Ashley Otero

Maternal immune activation (MIA) during pregnancy is linked to neurodevelopmental disorders, such as schizophrenia and autism spectrum disorder (ASD), in offspring. The current proposed pathway is based on work using animal models that initiate MIA using viral mimetics, which recapitulate a controlled, innate portion of the viral immune response. Our lab uses a mouse model of live H3N2 influenza A virus (IAV), which activates the complete adaptive and innate immune response. Furthermore, respiratory IAV infection is known to cause downstream dysregulation in the intestine despite no detectable virus outside of the respiratory tract. Our target is intestinal Th17 cells, which are implicated in MIA-driven developmental abnormalities and intestinal injury following IAV infection. We hypothesize that immune and microbial changes in the maternal gut as a result of viral infection lead to aberrant fetal brain development.