Abstract: The present invention relates to methods of treatment of programmed cell death (apoptosis) through the use of the HSV-1 gene &ggr;134.5 or the product of its expression, ICP34.5. The gene and its expression have been demonstrated to be required for HSV-1 neurovirulence, and in particular, to act as an inhibitor of neuronal programmed cell death which allows for viral replication. Use of the gene therapy, or the protein itself, can be expected to result in inhibition of programmed cell death in various neurodegenerative diseases. This invention also relates to novel vectors for gene therapy, including modified herpes virus. Methods are presented for conducting assays for substances capable of mimicing, potentiating or inhibiting the expression of &ggr;134.5 or the activity of ICP34.5. Also, methods are disclosed for the treatment of tumorogenic diseases, including cancer, and for treatment of herpes and other viral infections using inhibitors of &ggr;134.5 expression or ICP34.5 activity.

Abstract: The present invention relates to methods of treatment of programmed cell death (apoptosis) through the use of the HSV-1 gene &ggr;134.5 or the product of its expression, ICP34.5. The gene and its expression have been demonstrated to be.required for HSV-1 neurovirulence, and in particular, to act as an inhibitor of neuronal programmed cell death which allows for viral replication. Use of the gene therapy, or the protein itself, can be expected to result in inhibition of programmed cell death in various neurodegenerative diseases. This invention also relates to novel vectors for gene therapy, including modified herpes virus. Methods are presented for conducting assays for substances capable of mimicing, potentiating or inhibiting the expression of &ggr;134.5 or the activity of ICP34.5. Also, methods are disclosed for the treatment of tumorogenic diseases, including cancer, and for treatment of herpes and other viral infections using inhibitors of &ggr;134.5 expression or ICP34.5 activity.

Abstract: Methods for the identification of inducers and inhibitors of apoptosis are described. The method exploits the finding that the exposure of cells to apoptotic stress and its concurrent shutdown of cellular protein synthesis is accompanied by phosphorylation of IF-2.alpha. and a novel protein termed p90.