POSTER

S.H.

Fatemi¹, D.A. Pearce², A.I Brooks², R.W.

1Department of

Psychiatry, University of Minnesota; ²Center for Functional Genomics,

University of Rochester; ³Institute of Antiviral Research, Utah State

Schizophrenia and autism are severe Neurodevelopmental disorders with genetic

and environmental etiologies.  Some of the epidemiological evidence links

schizophrenic and autistic births to prenatal viral infections during the 1^st

and 2^nd trimesters of pregnancy.  We have studied the effects of

prenatal human influenza viral infection on day 9 of pregnancy in C57BL6 and

Balb-c mice and their offspring (Fatemi et al, 2003).  These studies showed the

deleterious effects of influenza on growing brains of exposed offspring, causing

abnormal corticogenesis (Fatemi et al 1999), pyramidal cell atrophy (Fatemi et

al 2002b) and alterations in levels of Reelin (Fatemi et al 1999), nNOS (Fatemi

et al 2000), SNAP-25 (Fatemi et al 1998), GFAP (Fatemi et al 2002a, 2003) and

GAD65/67 kDA proteins (Fatemi et al 2003).  Additionally, exposed animals

exhibit reduced prepulse inhibition and other abnormal behavior in adulthood

(Shi et al 2003).  In the current study, control and exposed day 0 Balb-c brains

were analyzed using cDNA microarray technology, spanning approximately 23,000

genes using established protocol (Elshatory et al 2003).  The results showed

downregulation of 29 genes by greater than 1.5 fold (range 1.5-19.58) in the

exposed brains vs. controls.  Several genes were also upregulated in the exposed

brains.  The identity and implications of alterations in these genes will be

discussed.  These results show for the first time that prenatal human influenza

viral infection on day 9 of pregnancy in Balb-c mice leads to alterations in a

large group of genes in the brains of exposed offspring. The generous support by

Jonty Foundation (SHF) and NIH (NIAID contract #1-A165291 to RWS) is greatly