In agreement with our previous reports the advances obtained in understanding central nervous system (CNS) viral infections make viruses attractive etiological candidates for the prenatal origin of
schizophrenia. Among these candidates is Herpes Simplex Hominis type I Virus (HSV-1) due its capacity to remain latent with periodic reactivation, its affinity for the limbic system, the region of
the brain involved in schizophrenia, its reactivation by endocrine changes, stress, radiation and immune alterations and for its relation to genetic predisposition. Presumptive evidence for a viral
etiology requires the demonstration of a virus, antigen or viral antibody. Our electron and immunoelectronmicroscopic
observations of viral particles and HSV-1 antigen in the temporal lobe of the brain of dead adults schizophrenic patients, of aborted fetuses from schizophrenic mothers and in experimental animals inoculated with cerebrospinal fluid [CSF] from schizophrenic patients made us to consider this virus as an etiological agent since Koch postulates have been partially fulfilled.