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

PubMed ID: 41605918

Author(s): Ausderau KK, Boerigter B, Razo ER, Gutkes J, Krabbe NP, Mitzey AM, Walsh S, Menna V, Drew JR Jr, Kabakov S, Eckes F, Spanton RV, Shah A, Sun A, Katz A, Kim C, Hartman A, Weiler AM, Rasmussen C, Nork TM, Basu P, Simmons HA, Ver Hoeve J, Capuano S, Aliota MT, Friedrich TC, Mohr EL. Prenatal Zika virus exposure disrupts social-emotional development and cortical visual function in infant macaques. Nat Commun. 2026 Jan 29. doi: 10.1038/s41467-026-68517-x. Online ahead of print. PMID 41605918

Journal: Nature Communications, Jan 2026

Prenatal Zika virus (ZIKV) exposure can result in outcomes ranging from severe birth defects to subtle developmental delays, yet the underlying mechanisms remain unclear. Using a translational rhesus macaque model, we assess visual, auditory, and neurodevelopmental outcomes through 12 months of age following first-trimester ZIKV inoculation. Pregnant macaques, either flavivirus-naive or with prior dengue virus (DENV) exposure, are inoculated with Asian or African ZIKV lineages. Maternal viremia duration, placental viral burden, and neutralizing antibody titers vary but are not associated with developmental outcomes. At 12 months, ZIKV-exposed infants exhibit altered maternal attachment behaviors and reduced inhibition toward novel sensory stimuli. Visual evoked potentials are impaired at 3 months but normalize by 12 months; hearing loss is more frequent but not statistically significant. These outcomes are driven by ZIKV exposure itself, independent of maternal infection characteristics. Our findings highlight the limitations of maternal biomarkers in risk prediction and support incorporating infant-focused developmental outcomes in studies of maternal interventions.