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Prenatal Zika virus exposure disrupts social-emotional development and cortical visual function in infant macaques

Karla K Ausderau1,2, Ben Boerigter1, Elaina R Razo3

  • 1Department of Kinesiology, University of Wisconsin-Madison, Madison, WI, USA.

Nature Communications
|January 28, 2026
PubMed

Insights

Prenatal Zika virus (ZIKV) exposure can cause developmental delays in infants. This study in macaques shows ZIKV itself, not maternal factors, drives these neurodevelopmental outcomes.

Area of Science:

  • Neuroscience
  • Virology
  • Developmental Biology

Background:

  • Prenatal Zika virus (ZIKV) exposure poses risks from severe birth defects to subtle developmental delays.
  • The precise mechanisms underlying ZIKV's impact on infant neurodevelopment remain largely unknown.
  • Rhesus macaques offer a translational model to study ZIKV's effects on prenatal and early-life development.

Purpose of the Study:

  • To investigate the neurodevelopmental outcomes in infants following first-trimester ZIKV exposure using a rhesus macaque model.
  • To assess the influence of maternal infection characteristics and prior dengue virus (DENV) exposure on ZIKV-induced developmental effects.
  • To evaluate visual, auditory, and behavioral outcomes up to 12 months of age.

Main Methods:

  • First-trimester ZIKV inoculation of pregnant rhesus macaques (flavivirus-naive or DENV-exposed) with different ZIKV lineages.
  • Monitoring of maternal viremia, placental viral load, and neutralizing antibody titers.
  • Assessment of infant visual evoked potentials, auditory function, and behavioral development (attachment, novelty response) at 3 and 12 months of age.

Main Results:

  • ZIKV-exposed infants displayed altered maternal attachment behaviors and reduced inhibition towards novel stimuli at 12 months.
  • Transient impairment of visual evoked potentials was observed at 3 months, normalizing by 12 months.
  • While hearing loss was more frequent in ZIKV-exposed infants, it did not reach statistical significance.
  • Maternal viremia, placental burden, and antibody titers did not correlate with infant developmental outcomes.

Conclusions:

  • ZIKV exposure itself, independent of maternal factors, is the primary driver of observed neurodevelopmental alterations.
  • Maternal biomarkers are limited in predicting infant risk following prenatal ZIKV exposure.
  • Future research and interventions should prioritize infant-focused developmental outcomes in ZIKV studies.

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