The Zika virus destroys cells that give rise to the brain cortex in the developing fetus, scientists reported Friday.
The Zika virus destroys cells that give rise to the brain cortex in the developing fetus, scientists reported Friday.
The finding, published in the journal Cell Stem Cell, may help explain how the virus might cause microcephaly, or unusually small heads, in infants whose mothers are infected during pregnancy.
“It’s an important advance and a step forward to clearly demonstrate that the virus kills brain cells,” said Dr. Mark R. Schleiss, the director of pediatric infectious diseases and immunology at the University of Minnesota Medical School, who was not involved in the study.
But other experts cautioned that it was conducted with cells cultured in a laboratory and may not reflect the virus’s effects in humans.
“It might be that the results wouldn’t be the same in a living system of actual cortical stem cells,” said Dr. Catherine Y. Spong, the acting director of the National Institute of Child Health and Human Development.
“The act of culturing these cells to evaluate them in an in vitro system may make them more susceptible to infection,” she said.
In their experiments, researchers at Johns Hopkins and elsewhere cultured cells that eventually form the cortex, the outer layer responsible for many higher functions, of the fetal brain.
In the laboratory, the scientists exposed the so-called cortical neural progenitor cells to the Zika virus, along with two other types of cells present in early fetal development. Three days after exposure, 90 percent of the progenitor cells were infected, while the two other types were much less compromised.
“We found the cell types responsible for forming the cortex are the target of the Zika virus,” said Hongjun Song, a senior author of the new paper and a professor of neurology and neuroscience at Johns Hopkins University School of Medicine.
Infected cortical neural progenitor cells were unable to divide normally and died more often, the researchers found. The number of viable cells decreased 72 hours after infection, compared with those not infected with the Zika virus.
Dr. William B. Dobyns, a pediatric neurologist at Seattle Children’s Research Institute, called the new paper “highly significant.”
If the cells that should form the brain’s cortex in a fetus “aren’t growing fast enough,” he said, “you get a small brain, but on top of that there’s cell death, which means whatever the size the brain is, it will shrink.” That reduction may lead to a conspicuous space between the skull and brain.
Dobyns recently reviewed the brain scans of infants with microcephaly in Brazil.
“This paper fits like a glove what I’m seeing on the brain scans,” Dobyns said, including abnormalities like an unusual space between severely shrunken brains and the inner skull, and a relatively smooth brain surface.
But the new study does not prove that the Zika virus is responsible for a reported increase in microcephaly in Brazil. Experts await more convincing evidence from a study of roughly 5,000 pregnant women, mostly in Colombia, who all were infected with the Zika virus early in their pregnancies.
The World Health Organization does not expect the results from that study until June at the earliest.
Sara Cherry, an associate professor of microbiology at the University of Pennsylvania, called the new study “really important” but noted that Song and his colleagues “used a virus strain that’s quite distinct from what is circulating in Latin America.”
The research team, which includes scientists from Florida State University and Emory, nonetheless believes its experimental model can help explain how Zika affects nervous system development and can help provide a way to screen drugs that may “stop the entry of the virus into these brain cells,” said Dr. Guo-li Ming, a senior author of the study and a neurology professor at Johns Hopkins.
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