Pregnant women are at higher risk of complications caused by the spreading Zika virus. One of the dreaded complications is giving birth to an infant with microcephaly. Though the link between the two is being established by various groups of health agencies and experts, a team of U.S. scientists may have the answer to how the virus destroys cells important to fetal brain development.
A new study by researchers from Johns Hopkins University School of Medicine and Emory University sheds light on the biology and possible physiology behind Zika, a virus that has been linked to babies born with abnormally smaller heads. The virus infects a type of neural stem cell from where the brain's outer layer called cerebral cortex emerges. This prevents these cells from dividing and growing into new brain cells.
Published in the journal Cell Stem Cell, the study involved laboratory experiments wherein the scientists used petri dishes. Researchers found that virus infects these stem cells, resulting in cell death and disruption of cell growth.
"This is a first step, and there's a lot more that needs to be done," said Hongjun Song, a neuroscientist and stem cell biologist at Johns Hopkins University School of Medicine.
"What we show is that the Zika virus infects neuronal cells in dish that are counterparts to those that form the cortex during human brain development," he added.
Though no known evidence shows what is really happening in the developing baby in the womb, the findings may point out to altered development of the brain as one mechanism that leads to microcephaly. The direct link between Zika virus and microcephaly, however, will more likely come from clinical studies.
In the laboratory, the researchers grew cortical neural progenitor cells, the stem cells involved in the development of the brain's cortex. They also grew other cell types including pluripotent stem cells and immature neurons. They exposed all three cell types to Zika virus and analyzed the results.
90 Percent Of Cortical Stem Cells Got Infected
They found that 90 percent of the cortical neural progenitor cells were infected in just three days of exposure to the virus. The virus attacked the cells and used them to produce more viruses.
Notably, the genes needed to fight the virus have not been switched on, leading to infected cells dying. Most of the infected cells died and others showed disruption in genes responsible in cell division. This may lead to formation of new cells that are ineffectively produced.
"There are case reports for the Zika virus where they show that certain brain areas appear to have developed normally, but it is mostly the cortical structures that are missing," said Guo-li Ming from Johns Hopkins' Institute for Cell Engineering.
Now that scientists have identified that the cortical neural progenitor cells are the targets of the virus, these can be used to screen potential treatment options for Zika virus infection to measure effectiveness and potency.
In the United States alone, there are already 153 travel-associated Zika virus disease cases. However, in other U.S. territories, there are now 107 locally acquired cases and one travel-associated case.