Project Summary/Abstract At its most extreme, fetal Zika virus infection causes microcephaly – the significant shrinking of the fetal brain and skull. Accumulating evidence suggests that microcephaly is just one possible outcome of fetal Zika virus infection, however, and that babies born with normal sized heads may have significant central nervous system pathology. The long-term consequences of this pathology are unknown, leaving open the possibility of a secondary epidemic resulting from compromised cognition and socioaffective processing that will occur as babies born during the epidemic age. The proposed work takes the first step in developing an understanding of the consequences of this pathology by mapping the cognitive and socioaffective of a cohort of nonhuman primates infected with Zika virus as fetuses and a group of procedure matched, non-infected controls. We will evaluate the extent to which maternal and fetal viremia influences cognitive, socioaffective, and neurological outcomes. Because macaques develop approximately four times faster than humans, we will be able to prospectively model pathology that arises – that is, we will be able to predict what pathology human babies, infected with Zika virus during the 2015-2016 epidemic, will experience as they grow up. Developmental modeling of this sort is critical for developing effective interventions and treatments to encourage healthy development and ameliorate psychopathology.