Abstract

In utero infection with Zika virus (ZIKV) during pregnancy can lead to the development of birth defects and postnatal deficits. A nonhuman primate (NHP) model of congenital ZIKV infection can help fill the gaps in knowledge where tissue studies are required to define viral pathogenesis and identify targets for therapeutic intervention. This model system has already identified critical features of ZIKV pathogenesis in congenital infection. Before translating these NHP studies to human clinical trials, we must understand the similarities and differences between human and NHP fetal immune system development, neural development, and infant assessment tools. Because of the overall similarity between fetal and infant development in humans and NHPs, this NHP model can complement human clinical trials by defining immune correlates of protection and evaluating therapeutic interventions.

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