Zika virus symposium: hope for the future
This morning, I attended a symposium on Zika virus research. As you have likely heard in the news, this virus has devastating neurodevelopmental consequences for gestating fetuses. However, this symposium gives me hope for the future – due to both advances in understanding how the virus affects cells and in possibilities for preventing the consequences of Zika infection on the brain.
The Zika virus impacts brain development. There are three major processes in cortical development – proliferation, migration and connection. Problems at each stage can lead to microcephaly, the primary defect seen in Zika-affected infants. A person with microcephaly has an abnormally small head, usually due to an abnormally small brain. Primary microcephaly can be caused by genetic or environmental factors, and many microcephalic genes are related to cell proliferation. The Zika virus targets neural stem cells over neurons and progenitor cells. Therefore, researchers are working out the mechanisms of the Zika virus’s effects on developing brains from multiple angles.
A common thread in the talks I saw (I confess I could not stay the whole time) was how Zika infection causes cell death and problems in the cell cycle. With these problems present, brain cells die or are not formed in the first place, leading to microcephaly. In Guo-li Ming’s talk, she showed that overexpression of NS2A, one of the 10 proteins expressed by the Zika virus, leads to decreased numbers of neural stem cells. By proteomic screen, they found that NS2A binds to several cell adhesion molecules. This is exciting because it provides an avenue for treatment. Cell adhesion molecules are important for setting up the overall structure and polarity of the developing brain that allows newly born brain cells to migrate properly. Without them, disorganization reigns and the brain does not form properly. They investigated the potential for myricetin, a known protease inhibitor for dengue virus, to alleviate Zika infection. They found that myricetin treatment reduced the spread of Zika infection in the brains of mice! This is exciting – there might be a treatment avenue here!
Much work remains to be done to elucidate the mechanisms of Zika infection, especially in the fetal brain. We still do not know how the Zika virus crosses the placenta and the blood-brain barrier to create the devastating microcephaly seen in humans. Yet, this symposium gives me confidence that tenacious scientists are working hard to figure it out.
P Garcez et al, 217, Sci Reports. Zika virus disrupts molecular fingerprinting of human neurospheres. https://www.nature.com/articles/srep40780?WT.feed_name=subjects_microbiology
CDC page on the Zika virus. https://www.cdc.gov/zika/hc-providers/infants-children/zika-syndrome-birth-defects.html
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