Emory researchers show how Zika may infect placenta, fetus

The placenta is supposed to help nourish a fetus in utero, get rid of waste and protect the growing embryo from infection.

But with the Zika virus, the placenta doesn’t shield a fetus from the disease; instead it appears to help the disease grow and travel to the developing fetus’s brain.

This is the finding of a new study by Emory University researchers, who are trying to determine exactly how the virus makes its way into fetal neural cells causing horrible birth defects.

Only a few viruses can make their way past the placental wall and go on to infect a growing fetus: rubella, HIV, herpes and hepatitis B and C. Zika joins that list. According to the Emory study published today in the scientific journal Cell Host Microbe, the virus infects immune cells in the outer portion of the placenta and grows there. As the virus replicates, it doesn’t kill the cell, but somehow moves from those cells to the innermost portion of the fetal compartment.

Researchers are still trying to figure out the exact mechanism the virus uses to get from those outer cells to the compartment. Determining that will help in the race to develop a vaccine for the only known mosquito-borne virus that causes severe birth defects. But the Emory researchers believe they have identified the type of cells in the placenta that are most likely to harbor the virus and set up a devastating chain of events.

“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.