Washington | The Zika virus infects a type of neural stem cell that gives rise to the brain’s cerebral cortex and turns them into viral replication factories, according to a new study that may help find the link between the virus and incomplete brain development.
On laboratory dishes, these stem cells were found to be havens for viral reproduction, resulting in cell death and disruption of cell growth. While this study does not prove the direct link between Zika and microcephaly, it pinpoints where the virus may be doing the most damage, researchers said.
The research, led by Guo-li Ming and Hongjun Song of the Johns Hopkins University School of Medicine and Hengli Tang of Florida State University in US, provides a new platform to learn about the Zika virus using neuronal cells derived from human induced pluripotent stem cells.
In future, the researchers hope to grow mini-brains from the stem cells to observe the long-term effects of Zika infection on neural tissue and to screen for potential therapeutics. 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, said Song. As humans are typically infected by Zika virus carried by mosquitoes, the researchers also grew their Zika virus stock in mosquito cells for a few days before applying the virus onto the human cells.
One concerning discovery was that the stem cells that Zika was found to infect, called cortical neural precursors, become factories for viral replication. From a single infection, the virus particles spread through a plate of stem cells within a span of three days. 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 Ming.
So a very important question that emerges from our work is whether the Zika virus specifically targets the neural progenitor mostly responsible for generating the cortex, Ming said. We are trying to fill the knowledge gap between the infection and potential neurological defects, said first author Tang.
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