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Infectivity of Immature Neurons to Zika Virus: A Link to Congenital Zika Syndrome
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文摘

The mechanism of Zika virus-mediated microcephaly is explored using infected undifferentiated, partially differentiated and terminally differentiated neuroblastoma cell lines.

Undifferentiated, progenitor neurons, as well as partially differentiated cells representative of an early developing fetal brain, were highly permissive to Zika virus In contrast, terminally differentiated neurons, representative of an adult brain, were highly resistant to Zika virus.

This study shows the differential susceptibilities of immature versus mature neurons and may shed light on the development of microcephaly in early prenatal fetuses and Guillain-Barré syndrome in adult humans exposed to Zika virus.

Cases of babies born with small head size (known as microcephaly) in the Zika virus infected areas of Brazil have created fear at a global scale. Generally, people wonder why Zika would cause small brain size in newborns whose mothers have been infected with the virus but do not have any apparent brain illness. This study explains the reasons behind such reported observations. We found that Zika virus primarily kills, or damages, brain cells that are growing very fast and are still immature, whereas, it has no effect on mature neurons found in an adult brain.

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