Growth of Zika virus in Brain Stem Cells Implies Involvement in Microcephaly

Infected hNPCs further released infectious ZIKV particles. ZIKV infection increased cell death and disrupted cell-cycle progression, resulting in attenuated hNPC growth.

Global gene expression analysis of infected hNPCs revealed transcriptional dysregulation, notably of cell-cycle-related pathways.

The results of this study point to hNPCs as being directly targeted by ZIKV. Furthermore, they describe an experimental model system to investigate the impact and mechanism of ZIKV on human brain development and provide a platform to screen therapeutic compounds.

“Studies of fetuses and babies with the telltale small brains and heads of microcephaly in Zika-affected areas have found abnormalities in the cortex, and Zika virus has been found in the fetal tissue,” said senior author Dr. Guo-li Ming, professor of neurology, neuroscience, psychiatry, and behavioral science at Johns Hopkins University. “While this study does not definitely prove that Zika virus causes microcephaly, it is very telling that the cells that form the cortex are potentially susceptible to the virus, and their growth could be disrupted by the virus.”

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