Prenatal viral infection in mouse causes differential expression of genes in brains of mouse progeny: a potential animal model for schizophrenia and autism

Abstract

Schizophrenia and autism are neurodevelopmental disorders with genetic and environmental etiologies. Prenatal viral infection has been associated with both disorders. We investigated the effects of prenatal viral infection on gene regulation in offspring of Balb-c mice using microarray technology. The results showed significant upregulation of 21 genes and downregulation of 18 genes in the affected neonatal brain homogenates spanning gene families affecting cell structure and function, namely, cytosolic chaperone system, HSC70, Bicaudal D, aquaporin 4, carbonic anhydrase 3, glycine receptor, norepinephrine transporter, and myelin basic protein. We also verified the results using QPCR measurements of selected mRNA species. These results show for the first time that prenatal human influenza viral infection on day 9 of pregnancy leads to alterations in a subset of genes in brains of exposed offspring, potentially leading to permanent changes in brain structure and function.