A method is presented for treating herpes simplex virus (HSV) infection comprising: (a) locally administering a substance that induces a delayed type hypersensitivity (DTH) response to a patient at a site of an HSV lesion to induce a DTH response at the site of the lesion during one or more outbreaks of the HSV infection.

Eliciting a systemic antitumor immune response can be efficacious for a patient who presents with or who is at risk of developing multiple metastatic tumors of a given cell type. To this end a pharmaceutical composition is employed that comprises a defective HSV vector, preferably containing an expressible nucleotide sequence encoding at least one immune modulator.

Eliciting a systemic antitumor immune response can be efficacious for a patient who presents with or who is at risk of developing multiple metastatic tumors of a given cell type. To this end a pharmaceutical composition is employed that comprises a defective HSV vector, preferably containing an expressible nucleotide sequence encoding at least one immune modulator.

Eliciting a systemic antitumor immune response can be efficacious for a patient who presents with or who is at risk of developing multiple metastatic tumors of a given cell type. To this end a pharmaceutical composition is employed that comprises a defective HSV vector, preferably containing an expressible nucleotide sequence encoding at least one immune modulator.

The present disclosure provides a bispecific single-chain antibody, recombinant oncolytic virus for expressing same and virus composition. The antibody named BiTEs-PD-L1 is a bispecific antibody capable of simultaneously binding CD3 and PD-L1 on the surfaces of tumor cells, and it can effectively activate T cells and guide T cells to kill tumor cells. The oncolytic virus oHSV2-BiTEs-PD-L1 is further developed by utilizing the BiTEs-PD-L1, it can reduce frequency and dosage of the administration. The present disclosure also confirmed several virus compositions with excellent antitumor effect.

The present disclosure relates, in part, to pharmaceutical compositions comprising one or more polynucleotides suitable for enhancing, increasing, augmenting, and/or supplementing the levels of Collagen alpha-1 (VII) chain polypeptide and/or Lysyl hydroxylase 3 polypeptide and/or Keratin type I cytoskeletal 17 polypeptide in a subject. The present disclosure also relates, in part, to pharmaceutical compositions and methods of use for providing prophylactic, palliative, or therapeutic relief of a wound, disorder, or disease of the skin in a subject, including a subject having, or at risk of developing, one or more symptoms of epidermolysis bullosa.

The present disclosure relates, in part, to pharmaceutical compositions comprising one or more polynucleotides suitable for enhancing, increasing, augmenting, and/or supplementing the levels of Collagen alpha-1 (VII) chain polypeptide and/or Lysyl hydroxylase 3 polypeptide and/or Keratin type I cytoskeletal 17 polypeptide in a subject. The present disclosure also relates, in part, to pharmaceutical compositions and methods of use for providing prophylactic, palliative, or therapeutic relief of a wound, disorder, or disease of the skin in a subject, including a subject having, or at risk of developing, one or more symptoms of epidermolysis bullosa.

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.

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 variants of herpes simplex virus (HSV) that selectively infect and replicate in cancer cells, including HSV strains that selectively infect and replicate in bladder cancer cells. Preferred HSV of the invention have intact endogenous Us11 and Us12 genes and have genes encoding ICP34.5 replaced with a gene encoding Us11 fused to an HSV immediate early (IE) promoter. The variant HSV of the invention also comprise one or more additional heterologous genes encoding immunomodulatory polypeptides. Methods and compositions using these variant HSV, for example, for treating cancer in a subject, are also provided.