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. 2009 Feb 17;35(3):528–548. doi: 10.1093/schbul/sbn187

Fig. 2.

Fig. 2.

A Hypothesis of How Prenatal Viral Infection Could Contribute to the Development of Schizophrenia. Prenatal viral infection may lead to (1) activation of DNA methyltransferase 1 (DNMT1) that in turn changes methylation of promoters for a variety of genes leading to altered levels of molecules such as glutamic acid decarboxylase 67-kDa protein (GAD67) and reelin (S.H. Fatemi, unpublished observations).74,75 These changes may result in abnormal development and altered γ-aminobutyric acid (GABA) signaling and subsequent genesis of schizophrenia; (2) activation of the maternal immune response leading to altered levels of cytokines including interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNF-α)44,45,48 that regulate normal brain development.50–52 Changes may lead to abnormal cortical development and, ultimately, schizophrenia; and (3) altered expression of genes that are involved in cell-cell communication and changes in cell structure due to chronic actin depolymerization (S.H. Fatemi and M. Peoples, unpublished observations, 2007) may lead to dysregulation of multiple signaling systems that have been observed in schizophrenia. *, Pathways that require more substantial support.