Fetal neurotropic infection results in long term disruptions of brain structure and function

Brisbane Convention & Exhibition Centre 

Typical brain development is shaped by genetic programming, environmental influences, and learning. For humans and nonhuman primates, there is a complex, protracted sequence of developmental events, including axon formation, synaptic refinement, and myelination that can extend well into adulthood. Structural maturation is reflected in the emergence of brain and behavioral functions, with touch recognized as the earliest sensory milestone achieved in utero [1].

Neurotropic infections, like Zika virus, can invade the brain with outcomes heavily influenced by developmental timing. First trimester infections have been linked to fetal loss and microcephaly, as seen in Congenital Zika Syndrome. In contrast, infections occurring in the mid-to-late trimesters often result in infants with normal appearing head sizes but an elevated risk of developmental delay [2].

The long-term consequences of disruptions during fetal brain development, particularly in primates, remain poorly understood. This study examines the effects of mid-term neurotropic infection within the context of normative structural and functional development using a macaque monkey model of fetal Zika virus infection (fZIKV).