Scenarios for a viral etiology of schizophrenia

Recent discoveries in the field of virus receptors have revolutionized our concepts of viral pathogenesis. The lysis of cells resulting from virus infection or immune recognition of infected cells is seen as merely one facet of a spectrum of pathogenic mechanisms which may be subtle and complex. This is particularly relevant to the central nervous and immune systems which share cell-surface receptors for various neuropeptides and neurotransmitters. A number of viruses are now known to share receptors for such endogenous ligands; indeed, some viruses (e.g., human immunodeficiency virus and vaccinia) may themselves be structural analogs of these ligands. There is, therefore, considerable scope for interference by viruses in the normal functioning of the brain and neuroendocrine systems. Brief reactive psychoses are occasionally reported as acute sequels to viral infections, but generally these are regarded as unrelated to schizophrenia. An opposite viewpoint is presented in the article: i.e., that the only reason these reactive psychoses do not progress to schizophrenia is that the majority of individuals affected are not predisposed genetically to schizophrenia. Conceivably, therefore, the genetic predisposition to schizophrenia may be attributable to genes which determine idiosyncratic differences in immune responsiveness to common viral pathogens.