Cognitive, socioaffective, and neural development following fetal Zika virus infection

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Project Summary 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 for this supplement augments the Parent Grant by carrying out evaluations of the consequences of this pathology on sensorimotor development 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 behavioral and neural measures of sensorimotor function. 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. Funding via this supplement will support the doctoral training of a scholar from a background that is underrepresented in, and typically excluded from, STEM.