Zika virus (ZIKV) is associated with severe neurodeve- lopmental impairments in human fetuses, including microencephaly. Previous reports examining neural progenitor tropism of ZIKV in organoid and animal models did not address whether the virus infects all neural progenitors uniformly. To explore this, ZIKV was injected into the neural tube of 2-day-old chicken embryos, resulting in nonuniform periventricular infec- tion 3 days later. Recurrent foci of intense infection were present at specific signaling centers that influ- ence neuroepithelial patterning at a distance through secretion of morphogens. ZIKV infection reduced transcript levels for 3 morphogens, SHH, BMP7, and FGF8 expressed at the midbrain basal plate, hypotha- lamic floor plate, and isthmus, respectively. Levels of Patched1, a SHH-pathway downstream gene, were also reduced, and a SHH-dependent cell popula- tion in the ventral midbrain was shifted in position. Thus, the diminishment of signaling centers through ZIKV-mediated apoptosis may yield broader, non- cell-autonomous changes in brain patterning.


This is the publishers version of Thawani A, Sirohi D, Kuhn RJ, Fekete DM. Zika Virus Can Strongly Infect and Disrupt Secondary Organizers in the Ventricular Zone of the Embryonic Chicken Brain. Cell Rep. 2018 Apr 17;23(3):692-700. doi: 10.1016/j.celrep.2018.03.080.

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