Prenatal infection as a risk factor for schizophrenia

Schizophr Bull. 2006 Apr;32(2):200-2. doi: 10.1093/schbul/sbj052. Epub 2006 Feb 9.


Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia. This line of investigation has been advanced by birth cohort studies that utilize prospectively acquired data from serologic assays for infectious and immune biomarkers. These investigations have provided further support for this hypothesis and permitted the investigation of new infectious pathogens in relation to schizophrenia risk. Prenatal infections that have been associated with schizophrenia include rubella, influenza, and toxoplasmosis. Maternal cytokines, including interleukin-8, are also significantly increased in pregnancies giving rise to schizophrenia cases. Although replication of these findings is required, this body of work may ultimately have important implications for the prevention of schizophrenia, the elaboration of pathogenic mechanisms in this disorder, and investigations of gene-environment interactions.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Biomarkers
  • Communicable Diseases / complications*
  • Communicable Diseases / epidemiology*
  • Female
  • Herpesvirus 2, Human / immunology
  • Herpesvirus 2, Human / pathogenicity*
  • Humans
  • Interleukin-8 / immunology
  • Pregnancy
  • Pregnancy Complications, Infectious / epidemiology*
  • Pregnancy Complications, Infectious / immunology
  • Pregnancy Complications, Infectious / microbiology*
  • Risk Factors
  • Schizophrenia / epidemiology*
  • Schizophrenia / etiology*
  • Schizophrenia / immunology
  • Time Factors
  • Toxoplasma / pathogenicity*
  • Tumor Necrosis Factor-alpha / immunology


  • Biomarkers
  • Interleukin-8
  • Tumor Necrosis Factor-alpha