A pair of studies, one published in the journal Cell and the other in Nature, could help scientists better understand the mosquito-borne infection and develop vaccines to prevent it.
"This is the first demonstration in an animal model of in utero transmission of Zika virus, and it shows some of the same outcomes we've been seeing in women and infants," said Michael Diamond, a professor of medicine, molecular microbiology and pathology and immunology at Washington University in St. Louis and co-senior author of the study in Cell.
In one of the experiments, researchers used pregnant mice that were genetically engineered to lack the ability fight off Zika.
The virus killed most fetuses within a week, the study found. Offspring that survived had severely stunted growth.
In another experiment using genetically normal mice, the fetuses did not die but showed impaired growth and neuron damage.
In neither experiment did the mice develop microcephaly, but researchers said this could come down to biological differences between people and mice.
"Unlike in humans, a significant amount of neurodevelopment in mice actually occurs after birth, especially in the cerebral cortex, which is the part of the brain damaged in microcephaly," Diamond said.
But researchers were particularly intrigued by the way Zika expanded inside the placenta, an organ that develops inside the uterus during pregnancy and nourishes the fetus.
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