Scientists around the world have been struggling to prove Zika’s link to microcephaly. Epidemiological data, which shows a correlation between the number of Zika infections and the number of microcephaly cases, only says so much. What is needed is a verifiable biological mechanism that links the virus to the shrinking of newborns’ brains.
Here’s what we know about that suspected link. In 2015, Brazil saw a big uptick in Zika infections. Though the disease is mostly benign in adults, there was a corresponding uptick in the number of children born with microcephaly. The country has confirmed some 640 cases since October, and it still has some 4,000 suspected cases to examine.
Microcephaly causes newborns to have abnormally small brains, which often leaves them with cognitive and physical disabilities. In rare cases, it can also lead to an early death. (Researchers now suspect that Zika may be linked to other fatal birth defects, too.)
Zika’s relationship with birth defects prompted the World Health Organization to declare a public health emergency last month—it is important that researchers now prove that the link is there. Two pieces of evidence have strengthened their convictions.
First, the Zika virus has been found a few times in the placenta and amniotic fluid (in which the baby floats in a mother’s womb) in microcephaly cases. Second, the virus was recently also found in the brain tissue of a microcephaly baby that died just after birth. Now, in a lab study on human cells, researchers from Florida State University have found the strongest evidence yet that Zika may indeed cause microcephaly.
The researchers started with pluripotent stem cells, which have the ability to convert into any kind of human cell. They then converted them into neural progenitor cells, which is the stage before cells become neurons—that is, brain cells. At this crucial step, the researchers infected some of the cells with the Zika virus and left others alone.
They report in Cell Stem Cell that difference was stark. The virus readily infected neural progenitor cells and spread to as many as 90% of all cells in those samples. After three days, around a third of cells died or couldn’t convert into healthy neurons. This is still not definitive evidence that the microcephaly is caused by the Zika virus, but it brings us a step closer.
Many unanswered questions remain. For instance, we don’t know yet what levels of exposure to the virus makes brain cells go haywire. The Florida State researchers’ results will also need to hold for cells in the human brain instead of just in a Petri dish. But, as Sika Zheng of the University of California, Riverside, puts it, “this is a timely report in searching for directions of targeted therapy.”