“It was known that the virus was getting into the placenta,” said Mehul Suthar, an assistant professor of pediatrics at Emory University School of Medicine and senior author of the new study. “But little was known about where the virus was replicating and in what cell type.”
The research team used cells from placenta donated by five non-infected women who had full-term births through C-sections at either Grady Memorial or Emory Midtown hospitals. The team found something surprising: the virus didn’t kill the cells that may protect against infection, called Hofbauer cells, which are made by the growing fetus. Zika continued to reproduce.
This could help explain why the first trimester and early second trimester are the most dangerous for Zika infection. The placenta simply isn’t developed enough at those stages to fend off an infection.
Still, researchers determined that resistance to Zika infection varied from donor to donor. That might help explain why not every woman who contracts Zika during her pregnancy has a baby affected by the virus.
“Not every pregnant woman who is infected by Zika transmits the virus to her fetus,” Suthar said in a statement. The mother’s genetics, her relative overall health, even when she got the disease might affect the probability of her baby getting Zika too.
“A better understanding of these factors could allow the design of preventive measures, and eventually antiviral therapies,” Suthar said.