Epidemiologic, immunologic, and pathologic evidence has suggested that, in a significant number of cases, schizophrenia may be related to infected with or activation of a viral disease of the brain. To further pursue this possibility, we previously undertook immunocytochemical and in situ hybridization studies of brain in which we sought evidence of specific viral antigens or genomes. With rare exceptions these studies did not disclose viral antigens (1). Intracerebral yielded negative results (2). Two new approaches have since been undertaken. Co-cultivation of schizophrenic and control CSF lymphocytes with human neuroblastoma cells (SH-EP). (2) Ino These studies demonstrated growth to higher density of cells treated with (freshly drawn) CSF cells from 10 of 12 patients with chronic schizophrenia from research wards of our unit at St. Elizabeths Hospital. In a second study, a spundown aliquot of CSF from twelve patients with acute or exacerbated schizophrenia and from 13 age-matched neurologic controls from the Oregon Health Sciences University in Portland, Oregon and cooperating hospitals were cultured with human neuroblastoma cells. In contrast to the SEH material, all of the Oregon cultures, both treated with schizophrenic and with control CSF, grew to the same high density. Current work is focused on isolating the factor(s) responsible for the higher growth in the SEH chronic schizophrenic cohort using nucleases and proteases and characterization of nucleic acid associated with the higher growth sample. We are also repeating the original study of CSF on a new group of Saint Elizabeths' patients and controls. In a third study, commenced in the spring of 1988, we inoculated previously frozen CSF from acute and chronic schizophrenic patients (n=14) and controls (n=13) intracranially in newly born mice (n=107). Systematic behavior tests were done on these animals at two months of age. Animals were sacrificed if sick or at one year after inoculation if no illness develops.
