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

Abstract: The present invention relates to an oncolytic virus which is, or is derived from, a clinical isolate which has been selected by comparing the abilities of a panel of three or more clinical isolates of the same viral species to kill tumor cells of two or more tumor cell lines in vitro and selecting a clinical isolate which is capable of killing cells of two or more tumor cell lines more rapidly and/or at a lower dose in vitro than one or more of the other clinical isolates in the panel.

Abstract: The present invention relates to oncolytic virus comprising: (i) a GM-CSF-encoding gene; and (ii) an immune co-stimulatory pathway activating molecule or an immune co-stimulatory pathway activating molecule-encoding gene.

Abstract: The present invention provides a method of treating cancer, which comprises administering a therapeutically effective amount of an oncolytic virus, an inhibitor of the indoleamine 2,3-dioxygenase (IDO) pathway and a further antagonist of an immune co-inhibitory pathway or an agonist of an immune co-stimulatory pathway to a patient in need thereof.

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

Abstract: The present invention relates to an oncolytic virus which is, or is derived from, a clinical isolate which has been selected by comparing the abilities of a panel of three or more clinical isolates of the same viral species to kill tumor cells of two or more tumor cell lines in vitro and selecting a clinical isolate which is capable of killing cells of two or more tumor cell lines more rapidly and/or at a lower dose in vitro than one or more of the other clinical isolates in the panel.

Abstract: The present invention relates to an oncolytic virus which is, or is derived from, a clinical isolate which has been selected by comparing the abilities of a panel of three or more clinical isolates of the same viral species to kill tumor cells of two or more tumor cell lines in vitro and selecting a clinical isolate which is capable of killing cells of two or more tumor cell lines more rapidly and/or at a lower dose in vitro than one or more of the other clinical isolates in the panel.

Abstract: The present invention relates to oncolytic virus comprising: (i) a GM-CSF-encoding gene; and (ii) an immune co-stimulatory pathway activating molecule or an immune co-stimulatory pathway activating molecule-encoding gene.

Abstract: The present invention provides a method of treating cancer, which comprises administering a therapeutically effective amount of an oncolytic virus, an inhibitor of the indoleamine 2,3-dioxygenase (IDO) pathway and a further antagonist of an immune co-inhibitory pathway or an agonist of an immune co-stimulatory pathway to a patient in need thereof.

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

Abstract: A method for altering the electronic and optical properties of a chemical compound having a band gap and a framework that includes ?-delocalized electrons. The method includes complexing a Lewis acid to a basic site within the framework to form a Lewis acid adduct having a band gap that differs from the band gap of the chemical compound. The ?max of the Lewis acid adduct can be shifted to a longer wavelength in comparison to the ?max of the chemical compound. In various versions, the chemical compound can be a conjugated oligomer, a conjugated polymer, or a small molecule comprising a conjugated ?-electron system. Electronic devices that include Lewis acid adducts are also provided.

Abstract: A method for altering the electronic and optical properties of a chemical compound having a band gap and a framework that includes ?-delocalized electrons. The method includes complexing a Lewis acid to a basic site within the framework to form a Lewis acid adduct having a band gap that differs from the band gap of the chemical compound. The ?max of the Lewis acid adduct can be shifted to a longer wavelength in comparison to the ?max of the chemical compound. In various versions, the chemical compound can be a conjugated oligomer, a conjugated polymer, or a small molecule comprising a conjugated ?-electron system. Electronic devices that include Lewis acid adducts are also provided.

Abstract: The present invention provides a herpes virus with improved oncolytic properties which comprises a gene encoding an immunomodulatory cytokine and which lacks a functional ICP34.

Abstract: Described are novel monomers bearing functionalities capable of initiating control free radical reactions, and a novel process using these initiating monomers in the co-polymerization of an olefin for the formation of well-controlled polyethylene graft polymers where the graft component is derived from controlled free radical polymerization reactions. The initiating monomers are produced by combining an amount of 5-norbornen-2-ol with a hydride or amine for a predetermined amount of time to form a mixture; and adding an amount of an alkyl or acyl halide to said mixture. Polymerization of an olefin with an initiating monomer is conducted in the presence of a metal compound, where the metal compound is comprised of a Group VIII transition metal complex.

Abstract: The present invention relates to clinical herpes simplex virus (HSV) isolates with improved oncolytic capabilities as compared to reference laboratory HSV strains. The present invention also relates to methods of producing HSV strains of the invention and to pharmaceutical compositions comprising a HSV strain of the invention.

Abstract: The present invention provides a herpes virus which lacks a functional ICP34.5 encoding gene and which comprises two or more of—(i) a gene encoding a prodrug converting enzyme; (ii) a gene encoding a protein capable of causing cell to cell fusion; and (iii) a gene encoding an immunomodulatory protein.

Abstract: An attenuated herpes virus which lacks a functional vhs gene or a functional equivalent thereof, but which has a functional UL43 gene or functional equivalent thereof, stimulates an immune response when dendritic cells are infected with the virus.

Abstract: An attenuated herpes virus capable of efficiently infecting a dendritic cell without preventing antigen processing occurring within the infected cell. The attenuated herpes virus and dendritic cells infected with the virus are useful immunotherapeutic methods of treating disease.

Abstract: The present invention provides the use of a replication competent herpes virus which (a) lacks a functional wild-type HSV ICP27 gene; and (b) comprises an ICP27 gene encoding an ICP27 protein which allows replication of said herpes virus to occur and which has a reduced ability to inhibit RNA splicing compared to wild-type HSV ICP27 in the production of an adeno-associated virus (AAV) vector.