Retroviruses and schizophrenia revisited

Abstract

Both genetic and environmental factors appear to contribute to the causation of schizophrenia. Evidence indicating that fetal development is disrupted in schizophrenia and the finding of an excess of winter births among schizophrenic patients have led to continued speculation that an intrauterine viral infection may cause developmental lesions, genetic mutations, or persistent infections that lead to schizophrenia. Certain unique characteristics of the retroviruses render them plausible as candidate "schizoviruses" and the involvement of an endogenous retrovirus would be compatible with some of the puzzling epidemiological findings in schizophrenia. Reverse transcriptase (RT) is a retrovirally encoded enzyme essential for retroviral integration into host DNA. While attempts to detect retroviral infections by measuring RT activity in the peripheral lymphocytes and serum of schizophrenic patients have been unsuccessful, such negative findings may simply mean that the virus is not active in peripheral lymphocytes. A more sensitive and comprehensive approach to detect a retrovirus is to search the genomes of schizophrenic patients directly for the presence of retroviral DNA sequences encoding RT and one possible approach is described.