New Study May Explain How Zika Virus Causes Microcephaly
One question underlies the race for a Zika vaccine: What is this virus, exactly, and how does it work? A new paper in the journal Cell Host & Microbe takes us one step closer to understanding by illuminating the relationship between Zika infection and microcephaly.
Babies with the congenital condition called microcephaly are born with unusually small heads and often have difficulties with brain development. Women who become infected with Zika virus while pregnant are at risk for transmitting the virus to their infants, who may be at higher risk for microcephaly. But just how Zika causes microcephaly has remained something of a puzzle.
To take a closer look, researchers at Stanford University cultured human stem cells in petri dishes and infected them with the virus. As the cells developed into embryos, the team was able to monitor exactly what went wrong with which cells.
Previous studies had focused on neural progenitor cells, which eventually grow into the nervous system. The Stanford team found a vital element in a second type of cell: cranial neural crest cells (CNCC). But where neural progenitor cells are easily killed off by the virus, cranial neural crest cells responded quite differently, secreting two kinds of cytokines, or inflammatory immune response signaling molecules, in reaction to the presence of the virus. That triggered the growth of more new neural cells—and sent the process of brain and skull development off the rails. Some cells split prematurely, and others died. The virus effectively interfered by confusing communication—or "crosstalk," as the researchers describe it—between cranial neural crest cells and neural progenitor cells.
"Our results suggest that CNCC infection by ZIKV may contribute to associated embryopathies through signaling crosstalk between developing face and brain structures," they write.
Co-senior author Joanna Wysocka is a chemical and systems biologist at the Stanford University School of Medicine. She says it’s possible that the virus is affecting still other cell types in addition to these two.
“Neural crest cells are one example,” she said in a press statement, “but such mechanisms may also be relevant to other tissues that come in contact with the developing brain during head formation and could be infected by Zika virus.”
Wysocka emphasized that microcephaly is a congenital issue and not a risk for adults who contract the virus.
The team’s findings are “remarkable,” physician Larry Brilliant tells mental_floss. (Brilliant was unaffiliated with the study.) The notion of crosstalk between the cell types is “phenomenally important,” he said, because “they lead to questions of [whether] therapeutic interventions might be possible even after the virus is transmitted.”
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