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, at least in mice.
Mice are not little people, of course, or every disease would have been cured by now and every chemical would be toxic, but it's a starting point for understanding the role of zika in birth defects beyond vague epidemiology.
The researchers administered Zika virus directly into the reproductive tract of pregnant mice that have an intact immune system, and 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.
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.
Nearly 94 percent of all pregnancies remained viable when a mock infection was introduced during the first trimester, while the viability of fetuses after Zika infection was reduced, regardless of which strain was used. Viability ranged from 56 percent from infection with the Brazil strain to 71 percent following infection with the Nigeria strain. That means anywhere from 29 to 44 percent of pregnancies were lost following infection. Since miscarriages can be caused by a multitude of factors, this Zika connection was not previously known. When the researchers infected the mice in the equivalent of the late second trimester instead, however, many fewer miscarriages occurred, suggesting that there is less vulnerability to Zika later in pregnancy.
The researchers also could see the activation of antiviral defenses in the placentas of pregnant mice infected with virus. To cause an infection, viruses work like a lock and key, attaching to specific receptors on cells to take hold and spread. The researchers identified receptors on cells in the placenta that the virus may use to cross into the fetus. These anti-viral pathways could be potential targets for treatments that could stop transmission, the researchers say.
Meghan S. Vermillion; Jun Lei; Yahya Shabi; Victoria K. Baxter; Nathan P. Crilly; Michael McLane; Diane E. Griffin; Andrew Pekosz; Sabra L. Klein and Irina Burd, "Intrauterine Zika virus infection of pregnancy immunocompetent mice models transplacental transmission and adverse perinatal outcomes", Nature Communications
