(CN) — For the first time, researchers have documented the brain development damage caused by a Zika virus infection during pregnancy, which could be crucial to testing therapeutic interventions.
In findings published Monday in the journal Nature Medicine, the researchers detailed their observations after infecting a nonhuman primate with Zika.
The team’s experiment adds more evidence to the growing body of research linking Zika to congenital brain disorders, essentially proving a definitive connection between the mosquito-borne virus and conditions like microcephaly — a condition that results in babies born with abnormally small heads and potential brain damage.
“Our results remove any lingering doubt that the Zika virus is incredibly dangerous to the developing fetus and provides details as to how the brain injury develops,” Kristina Adams Waldorf, the lead author of the study, said.
Adams Waldorf, a researcher at the University of Washington who specializes in maternal and fetal infections, said the findings can be valuable in the ongoing search for safe and effective treatments of Zika infections.
“This study brings us closer to determining if a Zika vaccine or therapy will prevent fetal brain injury, but also be safe to take in pregnancy,” she said.
Study co-author Michael Gale Jr. explained that the findings met Koch’s Postulate, which establishes the criteria for determining if a microorganism is a direct cause of a disease or disorder.
“This is the only direct evidence that shows that the Zika virus can cross the placenta late in pregnancy and affect the fetal brain by shutting down certain aspects of brain development,” he said.
Primates — including humans — share many features of brain development and pregnancy, like the structure of the placenta, the timing of nerve and brain development, as well as the resulting proportions of gray and white matter in the brain.
No previous experiments on animal models closely matched the effects of Zika infection during human pregnancy. The virus can cause fetal demise in mice, but mouse models have not enabled medical researchers to analyze the causal relationships between Zika infection and fetal brain disorders.
“We were shocked when we saw the first MRI of the fetal brain 10 days after viral inoculation. We had not predicted that such a large area of the fetal brain would be damaged so quickly,” study co-author Lakshmi Rajagopal said.
“By the time a pregnant woman develops symptoms, the fetal brain may already be affected and damaged.”
Zika is unique from other flaviviruses — a group of insect-carried viruses that cause illness — as the virus generally leads to mild symptoms in adults including fever, rash and muscle aches. About 20 percent of infected adults don’t experience symptoms at all.
However, contracting Zika during pregnancy can lead to congenital disorders that can destroy a fetal brain or prevent it from developing.
The study took place during equivalent of the third trimester of a human pregnancy, and the amount of the virus administered in the study was approximately equivalent to what a person might contract from a bite by an infected mosquito. The pregnant primate did not show any significant symptoms of infection.
The white matter of the fetal brain, which is important for coordinating communication between different parts of the brain, stopped growing roughly three weeks after viral infection. If the study had continued another month with the same trajectory of brain growth, microcephaly would have occurred.
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