Abstract
Zika virus (ZIKV) infection has a profound impact on the fetal nervous system. The postnatal period is also a time of rapid brain growth, and it is important to understand the potential neurobehavioral consequences of ZIKV infection during infancy. Here we show that postnatal ZIKV infection in a rhesus macaque model resulted in long-term behavioral, motor, and cognitive changes, including increased emotional reactivity, decreased social contact, loss of balance, and deficits in visual recognition memory at one year of age. Structural and functional MRI showed that ZIKV-infected infant rhesus macaques had persistent enlargement of lateral ventricles, smaller volumes and altered functional connectivity between brain areas important for socioemotional behavior, cognitive, and motor function (e.g. amygdala, hippocampus, cerebellum). Neuropathological changes corresponded with neuroimaging results and were consistent with the behavioral and memory deficits. Overall, this study demonstrates that postnatal ZIKV infection in this model may have long-lasting neurodevelopmental consequences.
Highlights
Zika virus (ZIKV) infection has a profound impact on the fetal nervous system
Controls and ZIKV-infected rhesus macaques (RMs) exhibited similar levels of anxiety, vocalizations, and stereotypies (Supplementary Table 1). These results show that ZIKV infection at 5 weeks of age resulted in atypical socioemotional behavior and impaired motor function at 12 months of age
Taken together these findings suggest that ZIKV infection during infancy resulted in quantifiable behavioral alterations at 12 months of age that may be consequences of the brain growth and function effects reported below
Summary
Zika virus (ZIKV) infection has a profound impact on the fetal nervous system. The postnatal period is a time of rapid brain growth, and it is important to understand the potential neurobehavioral consequences of ZIKV infection during infancy. The passage of ZIKV into the brain and its ability to infect human cortical neural progenitor cells[7] induces neuropathological changes that have been reported since the late 1950s8,9. Congenital ZIKV syndrome is a pattern of birth defects that includes severe microcephaly, thinning of the cerebral cortex with subcortical calcifications, macular scarring and retinal mottling, congenital contractures, and hypertonicity[6]. Infants born with this syndrome can develop seizures, hearing and vision problems, feeding difficulties, and gross motor abnormalities[16]. A recent follow-up of 216 toddlers with prenatal ZIKV exposure reported microcephaly in only 3.7%
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