) have shown promise in cancer treatment by selectively replicating in tumor cells and promoting antitumor immunity. However, their immunogenicity is relatively weak, necessitating further investigation. This study demonstrates that HSV-1-based OVs (oHSV) trigger ZBP1-mediated PANoptosis, a unique innate immune inflammatory cell death modality, leading to enhanced antitumor immune effects. Mechanistically, oHSV enhances the expression of interferon-stimulated genes, resulting in the accumulation of endogenous Z-RNA and subsequent activation of ZBP1. To further enhance the antitumor potential, *Fusobacterium nucleatum* outer membrane vesicles (*Fn*-OMV) were identified, which can increase the expression of PANoptosis execution proteins. The combination of *Fn*-OMV and oHSV exhibits potent antitumor immunogenicity. This study provides a deeper understanding of oHSV-induced antitumor immunity and suggests a promising strategy combining oHSV with *Fn*-OMV.Oncolytic viruses (OVs) have shown promise in cancer treatment by selectively replicating in tumor cells and promoting antitumor immunity. However, their immunogenicity is relatively weak, necessitating further investigation. This study demonstrates that HSV-1-based OVs (oHSV) trigger ZBP1-mediated PANoptosis, a unique innate immune inflammatory cell death modality, leading to enhanced antitumor immune effects. Mechanistically, oHSV enhances the expression of interferon-stimulated genes, resulting in the accumulation of endogenous Z-RNA and subsequent activation of ZBP1. To further enhance the antitumor potential, *Fusobacterium nucleatum* outer membrane vesicles (*Fn*-OMV) were identified, which can increase the expression of PANoptosis execution proteins. The combination of *Fn*-OMV and oHSV exhibits potent antitumor immunogenicity. This study provides a deeper understanding of oHSV-induced antitumor immunity and suggests a promising strategy combining oHSV with *Fn*-OMV.