Maternal immune activation influences social behavior development in a nonhuman primate model

Women exposed to infection during pregnancy have an increased risk of giving birth to a child who will later be diagnosed with neurodevelopmental disorders (NDDs) characterized by changes in social development, such as autism and schizophrenia. Preclinical rodent models of maternal immune activation (MIA) have established causal links between elevated maternal cytokines and offspring social deficits indicative of human NDDs.

Here, we use a unique nonhuman primate (NHP) MIA model to explore the longitudinal development of social behavior, given their phylogenetic similarity, social complexity, and translational potential for identifying the emergence of NDDs in humans. We explore social behavior (N=28 males) in pairs, social groups, and a dominance assessment.

MIA-exposed and control offspring developed a species-typical repertoire of social behavior and interacted with conspecifics. Yet, consistent with rodent and human studies, we found that MIA-exposed NHP offspring were, overall, less social towards familiar peers. We also found that MIA-exposed offspring were more likely to play with their treatment-matched pair mate during the weaning period, while controls did not exhibit a partner preference. There were also patterns suggesting that MIA exposure led to reduced contact with dams during infancy, greater withdrawals from pair-mates, and reduced positive social interactions with peers.

These results confirm that NHP models of MIA are consistent with evidence from rodent and human studies indicating that MIA exposure reduces overall sociality. They also suggest that social deficits may be specific to certain behaviors and more subtle or masked during observations in large social groups.