CONTEXT: -Pathology studies have been important in concluding that Zika virus 
infection occurring in pregnant women can result in vertical transmission of the 
agent from mother to fetus. Fetal and infant autopsies have provided crucial 
direct evidence that Zika virus can infect an unborn child, resulting in 
microcephaly, other malformations, and, in some cases, death.
OBJECTIVE: -To better understand the etiologic role and mechanism(s) of Zika 
virus in causing birth defects such as microcephaly, this communication analyzes 
the spectrum of clinical and autopsy studies reported from fetuses and infants 
who developed intrauterine Zika virus infection, and compares these findings 
with experimental data related to Zika virus infection.
DESIGN: -Retrospective analysis of reported clinical, autopsy, pathology, and 
related postmortem studies from 9 fetuses and infants with intrauterine Zika 
virus infection and microcephaly.
RESULTS: -All fetuses and infants examined demonstrated an overlapping spectrum 
of gross and microscopic neuropathologic abnormalities. Direct cytopathic 
effects of infection by the Zika virus were confined to the brain; in cases 
where other organs were evaluated, no direct viral effects were identified.
CONCLUSIONS: -There is concordance of the spectrum of brain damage, reinforcing 
previous data indicating that the Zika virus has a strong predilection for cells 
of the fetal central nervous system following vertical transmission. The 
occurrence of additional congenital abnormalities suggests that intrauterine 
brain damage from Zika virus interferes with normal fetal development, resulting 
in fetal akinesia. Experimental in vitro and in vivo studies of Zika virus 
infection corroborate the human autopsy findings of neural specificity.