Johns Hopkins researchers say that in early pregnancy in mice with complete immune systems, Zika virus can cross the placenta – intended to protect the developing fetus – and appears to lead to a high percentage of miscarriages and to babies born with thin brain tissue and inflammation in brain cells.
By administering Zika virus directly into the reproductive tract of pregnant mice that have an intact immune system, the researchers found that the Zika virus appears to create disorganization in the cellular layers of the placenta that keep toxins, bacteria and viruses from crossing. This disorganization could be how the virus penetrates the placenta to infect the fetus. The researchers also discovered a mechanism by which Zika may be keeping antiviral proteins in the body from doing their job of protecting cells from the virus.
These findings, published February 21 in Nature Communications, put scientists one step closer to developing targets for vaccines or other treatments for Zika. Currently there is no cure or treatment for the virus, which has been linked to serious neurological problems in infants whose mothers were exposed in early pregnancy. For much of 2016, Zika was considered a public health emergency by the World Health Organization.
“We need to find a way to stop transmission of Zika through the placenta into the fetus, because that is where the damage is being done,” says study co-leader Dr. Sabra L. Klein, an immunologist and microbiologist at the Johns Hopkins Bloomberg School of Public Health. “In the placentas of our mice, we’re seeing a defense against Zika being mounted, but falling short, especially in early pregnancy, a time that corresponds to the first trimester in humans.”