. Scientific Frontline: Zika Virus: Hidden Infant Development Risks

Thursday, June 4, 2026

Zika Virus: Hidden Infant Development Risks

The Zika virus, spread by mosquitos such as the Aedes aegypti above, is known to cause severe birth defects. A new study explored why 30% of babies born without these physical symptoms still go on to experience developmental problems including vision and hearing loss.
Photo: Jeff Miller / UW–Madison

Scientific Frontline: Extended "At a Glance" Summary
: Prenatal Zika Exposure and Neurodevelopment

The Core Concept: Prenatal exposure to the Zika virus can cause subtle, long-term neurodevelopmental and sensory processing disorders in infants who are born without visible physical defects.

Key Distinction/Mechanism: Unlike severe structural anomalies directly linked to the virus (such as microcephaly), these hidden deficits stem from neurological communication disruptions—including cortical visual dysfunction—that occur independently of the mother's observable infection characteristics or immune biomarkers.

Major Frameworks/Components:

  • Cortical Visual Dysfunction: A disruption in eye-to-brain communication causing early visual delays, even when the infant's eyes are structurally healthy.
  • Altered Social-Emotional Development: Manifested as prolonged maternal attachment, indicating underlying challenges with sensory processing, threat assessment, and emotional regulation.
  • Behavioral Disinhibition: An abnormally rapid approach to novel objects and situations, which serves as a clinical signal for early anxiety and delayed emotional learning.
  • Diagnostic Biomarker Limitations: Standard maternal indicators, such as viral load, placental infection status, and antibody responses, fail to predict which infants will experience these long-term developmental differences.

Branch of Science: Virology, Neurobiology, Developmental Biology, and Pediatrics.

Future Application: The development of enhanced, long-term neurodevelopmental screening protocols beyond standard newborn physical exams, enabling targeted, early therapeutic interventions for sensory and behavioral delays.

Why It Matters: Approximately 30% of asymptomatic Zika-exposed infants experience later developmental issues. Recognizing these hidden neurological impacts is critical for ensuring comprehensive pediatric care and underscores the ongoing need for preventative vaccines and mosquito control.

Even babies born without the virus’s notable physical symptoms may experience sensory, attachment, and anxiety issues, according to a new study.

Infants exposed to the Zika virus during pregnancy may face hidden developmental challenges, even if they appear healthy at birth. A recent study at the University of Wisconsin–Madison highlights the need for better developmental screening during a child’s first year of life.

The Zika virus is known to cause severe birth defects, such as brain damage and microcephaly (a condition characterized by an abnormally small head and brain). However, little is understood about why 30% of babies born without physical symptoms go on to experience developmental problems, including vision and hearing loss.

To better understand what happens to newborns affected by a Zika infection, UW–Madison occupational therapy professor Karla Ausderau and colleagues studied pregnant rhesus macaques at the Wisconsin National Primate Research Center. The animals were exposed to the Zika virus or a placebo early in their pregnancies. The scientists followed the resulting infant macaques through one year using behavioral tests, vision and hearing assessments, and social observations.

They found that, like human babies, macaques with prenatal virus exposure, regardless of maternal vaccination status, had an increased risk of vision delays, hearing loss, and changes in maternal attachment, despite having no outward symptoms at birth. The researchers recently published their findings in the journal Nature Communications.

Although the infant macaques’ eyes appeared structurally normal, researchers found disruptions in how the eyes communicated with the brain, an issue known as cortical visual dysfunction. This type of visual impairment is also seen in human children who struggle with vision despite having healthy eyes. Early visual delays appeared in the macaques as early as three months of age; however, those differences resolved by 12 months. These early vision changes did not predict later developmental challenges, but researchers note they may signal broader effects of prenatal exposure.

“Infants exposed to Zika before birth showed altered social-emotional development and changes in cortical visual function during infancy, even when they appeared healthy at birth. And we couldn’t predict those outcomes from the mother’s infection characteristics, which is a problem if we’re trying to identify which babies need closer follow-up,” says Emma Mohr, a UW–Madison pediatrics professor and coauthor of the new study.

The researchers also found that hearing loss appeared more often in Zika-exposed infants than in unexposed animals, although the difference was not statistically significant.

Social behavior told another important story. Zika-exposed infants spent more time clinging to their mothers than is typically expected at this age, and they gained more weight than the control group due to increased access to nursing. In rhesus macaques, close maternal contact normally decreases as infants grow more independent. Researchers believe this prolonged attachment may reflect difficulties with sensory processing, emotional regulation, and assessing threats—skills that are critical for healthy social development.

Zika-exposed infants also exhibited lower inhibition, approaching new objects and situations more quickly than expected. This risky behavior may signal early anxiety, delayed emotional learning, or challenges in interpreting sensory information from their environment.

The study found that maternal virus levels, placental infection, and antibody responses did not predict which infants experienced developmental differences, suggesting that common maternal biomarkers are poor indicators of a child’s long-term risk. Human studies have shown that a Zika infection during pregnancy can persist for months and increase the risk of miscarriage and brain abnormalities. However, those severe outcomes were not observed in this animal study, limiting conclusions about how maternal immune responses relate to the most severe cases.

The findings point to a clear message: prenatal Zika exposure alone can influence early development, even in the absence of visible birth defects.

“Children with prenatal Zika exposure need long-term neurodevelopmental follow-up, not just a clean bill of health at birth. The subtle differences we’re detecting wouldn’t be picked up on a routine exam, but they’re the kinds of things that can shape learning, behavior, and social development as kids grow,” Mohr says.

The study strengthens the case for routine developmental monitoring of all children exposed to Zika during pregnancy, regardless of symptoms at birth. Early detection could allow for timely interventions when delays emerge. The authors also stress that prevention remains the strongest defense.

“Vaccines and mosquito control are still the best tools we have,” says Mohr. “Once infection occurs, the damage may already be done.”

Funding: Support for this research was provided in part by grants from the National Institutes of Health (P01AI132132, R01AI153130, P30EY016665, and P50HD105353).

Published in journal: Nature Communications

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

Authors: Karla K. Ausderau, Ben Boerigter, Elaina R. Razo, Jake Gutkes, Nicholas P. Krabbe, Ann M. Mitzey, Shannon Walsh, Viktorie Menna, John R. Drew Jr, Sabrina Kabakov, Finn Eckes, Rachel V. Spanton, Anika Shah, Angelica Sun, Alex Katz, Charlene Kim, Amy Hartman, Andrea M. Weiler, Carol Rasmussen, T. Michael Nork, Puja Basu, Heather A. Simmons, James Ver Hoeve, Saverio Capuano, Matthew T. Aliota, Thomas C. Friedrich, and Emma L. Mohr

Source/CreditUniversity of Wisconsin–Madison | Jenn Bal

Edited by: Scientific Frontline

Reference Number: vi060426_01

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