Provided are modified therapeutic cells comprising a first heterologous nucleic acid sequence encoding a simian ICP47 (sICP47) protein or a functional variant thereof. In some embodiments, the modified therapeutic cell further comprises a second heterologous nucleic acid sequence encoding an agonist of a natural killer cell inhibitory receptor. Also provided are methods of treatment using the modified therapeutic cells.

The present invention discloses methods and compositions for modulating the quality of an immune response to a target antigen in a mammal, which response results from the expression of a polynucleotide that encodes at least a portion of the target antigen, wherein the quality is modulated by replacing at least one codon of the polynucleotide with a synonymous codon that has a higher or lower preference of usage by the mammal to confer the immune response than the codon it replaces.

Nucleic acid sequences encoding improved Herpes Simplex Virus Thymidine Kinases are provided, including their use in diagnostic and therapeutic applications. The thymidine kinases may be mutated using conservative mutations, non-conservative mutations, or both. Also provided are gene therapeutic systems, including viral and retroviral particles.

Provided herein are improved vaccines for HSV-2.

A modified Herpes Simplex Virus (HSV), which has a portion of gD (glycoprotein D) of the glycoproteic envelope deleted and a heterologous single chain antibody inserted in place of such deleted portion; the modified HSV is capable of infecting cells through receptor HER2/ErbB2 but not through receptors HVEM/HveA and nectin1/HveC; uses of the modified HSV and a process of the preparation thereof are also disclosed.

The present invention relates to an oncolytic virus comprising: (i) a fusogenic protein-encoding gene; and (ii) an immune stimulatory molecule-encoding gene.

The invention described herein provides a recombinant replication-defective vims derived from Herpesvirales order, wherein the virus is characterized by a complete deletion of a gene encoding ICP27, or a functional equivalent gene thereof. The invention also provides production cell lines for such recombinant replication-defective vims, wherein the cell lines have a coding sequence for ICP27 or a functional equivalent thereof, and wherein the coding sequence has no or minimal sequence overlap with the virus characterized by the complete deletion of the gene encoding ICP27. Method of using such recombinant replication-defective vims and production cell lines are also provided.

The present disclosure provides a system for the expression of target protein in conjunction with enhancer protein. The enhancer protein may be a viral protein that blocks nucleocytoplasmic transport. Also provided are polynucleotides, vectors, and cells comprising target protein and enhancer protein nucleic acid sequences.

Proposed are a recombinant herpes simplex virus having a modified glycoprotein gH for retargeting and the use thereof. Particularly, the recombinant herpes simplex virus is capable of infecting a target cell having a target molecule to which a cell-targeting domain specifically recognizes and binds due to the presence of the cell-targeting domain in the glycoprotein gH thereof, and is thus useful for anticancer therapy or gene therapy.

The present disclosure provides human IL-2 variants, recombinant oncolytic viruses comprising the IL-2 variant, compositions comprising the IL-2 variant or recombinant oncolytic virus, and use of the IL-2 variants, recombinant oncolytic virus, or compositions for treating cancer in an individual.