A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex virus type 2 (HSV-2), derived from the HG52 strain and encoding a bispecific antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the T-cell surface antigen CD3, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, oncolytic HSV-2 expressing anti-PD-L1/CD3 bispecific antibody BS-006 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, BS-006 promotes the secretion of anti-PD-L1/CD3 bispecific antibody by the infected tumor cells. The bispecific antibody targets and binds to both the CD3 on T-cells and the PD-L1 expressed on tumor cells. This results in the cross-linking of T-cells and tumor cells and may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against PD-L1-expressing tumor cells. At the same time, BS-006 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances CTL-mediated tumor cell lysis, which may further lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Deletion of ICP47 also leads to an increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and the oncolysis of tumor cells.